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Determinants of the Degree of Functional Mitral Regurgitation in Patients With Systolic Left Ventricular Dysfunction: A Quantitative Clinical Study
Abstract
Functional mitral regurgitation (FMR) occurs with a structurally normal valve as a complication of systolic left ventricular dysfunction (LVD). Determinants of degree of FMR are poorly defined; thus, mechanistic therapeutic approaches to FMR are hindered.
In a prospective study of 21 control subjects and 128 patients with LVD (defined as ejection fraction <50%, mean 31+/-9%) in sinus rhythm, we quantified simultaneously by echocardiography the effective regurgitant orifice (ERO) of FMR by using 2 methods: mitral deformation (valve and annulus) and left ventricular (LV) global (volumes, stress, function, and sphericity) and local (papillary muscle displacements and regional wall motion index) remodeling. A wide range of ERO (15+/-14 mm(2), 0 to 87 mm(2)) was observed, unrelated to ejection fraction (P:=0.32). The major determinant of ERO was mitral deformation, ie, systolic valvular tenting and annular contraction in univariate (r=0.74 and r=-0.61, respectively; both P:<0.0001) and multivariate (both P:<0. 0001) analyses, independent of global LV remodeling. Systolic valvular tenting was strongly determined by local LV alterations, particularly apical (r=0.75) and posterior (r=0.70) displacement of papillary muscle, with confirmation in multivariate analysis (both P:<0.0001), independent of LV volumes, function, and sphericity.
The presence and degree of FMR complicating LVD are unrelated to the severity of LVD. Local LV remodeling (apical and posterior displacement of papillary muscles) leads to excess valvular tenting independent of global LV remodeling. In turn, excess tenting and loss of systolic annular contraction are associated with larger EROs. These determinants of FMR warrant consideration for specific approaches to the treatment of FMR complicating LVD.
... Patients with myocardial infarction (MI) frequently experience left ventricular (LV) dilation and adverse remodelling, resulting in mitral complex incompetence and ultimately leading to mitral regurgitation (MR) [1][2][3] . The incidence rate of moderate or severe ischaemic MR (IMR) in this patient population is reported greater than 10% [4] . ...
... Any disagreements regarding the final included studies were resolved through discussion and consensus. The selection criteria were [1] : studies using an RCT design [2] , studies assessing patients with a diagnosis of moderate IMR, and [3] studies reporting at least one primary outcome. Studies were excluded if [1] included patients with mixed MR etiologies [2] , had no available data for analysis, or [3] did not include combined CABG. ...
... The selection criteria were [1] : studies using an RCT design [2] , studies assessing patients with a diagnosis of moderate IMR, and [3] studies reporting at least one primary outcome. Studies were excluded if [1] included patients with mixed MR etiologies [2] , had no available data for analysis, or [3] did not include combined CABG. ...
Background
The efficacy of mitral valve repair (MVR) in combination with coronary artery bypass grafting (CABG) for moderate ischaemic mitral regurgitation (IMR) remains unclear. To evaluate whether MVR + CABG is superior to CABG alone, the authors conducted a systematic review and meta-analysis of existing randomized controlled trials (RCTs).
Methods
The authors searched PubMed, Web of Science, and the Cochrane Central Register of Controlled Trials for eligible RCTs from the date of their inception to October 2023. The primary outcomes were operative (in-hospital or within 30 days) and long-term (≥ 1 year) mortality. The secondary outcomes were postoperative stroke, worsening renal function (WRF), and reoperation for bleeding or tamponade. The authors performed random-effects meta-analyses and reported the results as risk ratios (RRs) with 95% CIs.
Results
Six RCTs were eligible for inclusion. Compared with CABG alone, MVR + CABG did not increase the risk of operative mortality (RR, 1.244; 95% CI, 0.514–3.014); however, it was also not associated with a lower risk of long-term mortality (RR, 0.676; 95% CI, 0.417–1.097). Meanwhile, there was no difference between the two groups in terms of postoperative stroke (RR, 2.425; 95% CI, 0.743–7.915), WRF (RR, 1.257; 95% CI, 0.533–2.964), and reoperation for bleeding or tamponade (RR, 1.667; 95% CI, 0.527–5.270).
Conclusions
The findings of this meta-analysis suggest that MVR + CABG fails to improve the clinical outcomes of patients with moderate IMR compared to CABG alone.
... Mitral annulus diameter was measured in parasternal long-axis view at end-diastole. 19 Tenting area was measured as the area enclosed by the annular plane and two leaflets in parasternal long-axis view at the time of maximal MV closure in mid-systole as previously reported 19 ; coaptation height was measured as the minimum distance between mitral leaflet coaptation and the mitral annular plane as well. Comprehensive TTE was performed by multiple credentialed sonographers according to usual clinical practice. ...
... Mitral annulus diameter was measured in parasternal long-axis view at end-diastole. 19 Tenting area was measured as the area enclosed by the annular plane and two leaflets in parasternal long-axis view at the time of maximal MV closure in mid-systole as previously reported 19 ; coaptation height was measured as the minimum distance between mitral leaflet coaptation and the mitral annular plane as well. Comprehensive TTE was performed by multiple credentialed sonographers according to usual clinical practice. ...
... 23 In patients with functional MR, who had reduced LV function and mitral annulus enlargement, increased systolic LV pressure caused by critical AS might play a major role in improvement in functional MR after AVR. 19 Because functional MR severity is easily impacted by haemodynamic status, its improvement has been expected after AVR. 20,22 Mitral annulus enlargement would cause reduced mitral Figure 3 Cumulative survival according to MR improvement. ...
Aims:
Concurrent mitral regurgitation (MR) influences treatment considerations in patients with severe aortic stenosis (sAS). Limited information exists regarding haemodynamic effects of sAS on MR severity and outcome of these patients. We assessed the impact of aortic valve replacement (AVR) on MR according to mechanism in patients with sAS and MR.
Methods and results:
In patients with sAS who received surgical or transcatheter AVR from 2008 to 2017, those with effective mitral regurgitant orifice area (ERO) ≥ 10 mm2 prior to AVR were evaluated. The change in MR after AVR was considered significant when there was at least one grade difference. We compared the all-cause mortality of patients with and without improvement in MR. Of 234 patients with sAS and MR (age 80 ± 9 years, 52% male, ERO 19 ± 7 mm2 ), organic and functional MR were present in 166 (71%) and 68 (29%), respectively. MR improved in 136 (58%); improvement occurred with similar frequency in organic versus functional MR (59% and 57%, P = 0.88). Associated determinants were absence of atrial fibrillation in organic MR [odds ratio (OR) 2.09, 95% confidence interval (CI) 1.00-4.37; P = 0.049] and indexed aortic valve area (iAVA) ≤ 0.40 cm2 in functional MR (OR 3.28, 95% CI 1.13-9.47; P = 0.028). In the overall cohort, mitral annulus diameter < 3 cm (OR 1.74, 95% CI 1.02-2.97; P = 0.041) and QRS duration < 115 ms (OR 1.73, 95% CI 1.00-2.98; P = 0.049) were independently associated with improvement in MR. During median follow-up of 3.5 years, lack of improvement in MR was not associated with higher mortality in the overall cohort of patients with ERO ≥ 20 mm2 [adjusted hazard ratio (HR) 1.71, 95% CI 0.90-3.27; P = 0.10, adjusted for age, New York Heart Association III or IV, diabetes, and creatinine ≥ 2.0 mg/dL]. Lack of improvement in organic MR was associated with higher mortality (adjusted HR 3.36, 95% CI 1.40-8.05; P < 0.01). In patients with functional MR, change in MR was not associated with mortality (HR 1.24, 95% CI 0.44-3.47; P = 0.68).
Conclusions:
In nearly 60% of patients with sAS and MR, MR improved after AVR, even in the majority of patients with organic MR. Absence of atrial fibrillation in organic MR, iAVA ≤ 0.40 cm2 in functional MR, and mitral annulus diameter < 3 cm and QRS duration < 115 ms in the overall population were associated with MR improvement. Post-operative improvement in organic MR was associated with better survival.
... This finding suggests that ischemic injury predominantly affects the dynamic properties of PPMs, rather than anatomical ones, as previously demonstrated in echocardiographic studies [25]. Papillary dysfunction, indeed, seems to be determined not only by the necrosis and fibrosis of PPMs, caused by direct ischemic damage, but also by the redistribution of myocardial wall tension forces due to concomitant ventricular wall motion abnormalities [26]. TTE, implemented by speckle tracking, may provide an objective and quantitative assessment of PPMs and MV apparatus with high reproducibility, as demonstrated in patients with mild to moderate rheumatic mitral stenosis. ...
... The detection of the ischemic involvement of PPMs and subpapillary regions of the LV wall could help to identify patients who are at risk of developing MVR [26,30]. ...
Papillary muscle (PPM) involvement in myocardial infarction (MI) increases the risk of secondary mitral valve regurgitation or PPM rupture and may be diagnosed using late gadolinium enhancement (LGE) imaging. The native T1-mapping (nT1) technique and PPM longitudinal strain (PPM-ls) have been used to identify PPM infarction (iPPM) without the use of the contrast agent. This study aimed to assess the diagnostic performance of nT1 and PPM-ls in the identification of iPPM. Forty-six patients, who performed CMR within 14–30 days after MI, were retrospectively enrolled: sixteen showed signs of iPPM on LGE images. nT1 values were measured within the infarcted area (IA), remote myocardium (RM), blood pool (BP), and anterolateral and posteromedial PPMs and compared using ANOVA. PPM-ls values have been assessed on cineMR images as the percentage of shortening between end-diastolic and end-systolic phases. Higher nT1 values and lower PPM-ls were found in infarcted compared to non-infarcted PPMs (nT1: 1219.3 ± 102.5 ms vs. 1052.2 ± 80.5 ms and 17.6 ± 6.3% vs. 21.6 ± 4.3%; p-value < 0.001 for both), with no significant differences between the nT1 of infarcted PPMs and IA and between the non-infarcted PPMs and RM. ROC analysis demonstrated an excellent discriminatory power for nT1 in detecting the iPPM (AUC = 0.874; 95% CI: 0.784–0.963; p < 0.001). nT1 and PPM-ls are valid tools in assessing iPPM with the advantage of avoiding contrast media administration.
... The abnormal function of the LV inferior-posterior-lateral region or the LV remodeling due to myocardial infarction cause a posterior-lateral and apical displacement of the posterior papillary muscle thereby increasing the tethering forces. [10,11] Moderate FMR is common in patients needing myocardial revascularization, ranging from 10 to 50% [12]. In the most recent years, the usefulness of addressing moderate functional regurgitation concomitantly to CABG has been questioned: many observational studies and a randomized clinical trial of Cardiothoracic Surgical Trials Network (CTSN) showed the benefits of mitral valve repair during CABG by lowering the incidence or recurrence of MR [13,14], that came at the cost of an increasing rate of adverse neurologic events, longer Intensive Care Unit (ICU) stay and supraventricular arrhytmias [15][16][17]. ...
... Although very precise and useful for research purposes, this formula is too complex to be used in the daily clinical practice. Therefore, we have simplified it as a ratio between anterior and posterior straight length, measured from the apical fourchambers view at transthoracic echocardiography [10]. ...
Introduction
The treatment of moderate functionalmitral regurgitation (FMR) during coronary artery bypass grafting (CABG) is still debated. Our primary end point was to assess the improvement of “mitral valve reserve” (MVR) after CABG alone as a clinical demonstration of left ventricular (LV) recovery.
Materials and methods
Between June 2019 and June 2021, we prospectively enrolled 104 consecutive patients undergoing CABG with moderate FMR. Inclusion criteria were inferior-posterior-lateral wall hypokinesia and revascularization of the circumflex or right coronary artery. MVR was calculated as the ratio between anterior and posterior leaflets’ straight length. All patients were followed for 1 year. The improvement of MVR has been considered as a reduction of the ratio between anterior and posterior leaflets straight length.
Results
Compared to baseline, mean MVR was significantly reduced both at 6 (2.24 ± 0.95 vs. 1,91 ± 0.6; p = 0,047) and 12 months follow-up (2.24 ± 0.95 vs. 1,69 ± 0.49; p = 0,006). Left ventricular (LV) reverse remodeling, meant as improvement of LV ejection fraction and reduction of LV end-systolic volume index and mitral anulus diameter were evaluated at 6 months and 1 year. Mitral regurgitation grade were also significantly reduced at 6 months (p < .001).
Conclusion
The benefits of myocardial revascularization in term of improvement of mitral regurgitation’s degree can be explained by the changes of MVR. The patients with FMR, who could have more advantages from CABG alone, should be the ones who have LVESVi just moderately increased.
... Secondary or functional mitral regurgitation (MR) is due to changes in the geometry of the left ventricle (LV) secondary to ventricular dysfunction. 1 It occurs when an ischemic heart disease or a dilated cardiomyopathy of any etiology causes dilation of the LV, dilation of the mitral ring, and/ or displacement of the papillary muscle, resulting in poor coaptation of the valve cusps and valve regurgitation. 2 the American Heart Association indicates that 16,250 per million North Americans have secondary MR, 3,4 totaling more than 5 million cases in the United States of America alone, and this number is estimated to be even greater due to the continued growth and aging of the population. This is noteworthy, as secondary MR causes a poor prognosis and is an independent predictor of mortality. ...
... In MITRA-FR, the mean ERO was 31 mm 2 , whereas COAPT had a mean ERO of 41 mm. 2 Although the inclusion criterion for both studies was MR with grade from moderate to severe, the COAPT study followed the North American recommendations of 2008, 14 which classifies moderate to severe MR when the ERO is ≥ 30 mm 2 and/or 45 mL RV; MITRA-FR followed the European recommendations of 2012: 15 ERO ≥ of 20 mm 2 and/or 30 mL RV classified as moderate to severe MR. This disagreement is based on the concept that mortality in patients with secondary MR is significantly higher for lower levels of ERO and RV. ...
... The erroneous assumption that the leaflet tethering in ischemic MR resulted from apical displacement of the papillary muscles was initially made due to the use of tethering lengths (2D parameters) in earlier studies to evaluate the 3D displacement of the muscles [6][7][8][9][10][11][12][13][14]. However, subsequent studies looking at the effect of LVEDD enlargement in ischemic MR with a 3D assessment challenged this notion. ...
Objective
Ischaemic secondary mitral regurgitation (ISMR) after surgery is due to the displacement of papillary muscles resulting from progressive enlargement of the left ventricle end-diastolic diameter (LVEDD). Our aim was to prove that if the interpapillary muscle distance (IPMD) is surgically stabilized, an increase in LVEDD will not lead to a recurrence of ischaemic mitral regurgitation (MR).
Methods
Ninety-six patients with ISMR, who underwent surgical revascularisation and annuloplasty, were randomly assigned in a 1:1 ratio to undergo papillary muscle approximation (PMA). At the 5-year follow-up, we assessed the correlation between PMA and echocardiographic improvements, the effect size of PMA on echocardiographic improvements, and a prediction model for recurrent MR using inferential tree analysis.
Results
There was a significant correlation between PMA and enhancements in both the α and β angles (Spearman’s rho > 0.7, p < 0.01). The α angle represents the angle between the annular plane and either the A2 annular-coaptation line or the P2 annular-coaptation line. The β angle indicates the angle between the annular plane and either the A2 annular-leaflet tip line or the P2 annular-leaflet tip line. PMA led to substantial improvements in LVEDD, tenting area, α and β angles, with a large effect size (Hedge’s g ≥ 8, 95% CI ORs ≠ 1). The most reliable predictor of recurrent MR grade was the interpapillary distance, as only patients with an interpapillary distance greater than 40 mm developed ≥ 3 + grade MR. For patients with an IPMD of 40 mm or less, the best predictor of recurrent MR grade was LVEDD. Among the patients, only those with LVEDD greater than 62 mm showed moderate (2+) MR, while only those with LVEDD less than or equal to 62 mm had absent to mild (1+) MR.
Conclusion
Prediction of recurrent ischaemic MR is not independent of progressive LVEDD increase. PMA-based surgical procedure stabilises IPMD.
... The tenting area is calculated by quantifying the triangular area between the mitral valve leaflets and the mitral annulus. Increased mitral tenting is associated with a more severe mitral valve deformation and consequent worsening MR. 49,50 Similarly, tenting volume has been demonstrated to have a significant association with the degree of regurgitation. 51,52 An additional simple measurement that renders the degree of distortion of the mitral valve is the tenting height (also known as coaptation height). ...
The mitral valve apparatus is a complex structure consisting of several coordinating components: the annulus, two leaflets, the chordae tendineae, and the papillary muscles. Due to the intricate interplay between the mitral valve and the left ventricle, a disease of the latter may influence the normal function of the former. As a consequence, valve insufficiency may arise despite the absence of organic valve disease. This is designated as functional or secondary mitral regurgitation, and it arises from a series of distortions to the valve components. This narrative review describes the normal anatomy and the pathophysiology behind the mitral valve changes in ischemic and non-ischemic dilated cardiomyopathies. It also explains the value of a complete multiparametric assessment of this structure. Not only must an assessment include quantitative measures of regurgitation, but also various anatomical parameters from the mitral apparatus and left ventricle, since they carry prognostic value and are predictors of mitral valve repair success and durability.
... [14][15][16][17] Digitized image datasets of baseline compre- The tenting height which was a distance between the mitral leaflet coaptation and mitral annulus plane at early systole was measured as displacement of the mitral coaptation toward the left ventricular apex. 18 where PSV AOV = aortic valve peak systolic velocity, AVA c = aortic valve area calculated using the continuity equation, and AoA = crosssectional area of the ascending aorta. 19 We calculated the Zva = (SAP + MG)/stroke volume index, where SAP is the systolic arterial pressure and MG is the mean transvalvular pressure gradient, as previously described. ...
Introduction
This study aimed to investigate the mechanisms and clinical implications of mitral regurgitation (MR) in patients with severe aortic stenosis (AS) who received transcatheter aortic valve replacement (TAVR).
Methods
We conducted retrospective echocardiographic analyses at baseline and 6 months after TAVR in 140 patients with symptomatic AS (85 ± 5 years) who underwent TAVR. We defined significant MR as ≥ moderate based on evaluation of transthoracic echocardiography (TTE).
Results
There were 48 patients (34%) with preexisting MR at the baseline. Among measured TTE parameters, end‐systolic wall stress (ESWS), mitral annulus area, and mitral valve thickening index were independent factors associated with preexisting MR (odds ratio [OR]: 1.013, 95% confidence interval [CI]: 1.005–1.021; OR: 1.740, 95% CI: 1.314–2.376; OR: 2.306, 95% CI: 1.426–3.848; respectively). Six months after TAVR, there were 34 patients with post‐existing MR, A history of atrial fibrillation and ESWS after TAVR were independent factors (OR: 3.013, 95% CI: 1.208–7.556; OR: 1.013, 95% CI: 1.000–1.023; respectively). The Kaplan–Meier plot indicated that preexisting MR was a risk factor for heart failure–related events within 1 year of discharge after TAVR ( p = .012).
Conclusions
In patients who underwent TAVR for severe AS, preexisting MR was associated with having a thickened mitral valve and large mitral annulus size induced by high ESWS. These patients may have worse prognosis after TAVR and should be closely monitored in the long term.
... IMR occurs due to ischemic myocardial changes despite unaltered mitral leaflets and chordae. LV remodeling and papillary muscle displacement are usually listed as factors playing an important role in its development [18,[29][30][31][32]. ...
Background:
Mitral regurgitation (MR) is frequently observed in patients with myocardial infarction (MI). However, the incidence of severe MR in contemporary population is unknown.
Aims:
The study evaluates the prevalence and prognostic impact of severe MR in contemporary population of patients with ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI).
Methods:
The study group consists of 8062 patients enrolled in the Polish Registry of Acute Coronary Syndromes over the years 2017‒2019. Only the patients with full echocardiography performed during the index hospitalization were eligible. Primary composite outcome was 12-month major adverse cardiac and cerebrovascular events (MACCE) (death, non-fatal MI, stroke and heart failure [HF] hospitalization) compared between patients with and without severe MR.
Results:
5561 NSTEMI patients and 2501 STEMI patients were enrolled into the study. Severe MR occurred in 66 (1.19%) NSTEMI patients and 30 (1.19%) STEMI patients. Multivariable regression models revealed that severe MR is an independent risk factor of all-cause death in 12-month observation (odds ratio [OR], 1.839; 95% confidence interval [CI], 1.012‒3.343; P = 0.046) in all MI patients. Patients with NSTEMI and severe MR had higher mortality (22.7% vs. 7.1%), HF rehospitalization rate (39.4% vs. 12.9%) and MACCE occurrence (54.5% vs. 29.3%). Severe MR was associated with higher mortality (20% vs. 6%) and higher HF rehospitalization (30% vs. 9.8%), stroke (10% vs. 0.8%) and MACCE rates (50% vs. 23.1%) in STEMI patients.
Conclusions:
Severe MR is associated with higher mortality and MACCE occurrence in patients with MI in 12-month follow-up. Severe MR is an independent risk factor of all-cause death.
... In a series of 128 patients, investigators found apical and posterior displacement of the PM to be an important determinant of MV tethering, which in turn, strongly correlates to MR severity (R ¼ 0.74, R < 0.001), even after multivariate adjustment. 21 Interestingly, isolated PM dysfunction induced experimentally through ligation of corresponding arteries does not lead to secondary MR. 22 Indeed, in a series of 40 patients with prior inferior MI, reduction in PM longitudinal contraction is associated with lesser MR, suggesting it may even be protective against secondary MR. ...
Secondary mitral regurgitation (MR) refers to MR resulting from left ventricular or left atrial remodeling. In ischemic or nonischemic cardiomyopathy, left ventricular dilation (regional or global) leads to papillary muscle displacement, tethering, and leaflet malcoaptation. In atrial functional MR, MR occurs in patients with left atrial dilation and altered mitral annular geometry due to atrial fibrillation. In addition to cardiac remodeling, leaflet remodeling is increasingly recognized. Mitral leaflet tissue actively adapts through leaflet growth to ensure adequate coaptation. Leaflets, however, can also undergo maladaptive thickening and fibrosis, leading to increased stiffness. The balance of cardiac and leaflet remodeling is a key determinant in the development of secondary MR. Clinical management starts with detection, severity grading, and identification of the underlying mechanism, which relies heavily on echocardiography. Treatment of secondary MR consists of guideline-directed medical therapy, surgical repair or replacement, and transcatheter edge-to-edge repair. Based on a better understanding of pathophysiology, novel percutaneous mitral repair and replacement devices have been developed and clinical trials are underway.
... Mitral leaflet tethering is the main lesion of SMR and results in a restriction of systolic leaflet motion (Carpentier type IIIb), due to the displacement of papillary muscles (PM) along a posterior, apical, or lateral vector. 12,13 PM displacement, in turn, moves the chordae tendineae away from the coaptation line. ...
Background
Mitral valve apparatus is complex and involves the mitral annulus, the leaflets, the chordae tendinae, the papillary muscles as well as the left atrial and ventricular myocardium. Secondary mitral regurgitation is a consequence of regional or global left ventricle remodeling due to an acute myocardial infarction (75% of cases) or idiopathic dilated cardiomyopathy (25% of cases). It is associated with an increase in mortality and poor outcome. There is a potential survival benefit deriving from the reduction in the degree of severity of mitral regurgitation. So the correction of the valve defect can change the clinical course and prognosis of the patient. The rationale for mitral valve treatment depends on the mitral regurgitation mechanism. Therefore, it is essential to identify and understand the pathophysiology of mitral valve regurgitation.
Aim of the Study
The aim of this review is to describe the crucial role of transthoracic and trans‐esophageal echocardiography, in particular with three‐dimensional echocardiography, for the assessment of the severity of secondary mitral regurgitation, anatomy, and hemodynamic changes in the left ventricle. Moreover, the concept that the mitral valve has no organic lesions has been abandoned. The echocardiography must allow a complete anatomical and functional evaluation of each component of the mitral valve complex, also useful to the surgeon in choosing the best surgical approach to repair the valve.
Conclusions
Echocardiography is the first‐line imaging modality for a better selection of patients, according to geometrical modifications of mitral apparatus and left ventricle viability, especially in preoperative phase.
... In FMR, the coaptation reserve is progressively reduced until coaptation is no more possible. The main determinant of the reduction of coaptation reserve is the predominance of tethering forces: LV remodeling and dilation cause papillary muscles (PMs) dislocation away from the mitral annulus [14]. Consequently, PMs tend to pull MV leaflets apically and/or posteriorly through the attached chordae tendinae, thus augmenting tethering forces (Figure 1). ...
Valve leaflets and chordae structurally normal characterize functional mitral regurgitation (FMR), which in heart failure (HF) setting results from an imbalance between closing and tethering forces secondary to alterations in the left ventricle (LV) and left atrium geometry. In this context, FMR impacts the quality of life and increases mortality. Despite multiple medical and surgical attempts to treat FMR, to date, there is no univocal treatment for many patients. The pathophysiology of FMR is highly complex and involves several underlying mechanisms. Left ventricle dyssynchrony may contribute to FMR onset and worsening and represents an important target for FMR management. In this article, we discuss the mechanisms of FMR and review the potential therapeutic role of CRT, providing a comprehensive review of the available data coming from clinical studies and trials.
... Functional MR is a common finding in patients with HF and reduced LVEF and is caused by progressive cardiac remodelling, resulting in papillary muscle displacement and annular enlargement. 18 Previous studies have demonstrated that CRT may result in MR improvement, 19 due to the immediate effects of resynchronization between the papillary muscles 20 and the more delayed effects of LV reverse remodelling. 21 In addition, an improvement in MR severity after CRT implantation has been associated with improved outcomes. ...
Aims
Left atrial (LA) function is a strong prognostic marker in patients with heart failure and functional mitral regurgitation (MR). Although cardiac resynchronization therapy (CRT) has shown to improve MR severity, the interaction between a reduction in MR severity and an increase in LA function, as well as its association with outcomes, has not been investigated.
Methods and results
LA reservoir strain (RS) was evaluated with speckle tracking echocardiography in patients with at least moderate functional MR undergoing CRT implantation. MR improvement was defined as at least 1 grade improvement in MR severity at 6 months after CRT implantation. The primary endpoint was all-cause mortality. A total of 340 patients (mean age 66 ± 10 years, 73% male) were included, of whom 200 (59%) showed MR improvement at 6 months follow-up. On multivariable analysis, an improvement in MR severity was independently associated with an increase in LARS (odds ratio 1.008; 95% confidence interval 1.003–1.013; P = 0.002). After multivariable adjustment, including baseline and follow-up variables, an increase in LARS was significantly associated with lower mortality. MR improvers showing LARS increasement had the lowest mortality rate, whereas outcomes were not significantly different between MR non-improvers and MR improvers showing no LARS increasement (P = 0.236).
Conclusion
A significant reduction in MR severity at 6 months after CRT implantation is independently associated with an increase in LARS. In addition, an increase in LARS is independently associated with lower all-cause mortality in patients with heart failure and significant functional MR.
... Importantly, we also noted a steady decline in LVEDD after the LVR, and the grade of MR was significantly decreased. Apical and inferior-papillary-muscle displacement due to ischemic left-ventricular remodeling plays an important part in the generation of functional mitral regurgitation [Yiu 2000]. Furthermore, increasing the grade of MR after LVR is an important predictor for reintervention and was strongly associated with hospital readmission due to heart failure [Sartipy 2006]. ...
Background:
The prognosis of severe coronary artery disease (CAD) patients undergoing left ventricular restoration (LVR) and ineligible for concomitant coronary artery bypass grafting (CABG) is unclear. This study illustrates the clinical characteristics and the long-term survival of these patients in a retrospective cohort.
Methods:
From January 1999 to March 2021, a total of 78 patients underwent surgical left ventricular restoration without concomitant CABG at our center. The primary endpoint was the major adverse cardiovascular and cerebrovascular events (MACCE). Kaplan-Meier analysis was performed to calculate survival, and compared by log-rank test, followed by multiple adjustments using Cox regression.
Results:
The mean age was 55.3 ± 11.4 years. There were 76 (97.4%) true and 2 (2.6%) pseudo-aneurysms. Forty-six (59.0%) patients presented NYHA functional class III or IV. The mean EuroSCORE was 10.6 ± 3.2. Concomitant surgeries included mitral valve repair (N = 3), mitral valve replacement (N = 2), tricuspid valve repair (N = 2), ventricular septal defect closure (N = 18), maze procedure (N = 1), and appendage ligation (N = 1). Reoperation for bleeding was performed in one patient (1.3%). Prolonged ventilation was observed in 21 (26.9%) patients. Fourteen (17.9%) patients presented with low cardiac output and were supported with IABP. Operative death occurred in one (1.3%) patient. The median duration of echocardiographic follow-up was 53 months (interquartile range, 81.5) and was obtained in 46 (59.0%) patients. Left ventricular ejection fraction (LVEF) improved from 41.1% ± 10.5% to 45.6% ± 7.9% (P < 0.001), and the left ventricular end-diastolic dimension (LVEDD) fell from 57.8 ± 6.6 mm to 52.0 ± 6.2 mm (P < 0.001). The median patient follow-up time was 79.5 months (interquartile range, 53.5). Overall, 1-, 5-, and 10-year survival rates were 98.7%, 95.5% and 82.3%, respectively.
Conclusions:
Patients with severe CAD and ineligible for concomitant CABG are in critical condition, and LVR could be a reliable approach to improving cardiac function with satisfactory early and long-term outcomes.
... The mechanism of MR can be broadly divided into degenerative MR and functional MR, which is mostly characterized by mitral valve (MV) prolapse/flail, leaflet redundancy/thickening, and chordal dysfunction [3]. Ventricular functional mitral regurgitation (vFMR) is commonly attributed to local or global left ventricular (LV) dysfunction and remodeling without structural MV abnormalities [4]. Recently, atrial functional mitral regurgitation (aFMR) has been increasingly recognized and is characterized by severe mitral annular dilatation, insufficient leaflet remodeling and decreased annular contractility in patients with longstanding atrial fibrillation (AF) [5]. ...
In order to achieve the classification of mitral regurgitation, a deep learning network VDS-UNET was designed to automatically segment the critical regions of echocardiography with three sections of apical two-chamber, apical three-chamber, and apical four-chamber. First, an expert-labeled dataset of 153 echocardiographic videos and 2183 images from 49 subjects was constructed. Then, the convolution layer in the VGG16 network was used to replace the contraction path in the original UNet network to extract image features, and depth supervision was added to the expansion path to achieve the segmentation of LA, LV, and MV. The results showed that the Dice coefficients of LA, LV, and MV were 0.935, 0.915, and 0.757, respectively. The proposed deep learning network can achieve simultaneous and accurate segmentation of LA, LV, and MV in multi-section echocardiography, laying a foundation for quantitative measurement of clinical parameters related to mitral regurgitation.
... Các thông số đánh giá tái cấu trúc vùng thất trái (theo Yiu và cộng sự) [6]: Chỉ số đánh giá độ dịch chuyển về phía sau của cơ nhú: Khoảng cách giữa đỉnh cơ nhú sau và vòng van hai lá đo ở mặt cắt trục dọc cạnh ức trái ở đầu thì tâm thu. Khoảng cách giữa hai cơ nhú đo ở mặt cắt cạnh ức trái trục ngắn đầu thì tâm thu, CSVĐV cơ nhú trước được đánh giá trung bình CSVĐV các vùng thành trước giữa, thành trước đáy, thành bên giữa, thành bên đáy; CSVĐV cơ nhú sau được đánh giá trung bình CSVĐV các vùng thành dưới giữa, thành dưới đáy, thành sau giữa, thành sau đáy (Hình 3). ...
Mục tiêu: Khảo sát đặc điểm hình thái và mức độ hở van hai lá bằng siêu âm Doppler tim và mối liên quan với hình thái, chức năng thất trái ở bệnh nhân có hở van hai lá mạn tính do bệnh tim thiếu máu cục bộ mạn tính. Đối tượng và phương pháp: Đối tượng là 95 bệnh nhân đến khám và điều trị tại Viện Tim mạch Việt Nam được chẩn đoán xác định là hở van hai lá mạn tính do bệnh tim thiếu máu cục bộ mạn tính, trong đó 55 bệnh nhân có kiểu hình lều đóng đồng tâm, 40 bệnh nhân có kiểu hình lều đóng lệch tâm (nhóm nghiên cứu) và 25 người bình thường (nhóm chứng). Các bệnh nhân nhóm nghiên cứu được siêu âm tim đánh giá mức độ hở hai lá, hình thái đóng van hai lá và cấu trúc, chức năng thất trái. Kết quả: 100% bệnh nhân nhóm lều đóng đồng tâm có dòng hở trung tâm, 92,5% bệnh nhân nhóm lều đóng lệch tâm có dòng hở lệch tâm. So với nhóm chứng, các thông số đánh giá hình thái van hai lá (diện tích lều đóng, chiều cao lều đóng, diện tích vòng van hai lá) của 2 nhóm nghiên cứu đều cao hơn; nhóm lều đóng đồng tâm có diện tích lều và chiều cao lều đóng lớn hơn so với nhóm lều đóng lệch tâm (p<0,01). Chỉ số vận động vùng cơ nhú sau của nhóm lều đóng lệch tâm lớn hơn nhóm lều đóng đồng tâm (p<0,05). Các thông số đánh giá cấu trúc thất trái toàn bộ (Dd, Ds, Vd, Vs, chỉ số vận động vùng, chỉ số cầu hóa) của nhóm lều đóng đồng tâm lớn hơn nhóm lều đóng lệch tâm (p<0,05). Kết luận: Ở bệnh nhân có hở van hai lá mạn tính do bệnh tim thiếu máu cục bộ mạn tính, có sự khác biệt rõ rệt giữa nhóm lều đóng đồng tâm và lều đóng lệch tâm về hướng dòng hở, diện tích lều và chiều cao lều đóng. Nhóm lều đóng đồng tâm chủ yếu có tái cấu trúc thất trái toàn bộ, còn nhóm lều đóng lệch tâm chủ yếu có tái cấu trúc thất trái vùng.
... Significant right ventricular (RV) dilatation has therefore long been considered integral to the pathogenesis of FTR, analogous to the relationship between left ventricular (LV) dilatation and functional mitral regurgitation (FMR). In the left heart, large and uniform papillary muscles play a major role in supporting the mitral apparatus and LV dilatation pulls these apart, in turn stretching the mitral annulus (via traction on the chordae) [3] and producing FMR. By contrast to the situation in the left heart, the papillary muscles in the RV are smaller, not uniformly disposed and do not support the tricuspid annulus well. ...
Background
Significant right ventricular (RV) dilatation has long been considered integral to the pathogenesis of functional tricuspid regurgitation (FTR).
Objectives
To explore the relationship of RV dilatation and FTR in patients with ‘pure’ RV volume overload.
Methods
Patients (>17yrs) with RV dilatation due to pre-tricuspid shunts (atrial septal defect; ASD and/or partial anomalous pulmonary venous drainage; PAPVD) referred to our service (2000–2019) were retrospectively identified. Those with pulmonary hypertension, primum ASD or left-heart disease were excluded. Using standard cardiac MRI protocols, RV, right atrial and TV parameters were measured and compared.
Results
Of 52 consecutively eligible patients (42 ± 15yrs, 25 males), 25 had ASDs, 13 had PAPVD and 14 had both conditions. All were in sinus rhythm and none had pulmonary regurgitation. Left and right ventricular ejection fractions were normal (LVEF 63 ± 8%, RVEF 56 ± 8%). Indexed RV end-diastolic volumes (RVEDVi) were moderately increased (males 148 ± 33 mL/m² and females 141 ± 42 mL/m², range 95–267 mL/m²). Despite substantial RV volume overload, no patients had severe tricuspid regurgitation (TR). Only two had > mild TR. There was a weak correlation between tricuspid annular diameter and both degree of RV dilatation (r = 0.37; p = 0.01) and degree of TR (r = 0.38; p = 0.006). There was a similarly poor correlation between right atrial dimensions and the degree of TR (r = 0.34; p = 0.02).
Conclusion
When RV dilatation is simply due to volume overload, we find that significant TR is extremely rare. This gives an important and novel insight; that RV dilatation per se does not result in FTR.
... The left ventricular volumes and ejection fraction (EF) were assessed by the biplane Simpson disk method [5]. The mitral valve deformation (MDI -mitral deformation indexes) was evaluated by measuring the tenting area (TA), i.e., the area enclosed between mitral leaflets and the line of annular plane and the coaptation height (CH), i.e., the distance between leaflet coaptation and mitral annular plane from the parasternal long-axis view at mid-systole [6]. ...
B a c k g r o u n d: To assess and compare mid-term outcomes and the quality of life (QoL) in patients with multivessel coronary artery disease (MVD) and moderate ischemic mitral regurgitation (IMR), treated with either coronary artery bypass grafting (CABG; group I) or CABG + mitral annuloplasty (CABG+MA; group II) in 12-months follow-up after surgery. M e t h o d s: We prospectively analyzed 74 patients (50.7% female, 66 [67-72] years) with at least moderate IMR, 3-24 weeks after myocardial infarction (MI). The effective regurgitation orifice (ERO) was used for a quantitative IMR assessment. To evaluate QoL we used a Short Form-36 (SF-36) questionnaire. R e s u l t s: Patients in group II spent more time in the hospital, expired more infection complications and received more often in-hospital complications requiring use amines and intra-aortic balloon pump as compared to those in group I. Analysis of SF-36 showed that all patients treated surgically notable improved their QoL during 12 months of follow-up. C o n c l u s i o n s: We observed a significant improvement in QoL among patients with MVD in 12 months follow-up after surgery irrespective of treatment type.
... Pathological deformation typically occurs during acute ischemia, and it is a predictor of recovery and ischemic memory, and, recently, the ability of PSS and ESL to predict adverse cardiac outcomes has been demonstrated in a wide range of special population [48][49][50][51][52]. • Mitral valve complex (MVC) tissue longitudinal elongation. It is clear that LV sphericity is associated with impaired LVEF, functional mitral regurgitation (MR) and poor prognosis [53,54] in DCM. LV shape becomes spherical and myocardial tissue elongates transversally [55]. ...
Although the overall survival of patients with dilated cardiomyopathy (DCM) has improved significantly in the last decades, a non-negligible proportion of DCM patients still shows an unfavorable prognosis. DCM patients not only need imaging techniques that are effective in diagnosis, but also suitable for long-term follow-up with frequent re-evaluations. The exponential growth of echocardiography’s technology and performance in recent years has resulted in improved diagnostic accuracy, stratification, management and follow-up of patients with DCM. This review summarizes some new developments in echocardiography and their promising applications in DCM. Although nowadays cardiac magnetic resonance (CMR) remains the gold standard technique in DCM, the echocardiographic advances and novelties proposed in the manuscript, if properly integrated into clinical practice, could bring echocardiography closer to CMR in terms of accuracy and may certify ultrasound as the technique of choice in the follow-up of DCM patients. The application in DCM patients of novel echocardiographic techniques represents an interesting emergent research area for scholars in the near future.
... The left ventricular volumes and ejection fraction (EF) were assessed by the biapical Simpson disk method. The mitral valve deformation was evaluated by measuring the tenting area (TA), i.e., the area enclosed between mitral leaflets and the line of the annular plane and the coaptation height (CH), i.e., the distance between leaflet coaptation and the mitral annular plane from the parasternal long-axis view at mid-systole [24]. ...
Purpose:
Although coronary artery bypass grafting alone (CABGa), or, with mitral annuloplasty (CABGmp), is considered the best therapeutic strategy for patients with ischemic mitral regurgitation (IMR), some recurrences are still reported. The aim of this study was to evaluate the use of the mitral deformation indices (MDI) as a predictor of recurrence of mitral regurgitation in a 12-month follow-up after CABG alone.
Methods:
A total of 145 patients after myocardial infarction with significant IMR, eligible for CABG, were prospectively enrolled in the study. Mitral valve morphology, left ventricle function, IMR degree as assessed by effective regurgitation orifice area (ERO), myocardial viability, and MDI were assessed prior to surgery. Patients were referred for CABGa (gr.1; n = 90) or CABGmp (gr.2; n = 55) based on clinical assessment, and the results of rest and stress echocardiography (exercise echocardiography and low dose dobutamine echocardiography-DBX). One year after surgery, each patient underwent the evaluation of cardiovascular events. Univariable logistic regression analysis was used to identify the factors of recurrence of IMR in 1 year follow-up. Serial echo examinations were performed in all patients at discharge, and at 1 and 12 months after surgery.
Results:
Logistic regression analysis revealed that in CABGa, group preoperative changes of tenting area (TA) and coaptation high (CH) during DBX remained the predictors of the recurrence of IMR in 12 months follow-up. TAdbx > 1 cm2 provided a sensitivity of 90% and specificity of 29%, (AUC 0.6436). The best cut-off value for CHdbx was 0.4 cm (sensitivity 90%, specificity 34%; AUC 0.6432). In both groups (CABGa vs. CABGmp) no significant differences were observed in 12-month mortality (1.2% vs. 0%; p = 1.0), hospitalizations due to the heart failure (HF) exacerbation (5.9% vs. 8.5%; p = 0.72), and in the incidence of the composite endpoint (deaths/CV hosp/stroke) (7% vs. 8.5%; p = 0.742).
Conclusions:
The preoperative assessment of MDI changes during dbx can be used to identify patients with IMR qualified to CABG alone at increased risk of recurrence of IMR in 1 year follow-up. Mitral deformation analysis should be used for a better qualification of patients with IMR to the exact surgical approach.
... 12,13 TR aetiologies are currently divided into primary and secondary TR. Intrinsic abnormalities of the tricuspid valve leading to significant TR (primary) are rare and are seen in approximately 8-10% of patients with severe TR. 14,15 In contrast, secondary TR is the most frequent form of TR requiring surgical intervention. Secondary TR occurs mainly from tricuspid annular dilatation and increased tricuspid leaflet tethering because of right ventricular enlargement, which is often secondary to left HF from myocardial or valvular causes. ...
Ischaemic cardiomyopathy is a condition that arises when heart muscle is weakened because of coronary artery disease or a heart attack. Left ventricular (LV) dysfunction occurs when the left ventricle is either defective or damaged, thus disrupting healthy function. Normal LV function can be perturbed because of several causes. Some cardiac defects such as valvular malformations or conditions block the passage of blood into the body. Effective and cost-effective treatment is available for such patients that can reduce both morbidity and mortality. Herein, the authors present the case of a 69-year-old male who was brought to the emergency department with a history of hypertension on medication. Later, the patient was transferred to the cardiology department. The patient was brought to the hospital after midnight and had bleeding gums, and experienced bleeding from the site of needle puncture. Earlier reports showed that the international normalised ratio was >6.0, and the 2D echocardiogram showed large LV blood clots, mild LV dysfunction, mild mitral regurgitation, and aortic valve stenosis. Finally, the patient was diagnosed with ischaemic cardiomyopathy associated with LV dysfunction. During discharge, the patient and patient's representative were counselled in layman's language about the conditions and prognosis of the disease, the use and adherence to medications, lifestyle modifications, and were advised to review back to the cardiologist.
... Local or global LV dysfunction and remodelling cause papillary muscle (PM) displacement and mitral leaflet tethering resulting in reduced leaflet coaptation. 1,2 Long-standing atrial fibrillation (AF) may result in left atrial (LA) enlargement and mitral annular dilatation. Mitral annular dilatation plays an important role in the development of atrial FMR (A-FMR). ...
Aims
This study investigated geometric differences in mitral valve apparatus between atrial functional mitral regurgitation (A-FMR) and functional mitral regurgitation (FMR) with left ventricular (LV) dysfunction in patients with atrial fibrillation (AF) using 3D transoesophageal echocardiography (TOE).
Methods and results
In total, 135 moderate or greater FMR patients with persistent AF or atrial flutter underwent 3D TOE. Fifty-six patients had A-FMR, defined as preserved LV ejection fraction (LVEF) of ≥50% and normal LV wall motion. Seventy-nine patients had ventricular FMR (V-FMR), defined as LV dysfunction (LVEF of <50%) or LV wall motion abnormality. To evaluate mitral leaflet coaptation, the coapted area was calculated as follows: total leaflet area (TLA) in end-diastole − closed leaflet area in mid-systole. Although annular area (AA) did not significantly differ between the two groups, TLA was significantly smaller in A-FMR than in V-FMR (P = 0.005). TLA/AA, indicating the degree of the leaflet remodelling, was significantly smaller in A-FMR than in V-FMR (P < 0.001). A-FMR had significantly smaller posterior mitral leaflet tethering height and angle measured at three anteroposterior planes (lateral, central, and medial) than V-FMR (all P < 0.001). However, vena contracta width (VCW) measured on long-axis view on TOE and coapted area, which correlated with VCW (r = −0.464, P < 0.001), were similar between the two groups.
Conclusion
Mitral leaflet remodelling may be less in A-FMR compared with V-FMR. However, leaflet tethering was smaller in A-FMR than in V-FMR, and this may result in a similar degree of mitral leaflet coaptation and mitral regurgitation severity.
... The success of accepted therapies for ischemic MR have largely been based on their effect on diminishing leaflet tenting which impacts severity of MR more than left ventricular dysfunction, but this effect may be limited with isolated leaflet/annular interventions. 4,6,11,13 Comparison of PMA outcomes with other therapies as evidenced by animal studies, retrospective and prospective randomized trials demonstrate an advantage of PMA in allowing reverse remodeling and improvement in left ventricular ejection fraction (LVEF), 7-9 but long-term survival is not different to that of RA and overall survival of all therapies remain suboptimal. Nappi and colleagues reported a significant decrease in major adverse cardiac and cerebrovascular events in the PMA group, demonstrating its long-term protective effect on the ventricle, but they found no significant difference in all-cause mortality at 5 years with 22.9% for the PMA group and 29.2% for the RA group. ...
... F unctional mitral regurgitation (FMR) is a common complication in patients with ischemic and dilated cardiomyopathy, which is associated with developing heart failure and poor clinical outcome. 1) It is critical to understand the pathophysiology of FMR in order to establish strategies for its prevention and therapy. There is much experimental and clinical evidence 2,3) that tethering of the mitral valve (MV) leaflet by a dilated LV and papillary muscle displacement is a key mechanism for the generation of FMR in addition to mitral annular dilation. 4,5) Recently, mitral leaflet size has been recognized as a possible underlying mechanism of progression of FMR, [6][7][8][9] because the size of the MV leaflets is critical for preservation of the valve coaptation-zone and closure of the MV. 6) The size of MV leaflets may be dynamically influenced by multiple factors. ...
Preservation of the mitral valve (MV) size is essential for valve function, and a reduced MV coaptation-zone area increases the risk of developing functional mitral regurgitation (FMR). We aimed to determine if the MV leaflet and coaptation-zone areas were associated with the severity of atherosclerosis assessed by cardio-ankle vascular index (CAVI) in patients with normal left ventricle (LV) systolic function and size by real-time 3D echocardiography (RT3DE).
We performed RT3DE analysis in 66 patients with normal LV size and ejection fraction who underwent 2D echocardiography and CAVI. MV coaptation-zone areas were measured by custom 3D software and indexed by body surface area (BSA). The associations of clinical factors and mean CAVI with MV leaflet and coaptation-zone areas were evaluated by univariable and multivariable linear regression analyses.
On univariable analysis, MV leaflet area/BSA was significantly associated with age (r = −0.335, P = 0.0069) and mean CAVI (r = −0.464, P < 0.001), and MV coaptation-zone area was significantly associated with age (r = −0.626, P < 0.001), hypertension (r = −0.626, P < 0.001), dyslipidemia (r = −0.626, P < 0.001), E/e' (r = −0.626, P < 0.001), and CAVI (r = −0.740, P < 0.001). On multivariable analysis, mean CAVI was independently associated only with MV leaflet area/BSA (standardized coefficient = −0.611, P < 0.001) and MV coaptation-zone area/BSA (standardized coefficient = −0.74, P < 0.001).
In patients with normal LV systolic function and size, MV leaflet and coaptation-zone areas might be reduced according to advancing atherosclerosis. Patients with atherosclerosis might be at increased risk of developing FMR.
... Thus, one target of paramount importance is to characterize cardiac remodelling due to MR effects, which implies the specific assessment of LV [43][44][45] and LA geometry by echocardiography [46]-especially in SMR patients [3,5,6]. Despite recent technical improvements in echocardiography and automated features to analyze LA and LV volumes and function, conventional 2D echocardiography remains the current standard and enables the assessment of relevant cardiac parameters as illustrated in Table 4. Linear internal 2D measurements of LV diameters and LV wall thickness as well as LV volume measurements by 2D planimetry are still used in clinical practice [5,41,47]-especially for calculation of LV mass [41]. ...
The echocardiographic assessment of mitral valve regurgitation (MR) by characterizing specific morphological features and grading its severity is still challenging. Analysis of MR etiology is necessary to clarify the underlying pathological mechanism of the valvular defect. Severity of mitral regurgitation is often quantified based on semi-quantitative parameters. However, incongruent findings and/or interpretations of regurgitation severity are frequently observed. This proposal seeks to offer practical support to overcome these obstacles by offering a standardized workflow, an easy means to identify non-severe mitral regurgitation, and by focusing on the quantitative approach with calculation of the individual regurgitant fraction. This work also indicates main methodological problems of semi-quantitative parameters when evaluating MR severity and offers appropriateness criteria for their use. It addresses the diagnostic importance of left-ventricular wall thickness, left-ventricular and left atrial volumes in relation to disease progression, and disease-related complaints to improve interpretation of echocardiographic findings. Finally, it highlights the conditions influencing the MR dynamics during echocardiographic examination. These considerations allow a reproducible, verifiable, and transparent in-depth echocardiographic evaluation of MR patients ensuring consistent haemodynamic plausibility of echocardiographic results.
Graphic abstract
... Progressive left ventricular remodelling is frequently followed by a functional regurgitation of the structurally normal mitral valve (FMR). 1 Due to papillary muscle displacement, increased tethering forces on mitral chordae and annular dilatation, mitral valve (MV) leaflets lose their coaptation and take shape of a tent during systole. 2 Typically, the triangular area between mitral annulus and tented leaflets is described as MV tenting area. 3 MV tenting area can be quantitatively assessed by echocardiography and reflects both the global and regional left ventricular remodelling. ...
Objectives
Mitral valve (MV) tenting parameters are indicators of left ventricular remodelling severity and may predict outcome in functional mitral regurgitation (FMR). We hypothesised that indexing of MV tenting area to body surface area (BSA), to mitral annulus diameter or gender-adjusted analysis of tenting parameters may improve their prognostic value.
Methods
We identified retrospectively 240 patients with consecutive FMR (mean age 68±10 years; men=135) from our institutional database who underwent isolated MV annuloplasty during a period of 7 years (2010–2016). Using preoperative two-dimensional transthoracic echocardiographic images, MV tenting parameters including tenting area, tenting height and annulus diameter were systematically assessed. Follow-up protocol consisted of chart review and structured clinical questionnaire. Primary study endpoint was the composite of death and adverse cardiac events (ie, MV reoperation, cardiac resynchronisation therapy implantation, ventricular assist device implantation or heart transplantation).
Results
BSA-indexed MV tenting area was identified as independent predictor of primary study endpoint (HR 1.9; 95% CI 1.1 to 3.5; p=0.02). After cut-off point analysis, BSA-indexed MV tenting area >1.35 cm ² /m ² was significantly associated with primary study outcome (HR 2.3; 95% CI 1.3 to 4.0; p=0.003). Annulus-indexed MV tenting area showed only a tendency towards primary study endpoint prediction (HR 2.8; 95% CI 0.6 to 12.6; p=0.17). Between female and male patients, BSA-indexed MV tenting area was similar (1.42±0.4 cm ² /m ² vs 1.45±0.4cm ² /cm ² ; p=0.6) and gender was not associated with primary study outcome (HR 0.8; 95% CI 0.5 to 1.4; p=0.5).
Conclusion
In our FMR cohort, BSA-indexed MV tenting area showed the strongest association with negative outcomes following isolated MV annuloplasty. Patients with BSA-indexed MV tenting area >1.35cm ² /m ² could potentially benefit from additional surgical maneuvers addressing left ventricular remodelling.
... In addition, LVEDV index was the only independent determinant of MV coaptationzone area/BSA, suggesting a close relationship between MV coaptation-zone area and LV size. As previous studies suggested, 2,3,[5][6][7][8] MV coaptation-zone area, which is an essential component of complete MV closure, is significantly influenced by tethering and the subvalvular appara- tus. As previous study demonstrated, 2) LV dilation causes MV tethering and the reduction of MV coaptation-zone area. ...
Enlargement of the mitral valve (MV) has gained attention as a compensatory mechanism for functional mitral regurgitation (FMR). We aimed to determine if MV leaflet area is associated with MV coaptation-zone area and identify the clinical factors associated with MV leaflet size and coaptation-zone area in patients with normal left ventricle (LV) systolic function and size using real-time 3D echocardiography (RT3DE).
We performed RT3DE in 135 patients with normal LV size and ejection fraction. MV leaflet and coaptation-zone areas were measured using custom 3D software. The clinical factors associated with MV leaflet and coaptation-zone areas were evaluated using univariate and multivariate linear regression analyses.
There was a significant relationship between MV leaflet and coaptation-zone areas (r = 0.499, P < 0.001). MV leaflet area was strongly associated with body surface area (BSA) (r = 0.905, P < 0.001) rather than LV size and age. MV leaflet area/BSA was independently associated with male gender (P = 0.002), lower diastolic blood pressure (P = 0.042), and LV end-diastolic volume (LVEDV) index (P = 0.048); MV coaptation-zone area/BSA was independently associated with lower LVEDV index (P = 0.01).
In patients with normal LV systolic function and size, MV leaflet size has a significant impact on competent MV coaptation. MV leaflet area might be intrinsically determined by body size rather than age and LV size, and the MV leaflet area/BSA is relatively constant. On the other hand, some clinical factors might also influence MV leaflet and coaptation-zone area.
BACKGROUND
Patients with only moderate atrial secondary mitral regurgitation (asMR) frequently develop heart failure (HF). Mechanisms of HF with moderate asMR and the impact of mild asMR remain unclarified. Although mild/moderate primary mitral regurgitation is compensated by left ventricular (LV) dilatation, the LV is not dilated in asMR. We hypothesized that patients with mild asMR without LV dilatation may have impaired hemodynamics and higher risks of subsequent symptomatic HF deterioration.
METHODS
Stroke volume, cardiac output, and systolic pulmonary artery pressure were measured by echocardiography in 142 patients with isolated atrial fibrillation and 30 healthy controls. Patients with isolated atrial fibrillation prognosis was followed up.
RESULTS
In the 142 patients with isolated atrial fibrillation, asMR was no/trivial in 55, mild in 83, moderate in 4, while none had severe asMR. Compared with controls and patients with no/trivial asMR, LV end-diastolic volume index was not increased and hemodynamic parameters were abnormal in patients with mild asMR (LV end-diastolic volume index, 65±6 versus 58±8 versus 60±8 mL/m²; stroke volume index, 42±4 versus 35±4 versus 29±6 mL/m²; P <0.001 versus other 2 groups; cardiac output index, 2.8±0.4 versus 2.8±0.5 versus 2.3±0.6 L/min per m²; P <0.001; systolic pulmonary artery pressure, 21±3 versus 26±5 versus 37±9 mm Hg; P <0.001). Although the event-free rate of HF symptomatic deterioration or hospitalization in patients with no/trivial asMR during a median 13.9 months follow-up was 86.9% and 100%, the rate in mild asMR was 59.4% and 85.0% ( P <0.001 or P =0.032), respectively.
CONCLUSIONS
In the presence of isolated AF and no compensatory LV dilatation, impaired hemodynamics and higher risks of symptomatic HF deterioration were associated with mild asMR, requiring further studies of causalities.
Myocardial ischemia, compromising myocardial function in acute and subsequently in chronic, has important physiopathological repercussions on the mitral valve. It determines the so-called functional ischemic mitral regurgitation (fIMR), resulting from the complex mitral anatomy and interdependence with the cardiac muscle. It also depends on the area and extent of ischemia. Current diagnostic techniques, primarily cardiac echocardiography and nuclear magnetic resonance of the heart, allow to study this complex and give indications on therapeutic treatment. The therapy is articulated, involving different figures such as the electrophysiologist, the clinical and interventional cardiologist, and the cardiac surgeon. Overall, the approach to this pathology is multidisciplinary and still a field to be explored for a tailored treatment on the patient.
Ischaemic mitral prolapse (IMP) is a pathologic entity encountered in about one-third of patients undergoing surgery for ischaemic mitral regurgitation. IMP is generally the result of a papillary muscle injury consequent to myocardial infarction, but the recent literature is progressively unveiling a more complex pathogenesis. The mechanisms underlying its development are the impairment of one or more components of the mitral apparatus, which comprises the annulus, chordae tendineae, papillary muscle, and left ventricular wall. IMP is not only a disorder of valvular function but also entails coexistent aspects of a geometric disturbance of the mitral valve configuration and of the left ventricular function and dimension. A correct understanding of all these aspects is crucial to guide and tailor the correct therapeutic strategy to be adopted. Localisation of prolapse and anatomic features of the prolapsed leaflets and the subvalvular apparatus should be carefully evaluated as also constituting the major determinants defining patient outcomes. This review will summarise our current understanding of the pathophysiology of and clinical evidence on IMP, with a particular focus on surgical treatment.
Aims
In patients with obstructive hypertrophic cardiomyopathy (HCM) and mild septal thickness undergoing myectomy, resecting fibrotic anterior mitral leaflet (AML) secondary chordae moves the mitral valve (MV) away from the outflow tract and ejection flow, reducing the need for a deep septal excision. Aim of the present study was to assess whether chordal resection has similarly favourable effects in patients with important hypertrophy, who represent the majority of patients with obstructive HCM.
Methods and results
The MV position in the ventricular cavity, assessed from echocardiography as AML-annulus ratio, was compared before and after chordal resection in 150 consecutive HCM patients with important (≥20 mm) and 62 with mild (≤19 mm) septal thickness undergoing myectomy. Preoperatively, MV position was displaced towards the septum to a similar extent in both groups. Postoperatively, AML-annulus ratio increased of an equal degree in both groups, from 0.43 ± 0.05 to 0.55 ± 0.06 (P < 0.001) a 28% increase, and from 0.43 ± 0.06 to 0.55 ± 0.06 (P < 0.001) a 26% increase, respectively, indicating a similar MV shift away from the outflow tract. When AML-annulus ratio was compared in the study cohort and 124 normal subjects, MV position was within normal range in <4% of patients preoperatively and normalized in >50% postoperatively.
Conclusions
In obstructive HCM, displacement of the MV apparatus into the outflow tract interferes with the ejection flow. Resection of fibrotic secondary chordae moves the MV apparatus away from the outflow tract and enlarges the outflow area independently of septal thickness, facilitating septal myectomy by reducing the need for a deep muscular excision.
Introduction
Although randomized trial data exist for 2-y outcomes comparing isolated coronary artery bypass grafting (CABG) versus CABG with concomitant mitral valve repair (CABG + MVr) for the treatment of moderate ischemic mitral regurgitation (IMR), longer term outcomes are unclear. This study evaluated the longitudinal outcomes of isolated CABG for moderate IMR.
Methods
Patients with moderate IMR undergoing isolated CABG from January 2010 to February 2018 at a single institution were included. Outcomes included longitudinal freedom from heart failure readmission, survival, rates of persistent mitral regurgitation (MR), and freedom from mitral valve reinterventions. A subanalysis was conducted comparing CABG versus CABG + MVr. Multivariable Cox regression was used for risk adjustment.
Results
A total of 528 patients with moderate IMR underwent isolated CABG. Postoperatively, 26% of patients had at least moderate MR at 1-mo follow-up, although at 5 y progression to severe MR was rare (2.2%) as were mitral valve reinterventions (0.2%). Survival at 30 d (95.8%), 1 y (89.6%), and 5 y (76.6%) was acceptable. Furthermore, the freedom from readmission for heart failure was also acceptable at 30 d (92.6%), 1 y (79.9%), and 5 y (65.0%) postoperatively. In a subanalysis comparing CABG versus CABG + MVr, unadjusted and risk-adjusted survival, freedom from heart failure readmissions, mitral valve reinterventions, and degrees of MR were comparable between the groups at all intervals (all P > 0.05).
Conclusions
The majority of patients with moderate IMR can undergo isolated CABG with acceptable rates of heart failure readmissions, survival, progression to severe MR, and the need for subsequent mitral interventions. These data support the use of isolated CABG in patients with moderate IMR.
Objectives:
We evaluate the mid-term results of mitral valve (MV) repair with patch augmentation of the posterior leaflet in secondary mitral regurgitation.
Methods:
Patients were included after diagnosis of a severe symptomatic secondary MV insufficiency with grade III and IV according to the Carpentier classification IIIb. Indication for a patch augmentation technique was a dilatation of the left ventricle leading to a displacement of the papillary muscles, causing restricted leaflet motion and a marked leaflet tenting height. Data were collected prospectively between December 2011 and March 2020.
Results:
In total, 174 patients (mean age: 65 ± 12 years) received an MV repair with patch augmentation of the posterior leaflet and a true-sized remodelling annuloplasty (mean size 30.8 mm). Causes of the MV incompetence were dilatative cardiomyopathy in 126 patients and ischaemic myocardial disease in 48 patients. Concomitant bypass surgery was performed in 28 patients, and the tricuspid valve was repaired in 68 patients. The mean follow-up was 40 ± 28.2 months. There was no 30-day mortality. In-hospital mortality was 1.2% (n = 2); late mortality was 10.9% (n = 19). At 8 years, overall survival was 62.48%, freedom from moderate or severe recurrent mitral regurgitation was 91.9% and freedom from reoperation due to MV insufficiency was 97.1%.
Conclusions:
Augmentation of the posterior MV leaflet in addition to remodelling annuloplasty is a safe and reproducible mitral reconstruction technique that renders sustainable MV competence.
Functional mitral regurgitation (FMR) occurs as a result of global or segmental left ventricular (LV) dysfunction or left atrial (LA) dilatation, leading to mitral annular dilatation, papillary muscle displacement, and mitral valve (MV) leaflet tethering and leaflet remodeling. The prevalence of FMR continues to rise in the United States. Even mild FMR is associated with adverse clinical outcomes. Echocardiography is the primary imaging modality to assess the type and severity of mitral regurgitation. FMR treatment depends on the etiology. Evidence based pharmacologic and cardiac resynchronization therapies for underlying LV dysfunction remain the mainstay of treatment. Patients who remain symptomatic despite optimal medical therapy can be considered for surgical or percutaneous MV intervention. This article reviews the pathophysiology, imaging evaluation, and therapeutic options of FMR, highlighting the most recent developments in a rapidly evolving field.
Background
Left atrial (LA) size is a marker of disease severity and is related to worse outcomes in secondary mitral regurgitation (MR). The prognostic value of LA function assessed by left atrial reservoir strain (LARS) however, remains unknown. We aimed to investigate the prognostic implications of LARS in patients with significant secondary MR.
Methods
LARS was evaluated by speckle tracking echocardiography in patients with more than mild (grade ≥2) secondary MR. The population was divided in 2 groups according to the median LARS value (9.8%). The primary endpoint was all-cause mortality.
Results
A total of 666 patients (mean age 66±11 years, 68% male) were included. On multivariable analysis, more severe MR was independently associated with more impaired LARS (LARS <9.8%) (OR 0.419; 95% CI 0.249 – 0.704; p=0.001). During a median follow-up of 5 (2 – 10) years, 383 (58%) patients died. Patients with LARS <9.8% had significantly lower survival rates at 1-, 2-, and 5-year follow-up (85%, 70%, and 45%, respectively) when compared to patients with LARS ≥9.8% (96%, 93%, and 78%, respectively) (p<0.001). After multivariable adjustment (including LA volume and left ventricular global longitudinal strain (LV GLS)), more preserved LARS (≥9.8%) (HR 0.499; 95% CI 0.386 – 0.645; p<0.001) was independently associated with lower all-cause mortality. LARS provided incremental prognostic value over LA volume and LV GLS.
Conclusions
LARS is independently associated with all-cause mortality in patients with significant secondary MR, and has incremental prognostic value over LA volume and LV GLS. LARS may improve risk stratification of patients with secondary MR.
Background
Functional mitral regurgitation(FMR) in patients with cardiomyopathy correlates with morbidity and mortality in heart failure. The response of FMR to cardiac resynchronization therapy(CRT) varies.
Objectives
The aim of our study was to analyze the incidence and severity of FMR in patients with non-ischemic cardiomyopathy(NICM) and left bundle branch block(LBBB) and the response to left bundle branch pacing(LBBP).
Methods
Patients who had undergone LBBP for NICM, LBBB and FMR between 2019 to 2021 were included retrospectively in the study.
Results
A total of 79-patients were identified and six patients excluded(5-no consistent LBB-capture and 1-prosthetic-mitral valve). Patients(n=73) were divided into two groups based on the severity of FMR– Group-I(mild FMR)(n=35;48%) and Group-II(significant FMR)(n=38;52%). The mean follow-up duration was comparable in both groups. Group-II was characterized by higher NT-pro BNP levels, NYHA-function class and larger left-ventricular dimensions. LBBP resulted in significant reduction in QRS duration in both group-I(113.8±12.7ms;p<0.0001) and group-II(117.3±10.3ms;p <0.0001). LBBP resulted in similar percentage reduction in QRS duration(-31±10% vs -33±8%;p = 0.34), LVEDD(-8±10% vs -11±12%;p= 0.25), LVEDV(-26±12% vs -31±27%;p= 0.31) and LVESV(-39±16% vs -37±30%;p= 0.72) in group-I and group-II respectively. The percentage change(+59±39% vs +59±41%;p-1.0) and absolute change(+19.9±10.4% vs +17±10.04%;p-0.22) in LVEF were similar in both the groups. In group-II, 31-patients (82%) showed significant reduction in FMR-severity during follow-up. No patients in group-I showed worsening of FMR.
Conclusion
LBBP resulted in excellent electrical resynchronization with significant reduction in the severity of FMR in the majority of patients with significant FMR and no worsening of FMR from baseline in any patient.
Aim
To evaluate insufficient rotational movement of the left ventricle (LV) as a potential novel mechanism for functional regurgitation of the mitral valve (FMR).
Methods and results
We compared reference subjects and patients with LV dysfunction (LVD, ejection fraction EF < 50%) with and without FMR (regurgitant volume RVol>10 mL). Subjects without structural mitral valve pathology undergoing cardiac MRI were evaluated. Delayed enhancement, global LV remodeling parameters, systolic twist and torsion were measured (using manual and novel automated cardiac MRI tissue-tracking). The study included 117 subjects with mean ± SD age 50.4 ± 17.8 years, of which 30.8% were female. Compared to subjects with LVD without FMR (n = 31), those with FMR (n = 37) had similar clinical characteristics, diagnoses, delayed enhancement, EF, and longitudinal strain. Subjects with FMR had significantly larger left ventricles (EDVi:136.6 ± 41.8 vs 97.5 ± 26.2 mL/m, p < 0.0001) with wider separation between papillary muscles (21.1 ± 7.6 vs 17.2 ± 5.7 mm, p = 0.023). Notably, they had lower apical (p < 0.0001) but not basal rotation and lower peak systolic twist (3.1 ± 2.4° vs 5.5 ± 2.5°, p < 0.0001) and torsion (0.56 ± 0.38°/cm vs 0.88 ± 0.52°/cm, p = 0.004). In a multivariate model for RVol including age, gender, twist, LV end-diastolic volume, sphericity index and separation between papillary muscles, only gender, volume and twist were significant. Twist was the most powerful correlate (beta −2.23, CI -3.26 to −1.23 p < 0.001). In patients with FMR, peak systolic twist negatively correlates with RVol (r = −0.73, p < 0.0001).
Conclusion
Reduced rotational systolic LV motion is significantly and independently associated with RVol among patients with FMR, suggesting a novel pathophysiological mechanism and a potential therapeutic target.
Objectives:
Despite coherent guidelines, management of functional-tricuspid-regurgitation (FTR) consequences on outcome in the context of degenerative-mitral-regurgitation (DMR) remains controversial due to lacking series of large magnitude with rigorous application of tricuspid guidelines and strict long-term echocardiographic follow-up. Thus we aimed at gatering such a cohort to examine outcomes of patients undergoing DMR surgery following tricuspid surgery guidelines.
Methods:
All consecutive patients with isolated DMR 2005-2015 operated on with baseline FTR-assessment and tricuspid-annulus-diameter (TAd) measurement were identified. Operative complications, postoperative tricuspid-regurgitation incidence and survival were assessed overall and stratified by guideline-based tricuspid annuloplasty (TA) indication (severe FTR or TAd ≥ 40mm).
Results:
Among 441 DMR patients undergoing mitral repair (66 ± 13years, 30% female, ejection-fraction 66±10%, systolic-pulmonary-artery-pressures 39±12mmHg) followed 6 [3-9] years, patients with TA (n=234--53%) had generally similar presentation vs. without TA (n=207--47%; all P≥0.2) except for more atrial fibrillation and larger left-ventricle (both P≤0.0003). Patients with TA showed longer bypass time, more maze-procedures (all P≤0.001), but hospital stay, renal-failure, pacemaker-implantation and operative mortality (overall 0.9%) were comparable (all P≥0.2). Postoperative incidence of moderate/severe FTR (0% at 1-year) became over time higher among patients without TA (5-year 8[4-13]% vs. 3[1-11]% and 10-year 10[6-16]% vs. 4[1-16]%, P=0.01). Survival[95%-confidence interval] throughout follow-up was 85[77-89]% at 10-year, with hazard-ratio 0.57[0.29-1.10], P=0.09. for patients with TA vs. without.
Conclusions:
In this large surgical DMR cohort, guideline-based FTR management was safe and effective. While long-term mortality did not reach significance, post-operative incidence of moderate/severe FTR, overall low, was nevertheless higher in patients who did not appear to require TA at surgery and linked to tricuspid annular dimension. Thus, future multicenter prospective cohorts with long-term follow-up are warranted to re-examine thresholds for TA performance and impact on survival.
This chapter discusses different heart diseases, which are abnormalities that affect normal functioning of the electrical system, valves, muscles, and arteries of the heart. The main focus is on mitral valve disease, which is the second most common valvular lesion, preceded only by aortic stenosis (AS). Study of mitral regurgitation (MR) is understood to cover all other mitral valve diseases. If MR does not progress, then the amount of regurgitation is small (i.e., MR is mild with less backward leakage). However, if there is significant MR, then the left ventricle must do more work to fulfill the oxygenated blood demand of the body. The long period of this disease may lead to heart failure, therefore early diagnosis is important. As such, this chapter highlights some special diagnostic methods, including different types of echocardiography.
Objectives
The aim of this work was to identify the key morphological and functional features in secondary mitral regurgitation (sMR) and their prognostic impact on outcome.
Background
Secondary sMR in patients with heart failure and reduced ejection fraction typically results from distortion of the underlying cardiac architecture. The morphological components which may account for the clinical impact of sMR have not been systematically assessed or correlated with clinical outcomes.
Methods
Morphomic and functional network profiling were performed on a cohort of patients with stable heart failure optimized on guideline-based medical therapy. Principal component (PC) analysis and subsequent cluster analysis were used to condense the morphomic and functional data first into PCs with varimax rotation (PCVmax) and second into homogeneous clusters. Clusters and PCs were tested for their correlations with clinical outcomes.
Results
Morphomic and functional data from 383 patients were profiled and subsequently condensed into PCs. PCVmax 1 describes high loadings of left atrial morphological information, and PCVmax 2 describes high loadings of left ventricular (LV) topology. Based on these components, 4 homogeneous clusters were derived. sMR was most prominent in clusters 3 and 4, with the morphological difference being left ventricular size (median end-diastolic volume 188 mL [interquartile range: 160 mL-224 mL] vs 315 mL [264 mL-408 mL]; P < 0.001). Clusters were associated with mortality (P < 0.001), but sMR remained independently associated with mortality after adjusting for the clusters (adjusted HR: 1.42; 95% CI: 1.14–1.77; P < 0.01). The detrimental association of sMR with mortality was mainly driven by cluster 3 (HR: 2.18; 95% CI: 1.32-3.60; P = 0.002), the “small LV cavity” phenotype.
Conclusions
These results challenge the current perceptions that sMR in heart failure with reduced ejection fraction results exclusively from global or local LV remodeling and are suggestive of a potential role of the left atrial component. The association of sMR with mortality cannot be purely attributed to cardiac morphology alone, supporting other complementary key aspects of mitral valve closure consistent with the force balance theory. Unsupervised clustering supports the association of sMR with mortality predominantly driven by the small LV cavity phenotype, as previously suggested by a conceptional framework and termed disproportionate sMR.
Background
Non valvular, ischemic regurgitation (MR) occurs secondary to myocardial infarction or acute ischemia. The presence of ischaemic MR is associated with increased morbidity and mortality. The severity of ischaemic MR is directly proportional to the severity of the LV dysfunction causing the MR. The present study was carried out to estimate the burden, clinical presentation and prognosis of non valvular MR among patients with coronary artery disease.
Methods
This cohort study was carried out among 75 adults aged over 25 years with electrocardiographic evidence of coronary artery disease. Clinical examination and periodic electrocardiography was done for evaluating the ischemic status and echocardiogram was done to assess the status of mitral regurgitation. Ejection fraction was measured by Simpsons method and regional wall motion abnormality was qualitatively evaluated.
Results
In this study, 60% of the participants had mild MR while 22.9% had moderate MR. In correlation with STEMI, inferior/posterior wall MI with right ventricular extension showed presence of MR in 100% of the cases. There was a statistically significant difference in the incidence of congestive cardiac failure among the patients with severe MR (66.7%) and mild MR (25%) compared to those without CCF (p < 0.01).
Conclusion
Ischemic MR is characteristically dynamic and can change substantially with changes in loading conditions. This study has laid down the basis for evaluating future role of new adjunctive surgical techniques and of percutaneous interventions.
One of the important complications which causes the increase of mortality and economic burden on patient is the ischemic MR. Its main pathophysiology is the remodeling of the LV after MI which causes the hemodynamic load and heart failure. However, the data on relationship between ischemic MR and duration of heart failure is very few. We prospectively studied 300 patients who admitted for acute myocardial infarction in our hospital. All patients were assessed by echocardiography and graded MR as mild, moderate, and severe according to regurgitant jet area which is less than 20%, 20 – 40%, and more than 40% of the left atrial area, respectively. The median duration of follow up was 1 year (range 6-12 months). Mild and moderate or severe ischemic MR was present in 40.2 and 6.4% of patients respectively. The hazard ratios for HF were 2.9 (95% condence interval (CI), 1.9–4.3; P<.001) and 3.7 (95% condence interval (CI), 2.1-6.5; P<.001) in patients with mild and moderate or severe ischemic MR respectively, with compared to patients without ischemic MR, after adjusting for ejection fraction and other clinical variables like age, sex, Killip class, previous infarction, hypertension, diabetes mellitus, anterior wall infarction, ST elevation infarction and coronary revascularization. In patients with mild ischemic MR, the adjusted hazard ratio for death was 1.1 (95% CI 0.7-1.7; P=.42), where as in moderate or severe ischemic MR it was 2.1 (95% CI 1.3-3.5; P=.02).
Objectives:
The aim of this study was to examine the temporal association between the onset of functional mitral regurgitation and the development of changes in left ventricular shape, chamber enlargement, mitral anulus dilation and regional wall motion abnormalities during the course of evolving heart failure.
Background:
Despite extensive characterization, the exact etiology of functional mitral regurgitation in patients with chronic heart failure remains unknown.
Methods:
Heart failure was produced in seven dogs by multiple sequential intracoronary microembolizations. Serial changes in left ventricular chamber volume and shape were evaluated from ventriculograms. Changes in mitral anulus diameter and ventricular regional wall motion abnormalities were evaluated echocardiographically. The presence and severity of mitral regurgitation were determined with Doppler color flow mapping. Measurements were obtained at baseline and then biweekly until mitral regurgitation was first observed.
Results:
No dog had mitral regurgitation at baseline but all developed mild to moderate regurgitation 12 +/- 1 weeks after the first embolization. The onset of mitral regurgitation was not associated with an increase in left ventricular end-diastolic volume relative to baseline (58 +/- 3 vs. 62 +/- 3 ml), mitral anulus diameter (2.4 +/- 0.1 vs. 2.4 +/- 0.1 cm) or wall motion abnormalities of left ventricular wall segments overlying the papillary muscles. In contrast, the onset of mitral regurgitation was accompanied by significant changes in global left ventricular shape evidenced by increased end-systolic chamber sphericity index (0.22 +/- 0.02 vs. 0.30 +/- 0.01) (p < 0.01) and decreased end-systolic major axis/minor axis ratio (1.71 +/- 0.05 vs. 1.43 +/- 0.04) (p < 0.001).
Conclusions:
These data indicate that transformation of left ventricular shape (increased chamber sphericity) is the most likely substrate for the development of functional mitral regurgitation.
The mechanism and temporal manifestation of functional mitral regurgitation after acute myocardial ischemia were examined in eight dogs. Regional ischemia was produced by selective micro-embolization of the left circumflex coronary artery. Mitral regurgitation and regional left ventricular wall motion abnormalities were evaluated with use of Doppler color flow mapping and two-dimensional echocardiography, respectively. Measurements were made at baseline (before embolization) and were repeated at 30 min and 3 weeks after embolization.Mitral regurgitation developed in all dogs 30 min after embolization and completely subsided 3 weeks later. There was no evidence of mitral valve prolapse, mitral anulus dilation or left ventricular segmental dyskinesia at any time during the study. Regional wall motion analysis showed only hypokinesia of the left ventricular segment overlying the papillary muscle at 30 min with subsequent normalization of the segment at 3 weeks. Mitral regurgitation was accompanied by an increase of the end-systolic distance between the mitral anulus plane and the point of coaptation of the mitral leaflets. This distance was 0.5 ± 0.1 cm at baseline, increased to 0.9 ± 0.1 cm 30 min after the embolization (p < 0.001) and returned to near baseline (0.6 ± 0.1 cm) 3 weeks after the embolization.These data indicate that mitral valve prolapse, mitral anulus dilation and regional left ventricular dyskinesia are not necessary conditions for the development of functional mitral regurgitation after acute myocardial ischemia. Instead, hypokinesia of the ventricular segment overlying the papillary muscle and leading to retraction of the mitral leaflets toward the apex appears to be a sufficient condition for incomplete leaflet coaptation.
Standard mitral valve replacement (MVR) in patients with chronic mitral regurgitation consistently results in a decrease in postoperative left ventricular (LV) ejection performance. This fall in ejection performance has been attributed, at least in part, to unfavorable loading conditions imposed by the elimination of the low-impedance pathway for LV emptying into the left atrium. In contrast to standard MVR in which the chordae tendineae are severed, however, MVR with chordal preservation (MVR-CP) does not usually decrease LV ejection performance despite similar removal of the low-impedance pathway. The purpose of the present study was to define the mechanisms responsible for this discordance in postoperative ejection performance between MVR with and without chordal preservation.
Echocardiography and sphygmomanometer blood pressures were obtained in 15 patients with pure chronic mitral regurgitation before and 7-10 days after mitral valve surgery. These measurements were used to calculate ventricular volume, wall stress, and ejection fraction. Seven patients underwent MVR with chordal transection (MVR-CT), and eight patients underwent MVR-CP. MVR-CT resulted in no postoperative change in LV end-diastolic volume, a significant increase in LV end-systolic volume, a significant increase in end-systolic stress, from 89 +/- 9 to 111 +/- 12 g/cm2 (p < 0.05), and a significant decrease in ejection fraction, from 0.60 +/- 0.02 to 36 +/- 0.02 (p < 0.05). In contrast, patients who underwent MVR-CP had a significant decrease in LV end-diastolic and end-systolic volumes. End-systolic wall stress actually fell from 95 +/- 6 to 66 +/- 6 g/cm2 (p < 0.05), and ejection fraction was unchanged (0.63 +/- 0.01 before and 0.61 +/- 0.02 after mitral valve surgery) instead of reduced.
MVR-CT resulted in a decrease in ejection performance caused in part by an increase in end-systolic stress, which in turn increased end-systolic volume. Conversely, MVR-CP resulted in a smaller LV size, allowing a reduced end-systolic stress and preservation of ejection performance despite closure of the low-impedance left atrial ejection pathway.
The relationship between left ventricular (LV) shape and functional mitral regurgitation (MR) was examined in 18 dogs with long-standing heart failure produced by multiple sequential intracoronary microembolizations. Global LV shape changes were evaluated from angiographic silhouettes obtained at baseline (before embolization) and during heart failure. LV shape changes at end systole and end diastole were quantitated based upon the ratio of the major-to-minor axis and the sphericity index. Among the 18 dogs studied, 11 developed 1+ to 3+ MR during heart failure and seven did not. There was no difference among the two groups with respect to hemodynamics, LV ejection fraction, chamber volume, and regional wall motion. A significant difference, however, was observed between the two groups with respect to the global indexes of LV shape. In dogs with MR, the end-systolic major-to-minor axis ratio decreased 29 +/- 3% between baseline and heart failure compared with only a 16 +/- 3% decrease in dogs without MR (p less than 0.01). In dogs with MR, the end-systolic sphericity index increased 72 +/- 11% between baseline and heart failure compared with an increase of only 30 +/- 5% in dogs without MR (p less than 0.02). Significant and directionally similar differences were observed during end diastole. These data indicate that in heart failure functional MR is associated with a more spherical LV and is not the result of simple LV chamber enlargement. Shape changes of the LV that occur in heart failure may be an important determinant of functional MR.
To assess the influence of mitral regurgitation (MR) on the response to captopril therapy for congestive heart failure (CHF), 30 patients with idiopathic dilated cardiomyopathy in New York Heart Association functional class III were studied. Left ventricular end-diastolic diameter and stroke volume were measured by Doppler echocardiography, and exercise tolerance by exercise testing before and at 1, 3 and 12 months after treatment. Patients were classified into 2 groups: those with (n = 14) and those without (n = 16) MR. No significant differences were observed between the 2 groups in pretreatment studies. Exercise tolerance increased significantly in the group with MR (p less than 0.001) during the year of follow-up, from 514 +/- 193 seconds at baseline study to 671 +/- 178 seconds (p less than 0.0005) at 1 month, 688 +/- 127 seconds (p less than 0.0005) at 3 months and 690 +/- 108 seconds (p less than 0.01) at 12 months. The group without MR had no significant changes. Stroke volume increased significantly only in the MR group during follow-up (p less than 0.01), changing from 43 +/- 9 ml at baseline study to 52 +/- 11 ml (p less than 0.01) at 1 and 49 +/- 11 ml (p less than 0.01) at 3 months. At 12 months the increase was not statistically significant. Left ventricular end-diastolic diameter decreased more in the group with than without MR, although the differences were not significant. Thus, the presence of dynamic MR appears to be an important factor in the therapeutic response to captopril therapy for CHF.
The relation between left ventricular (LV) shape and functional mitral regurgitation (MR) was evaluated in 39 patients with congestive heart failure. Heart failure was due to coronary artery disease in 23 patients (group I) and to idiopathic dilated cardiomyopathy in 16 (group II). LV shape was quantitated based on the ratio of LV major-to-minor axis and LV sphericity index calculated at end-systole and end-diastole. In group I, 9 patients had angiographic evidence of MR and 14 did not. In group II, 10 patients had MR and 6 did not. Within each group, there were no differences between patients with and without MR with regard to LV chamber volume and regional segmental wall motion abnormalities. In both groups, however, a significant difference was observed between patients with and without MR with respect to end-systolic and end-diastolic LV shape indexes. In group I, the end-systolic major-to-minor axis ratio was lower in patients with (1.42 +/- 0.04) than without (1.72 +/- 0.05) MR (p less than 0.001). Similar differences were observed in group II (1.41 +/- 0.06 vs 1.69 +/- 0.04) (p less than 0.01). In group I, the end-systolic sphericity index was also greater in patients with (0.32 +/- 0.02) than without (0.25 +/- 0.01) MR (p less than 0.02). Similar differences were observed in group II (0.37 +/- 0.03 vs 0.26 +/- 0.01) (p less than 0.02). These data indicate that in patients with severe heart failure, functional MR is present in those who manifest a more spherical LV cavity.
Ninety-one patients with dilated cardiomyopathy were studied by two-dimensional, pulsed, and color Doppler echocardiography (1) to detect and quantify mitral regurgitation (MR), (2) to record apical flow velocities in systole and diastole, and (3) to detect the presence of left ventricular thrombi. MR was detected in 57% of the patients and thrombi were present in 40%, but the occurrence of both MR and thrombus was rare (8%). Apical flow velocity was significantly higher throughout the cardiac cycle in the group with MR (diastole 15 +/- 7 vs 9 +/- 7 cm/sec; systole 29 +/- 12 vs 16 +/- 13 cm/sec; p less than 0.001 for both), accounting for the rarity of thrombi in this group. Follow-up data on 89% of the patients showed markedly decreased survival in the group with MR (22% vs 60% at 32 +/- 6 months, p less than 0.005), and this was evident even in patients with mild MR. Thus although MR is a noninvasively obtainable marker of a large subgroup of patients with dilated cardiomyopathy "protected" from left ventricular thrombus formation, it is a sensitive marker of decreased survival.
The aim was to study the nature, magnitude, and time course of left ventricular structural adaptations to evolving heart failure.
17 male mongrel dogs, weight 24.9(SD 3.7) kg, underwent rapid ventricular pacing (250 beats.min-1) until severe heart failure developed. Two dimensional echocardiographic and Doppler studies were performed at control, then weekly to severe heart failure. Haemodynamic measurements were made at control and severe heart failure. All studies were performed with the animals conscious during temporary sinus rhythm.
Left ventricular diastolic volume gradually increased and the left ventricle assumed a more globular shape associated with significant wall thinning. Both the change in diastolic volume after one week of pacing and at the time of severe heart failure correlated with the time to peak heart failure. Mitral regurgitation was mild after one week of pacing, became moderate in most animals at severe heart failure, and lagged temporarily behind the increase in cardiac dimensions. The percentage increase in mitral annular size was significantly less than the increase in left ventricular cross sectional area.
In pacing induced heart failure (1) marked left ventricular remodelling occurs, (2) the extent of left ventricular dilatation, both early and late, correlates directly with the time required for the development of severe heart failure, (3) mitral regurgitation is an epiphenomenon and is most likely to be caused by the increase in left ventricular cross sectional area.
Afterload reduction therapy can acutely improve hemodynamic function in patients with advanced heart failure; however, it is unknown if initial reductions in mitral and tricuspid regurgitation and atrial volumes can be sustained with oral therapy. Atrial volumes and atrioventricular valve regurgitation were measured using 2-dimensional and Doppler echocardiography with color-flow imaging in 14 patients with dilated heart failure (ejection fraction 17 +/- 4%) before and after 3 +/- 1 days of intensive vasodilator and diuretic therapy tailored to hemodynamic goals. Echocardiography was repeated again after 6 +/- 2 months on oral vasodilators and a flexible diuretic regimen. Acute therapy reduced systemic vascular resistance from 1,760 +/- 460 to 1,010 +/- 310 dynes.s.cm-5, pulmonary artery wedge pressure from 30 +/- 5 to 17 +/- 4 mm Hg, and right atrial pressure from 13 +/- 5 to 7 +/- 3 mm Hg, and led to a 61% increase in stroke volume (from 36 +/- 10 to 58 +/- 14 ml) (p less than 0.01). Mitral and tricuspid regurgitation, determined by color-flow fraction, initially decreased from 0.34 +/- 0.17 to 0.20 +/- 0.20 and from 0.33 +/- 0.15 to 0.13 +/- 0.13, respectively (p less than 0.001). This reduction was sustained at 6 months. Significant decreases occurred with acute therapy, with further reductions at 6 months in both mean left atrial volume (from 100 +/- 25 to 80 +/- 19 to 65 +/- 15 cm3) and right atrial volume (from 85 +/- 23 to 64 +/- 23 to 52 +/- 14 cm3) (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac performance and mitral regurgitation were measured by Doppler echocardiography and right heart catheterization in 12 patients with severe congestive heart failure who performed isometric exercise during control and intravenous administration of dobutamine and nitroglycerin. During control isometric exercise, mitral regurgitant volume increased from 18 +/- 13 to 31 +/- 17 ml (p less than 0.01), while forward stroke volume, by both thermodilution and Doppler echocardiography, substantially decreased. At rest, dobutamine decreased mitral regurgitant volume from 18 +/- 13 to 11 +/- 10 ml (p less than 0.05), while forward stroke volume increased from 46 +/- 13 to 55 +/- 15 ml (p less than 0.05). During isometric exercise, dobutamine tended to decrease mitral regurgitant volume (24 +/- 12 vs. 31 +/- 17 ml; NS) when compared with control exercise. At rest, nitroglycerin decreased mitral regurgitant volume from 18 +/- 13 to 11 +/- 11 ml (p less than 0.05), while forward stroke volume, by both thermodilution and Doppler echocardiography, substantially increased. Similarly, during isometric exercise, nitroglycerin decreased mitral regurgitant volume from 31 +/- 17 to 20 +/- 14 ml (p less than 0.05), while significantly increasing forward stroke volume. At control rest, the median mitral regurgitant fraction was 24% for the 12 patients. Neither dobutamine nor nitroglycerin changed significantly forward stroke and mitral regurgitant volumes at rest and during isometric exercise in the six patients with resting mitral regurgitant fraction below the median. In contrast, dobutamine and nitroglycerin significantly decreased mitral regurgitant volume and increased forward stroke volume both at rest and during isometric exercise in the six patients with mitral regurgitant fraction greater than the median.(ABSTRACT TRUNCATED AT 250 WORDS)
A transformation from the normal elliptical shape of the left ventricle that may accompany various disease states and that may be indicative of myocardial remodeling, has not been completely addressed in part because of the need for a descriptor of shape that is independent of chamber size. Accordingly, the goal of this study was twofold: to derive dimensionless echocardiographic descriptors of left ventricle chamber shape that are independent of chamber volume and to use these descriptors to quantitatively compare the shape of left ventricles that were either of normal size (81 +/- 17 ml, 19 patients) or were enlarged secondary to idiopathic cardiomyopathy (194 +/- 61 ml, 46 patients) or chronic aortic or mitral valve incompetence (196 +/- 67 ml, 14 patients). Two-dimensional and M-mode determined descriptors of left ventricle shape based on its width, length, and area were found to be independent of left ventricle volume. These descriptors were significantly greater in cardiomyopathy compared with the normal or dilated left ventricle secondary to valvular incompetence, indicating that the left ventricle had become nearly spherical. A spherical shape of the left ventricle was not observed with valvular incompetence. The ability to classify a patient as having either a normal or a cardiomyopathic left ventricle by discriminant function analysis was enhanced when both left ventricle size and shape were considered. In a prospective study using discriminant function and fractional shortening, we found that patients with valvular incompetence could be classified as having either a normal discriminant function and fractional shortening, an abnormal discriminant function and normal fractional shortening, or an abnormal discriminant function and fractional shortening.(ABSTRACT TRUNCATED AT 250 WORDS)
At a time when hospital mortality for adult cardiac operations is continuing to fall, the ischemic mitral regurgitation subset remains at relatively high risk. Based on analysis of available data, efforts to improve results might be directed toward a more general application of mitral valve reconstruction in this population. Other promising therapeutic measures include the liberal use of reperfusion therapy in the acute papillary muscle dysfunction group, better selection of patients for operation, and, perhaps, operative recommendation to a greater proportion of the more stable patients who previously were treated medically. Incorporating these therapeutic concepts into routine clinical practice may improve the overall prognosis of this difficult subgroup.
We have presented recommendations for the optimum acquisition of quantitative two-dimensional data in the current echocardiographic environment. It is likely that advances in imaging may enhance or supplement these approaches. For example, three-dimensional reconstruction methods may greatly augment the accuracy of volume determination if they become more efficient. The development of three-dimensional methods will depend in turn on vastly improved transthoracic resolution similar to that now obtainable by transesophageal echocardiography. Better resolution will also make the use of more direct methods of measuring myocardial mass practical. For example, if the epicardium were well resolved in the long-axis apical views, the myocardial shell volume could be measured directly by the biplane method of discs rather than extrapolating myocardial thickness from a single short-axis view. At present, it is our opinion that current technology justifies the clinical use of the quantitative two-dimensional methods described in this article. When technically feasible, and if resources permit, we recommend the routine reporting of left ventricular ejection fraction, diastolic volume, mass, and wall motion score.
Mitral regurgitation (MR) has long been known to accompany left ventricular dilatation, yet the underlying mechanism has been a source of controversy. Anular dilatation, lack of sphincteric contraction of the mitral valve ring and malalignment of the papillary muscles have all been considered possible etiologies. Chandraratna and Aronow1 found that the dimensions of the mitral anulus, as measured by echocardiography in the 2-dimensional long-axis parasternal view, did not correlate with the clinical presence of MR in patients with dilated cardiomyopathy. Boltwood et al,2 on the other hand, designed a spatial reconstruction of the mitral anulus using rotational cross-sectional echocardiography, and found that dilatation of the mitral anulus in cardiomyopathy was closely correlated with MR. In both studies,1,2 the presence of MR was determined solely by auscultation. In another report of patients with dilated cardiomyopathy, the mitral ring diameter and the degree of ring contraction measured echocardiographically did not correlate with the presence or absence of MR, which was detected on left ventriculography in 63% of patients.3 In a study using both 2-dimensional and Doppler techniques, all subjects with cardiomyopathy were found to have MR and tricuspid regurgitation (TR) was noted in 93%.4 We designed this study to determine how frequently Doppler flow examination could detect MR or TR in patients with cardiomyopathy. In addition, we wanted to determine if the size of the mitral anulus by simple 2-dimensional measurements would correlate with the presence and severity of MR as detected by Doppler echocardiography.
Ischemic mitral regurgitation is a serious and increasingly common clinical disorder, but at present, little is known of the associated prognostic implications, especially in specific therapeutic subgroups. Over a 6.5-year period beginning January 1, 1981, postinfarction mitral regurgitation was demonstrated ventriculographically in 2,343 (19%) of 11,748 patients having significant coronary artery disease defined at cardiac catheterization. Moderate or severe regurgitation was observed in 381 (3%), and among these patients, four treatment groups were defined: Group I (medical, n = 165), Group II (reperfusion, n = 63), Group III (coronary artery bypass only, n = 94), and Group IV (valve replacement or repair in addition to coronary bypass, n = 59). Multivariable regression analysis of survival data in the overall population and in specific treatment groups was performed with the Cox proportional hazards model. Defined and undefined selection biases precluded formal quantitative survival comparisons among some treatment groups; however, unadjusted and adjusted survival analysis for each group revealed several interesting concepts. First, increasing severity of mitral regurgitation had a progressively negative impact on survival prognosis regardless of treatment. Congestive heart failure, the number of associated disorders, acute presentation requiring cardiac care unit admission, diminished ejection fraction, increasing coronary obstruction, and advanced age all worsened prognosis (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Measurements of mitral and aortic valve flows were obtained with two-dimensional Doppler echocardiography in 25 patients with isolated mitral (n = 19) or aortic (n = 6) regurgitation and regurgitant fraction was calculated as the difference between the two flows divided by the flow through the regurgitant valve. Results were compared with measurements of regurgitant fraction determined by combined left ventricular angiography and thermodilution. Regurgitant fraction averaged 56 +/- 18% (range 19 to 79) by Doppler echocardiography and 48 +/- 17% (range 13 to 72) by angiography. A significant correlation was observed between the two methods (r = 0.91; SEE = 7%). In contrast, no significant correlation was found between regurgitant fraction measured by either method and the angiographic 1+ to 4+ qualitative classification of regurgitation. Doppler echocardiography appears to be an accurate method for the non-invasive quantification of severity of regurgitation in isolated left-sided valve lesions.
The evaluation and care of patients with mitral regurgitation would be facilitated by an easy, reproducible and noninvasive method that could quantitate the hemodynamic burden. In this study, we describe a new Doppler echocardiographic method that measures the regurgitant fraction and we compare it with angiographic and scintigraphic methods. A total of 27 patients with mitral regurgitation were evaluated by echocardiography and either cardiac catheterization or scintigraphy. With two-dimensional echocardiography, diastolic and systolic volumes were measured to derive the left ventricular stroke volume (LVSV). The forward stroke volume (FSV) was obtained from the product of M mode-derived aortic valve area and ascending aortic flow velocity integral assessed by continuous-wave Doppler. Regurgitant fraction was calculated as follows: (LVSV - FSV)/LVSV. Comparisons showed that regurgitant fraction calculated by Doppler echocardiography correlated with regurgitant fraction determined by both cardiac catheterization (r = .82) and by scintigraphy (r = .89). There was, however, an important interobserver variability within each method: 10%, 13%, and 11% for Doppler echocardiography, angiography, and scintigraphy, respectively. In conclusion, Doppler echocardiography can be used to quantitate mitral regurgitation. Serial noninvasive determinations of regurgitant fraction may be useful in the evaluation of therapy and in the follow-up of patients with mitral insufficiency.
This review deals with the functional anatomy of the six components of the mitral apparatus, namely, the left atrial wall, annulus, leaflets, chordae tendineae, papillary muscles, and left ventricular wall. Each component is considered individually, in the context of the apparatus as a whole, in relation to the mode of closure of the normal mitral valve, and in the light of many acquired and congenital disorders that disturb the harmony of the finely coordinated mitral mechanism and render it incompetent.
The left atrium is related to mitral valve competence in terms of contraction and relaxation and in terms of dilatation of its posterior wall. The annulus not only serves as a fulcrum for the leaflets but exhibits sphincteric contraction in systole that decreases the size of the orifice. The two leaflets differ in shape but are nearly identical in area, and together are about two and one half times the area of the orifice that they are required to close. Leaflet abnormalities causing acquired or congenital mitral regurgitation result from deficient leaflet tissue, excessive leaflet tissue, or restricted leaflet mobility. Chordae tendineae are considered according to their leaflet attachments, ventricular attachments, thicknesses, lengths, and arborization patterns. Mitral regurgitation due to chordal abnormalities results from chordae that are abnormally long, abnormally short, ectopically inserted, or ruptured. In this context, systolic clicks and late systolic murmurs are discussed, and severe acute mitral regurgitation is contrasted with severe chronic mitral regurgitation. The papillary muscles and the left ventricular wall represent the two muscular components of the mitral apparatus. An appraisal of papillary muscle dysfunction includes dysfunction with loss in continuity (rupture) and dysfunction without loss in continuity (fibrosis, ischemia, replacement). Finally, the role of altered left ventricular shape is discussed in the context of mitral regurgitation, and the effect of dilatation is ascribed chiefly to alterations in the position of papillary muscles and their directional axes of tension.
We sought to elucidate the mechanism of mitral regurgitation (MR) in dilated cardiomyopathy (DCM). Quantitative two-dimensional echocardiographic examinations were performed in 27 patients, 18 with DCM (nine with MR on physical examination, nine without MR) and nine without underlying heart disease. The MR and 'no MR' patients were clinically comparable. Spatial reconstructions from multiple apical cross sections were used to estimate the mitral leaflet area needed to occlude the orifice for a given midsystolic coaptation configuration (LEAF), as well as mitral annular area index, left ventricular volume, and left atrial volume. Similarly, reconstructions from parasternal short-axis views were used to estimate central chordae tendinae length and angulation. From selective parasternal views papillary muscle (PM) length and contraction and the tethering length from the PM base to annular plane were measured. The MR group was characterized by markedly enlarged occlusional leaflet area (LEAF 19.8 ± 3.1 in MR vs 13.8 ± 2.8 in no MR groups vs 6.3 ± 0.9 cm2 in normal group; p < .01), striking mitral annular dilatation (midsystolic annular area index 7.5 ± 0.8 in MR vs 4.6 ± 0.9 in no MR group vs 2.9 ± 0.4 cm2/m2 in normal group; p < .01), and left atrial enlargement (end-systolic left atrial volume 129 ± 39 in MR vs 73 ± 14 in no MR group vs 29 ± 5 ml in normal group; p < .01). Chordal length and angulation, PM length, contraction, and tethering length, and left ventricular volume were not significantly different in the MR vs the no MR group. Noncoaptation of the mitral leaflets at their free margins was not observed in any MR patient. With the use of stepwise linear regression LEAF was determined chiefly by annular size (R2 .868), with left ventricular size having little additional influence (R2 increment .071). Thus, DCM is associated with enlargement of the mitral anulus, which is more pronounced in those patients with MR. Based on the quantitative estimates of occlusional leaflet area, we postulate that mitral leaflet tissue can stretch somewhat to accommodate dilatation of the mitral complex, but as the requirement for occlusional leaflet area increases less tissue is available for coaptation. Thus, although coaptation continues to occur, the valvular seal becomes ineffective once a critical LEAF is reached. The chief determinant of LEAF is the mitral annular size, while left ventricular size is a less important factor.
Clinical acceptance of an association between papillary muscle dysfunction and mitral regurgitation is widespread, despite the lack of objective support. To evaluate a possible association, we performed echocardiographic examinations on 22 patients with prior myocardial infarction and clinical evidence of papillary muscle dysfunction, 40 patients with prior myocardial infarction and no clinical evidence of papillary muscle dysfunction, and 20 normal subjects. There was a unique pattern of incomplete mitral leaflet closure in a high percentage (91%) of infarct patients with mitral regurgitation. In these patients, one or both leaflets were effectively arrested within the cavity of the left ventricle during ventricular systole. Dyskinetic wall motion in the region immediately surrounding one of the papillary muscles was present in 23 of 24 patients (96%) with demonstrated incomplete closure. This study provides the first objective evidence that de novo mitral regurgitation in patients with prior myocardial infarction is due to dyskinesis involving the left ventricular myocardium beneath one of the papillary muscles, producing increased tension on the mitral leaflets and preventing normal closure.
Changes in the geometric and intravalvular relationships between subunits of the ovine mitral valve were measured before and after acute posterior wall myocardial infarction in three dimensions by means of sonomicrometry array localization. In 13 sheep, nine sonomicrometer transducers were attached around the mitral anulus and to the tip and base of each papillary muscle. Five additional transducers were placed on the epicardium. Snares were placed around three branches of the circumflex coronary artery. One to 2 weeks later, echocardiograms, dimension measurements, and left ventricular pressures were obtained before and after the coronary arteries were occluded. Data were obtained from seven sheep. Coronary occlusion infarcted 32% of the posterior left ventricle and produced 2 to 3+ mitral regurgitation by Doppler color flow mapping. Multidimensional scaling of dimension measurements obtained from sonomicrometry transducers produced three-dimensional spatial coordinates of each transducer location throughout the cardiac cycle before and after infarction and onset of mitral regurgitation. After posterior infarction, the mitral anulus enlarges asymmetrically along the posterior anulus, and the tip of the posterior papillary muscle moves 1.5 +/- 0.3 mm closer to the posterior commissure at end-systole. The posterior papillary muscle also elongates 1.9 +/- 0.3 mm at end-systole. The left ventricle enlarges asymmetrically and ventricular torsion along the long axis changes. The development of postinfarction mitral regurgitation appears to be the consequence of multiple small changes in ventricular shape and contractile deformation and in the spatial relationship of mitral valvular subunits.
Uncontrollable severe mitral regurgitation is a frequent complication of end-stage cardiomyopathy, significantly contributing to heart failure in these patients, and predicts a poor survival. Although elimination of mitral valve regurgitation could be most beneficial in this group, corrective mitral valve surgery has not been routinely undertaken in these very ill patients because of the presumed prohibitive operative mortality. We studied the early outcome of mitral valve reconstruction in 16 consecutive patients with cardiomyopathy and severe, refractory mitral regurgitation operated on between June 1993 and April 1994. There were 11 men and five women, aged 44 to 78 years (64 +/- 8 years) with left ventricular ejection fractions of 9% to 25% (16% +/- 5%). Preoperatively all patients were in New York Heart Association class IV, had severe mitral regurgitation (graded 0 to 4+ according to color flow Doppler transesophageal echocardiography) and two were listed for transplantation. Operatively, a flexible annuloplasty ring was implanted in all patients. Four patients also had single coronary bypass grafting for incidental coronary disease. In four patients the operation was performed through a right thoracotomy because of prior coronary bypass grafting, and four patients also underwent tricuspid valve reconstruction for severe tricuspid regurgitation. No patient required support with an intraaortic balloon pump. There were no operative or hospital deaths and mean hospital stay was 10 days. There were three late deaths at 2, 6, and 7 months after mitral valve reconstruction, and the 1-year actuarial survival has been 75%. At a mean follow-up of 8 months, all remaining patients are in New York Heart Association class I or II, with a mean postoperative ejection fraction of 25% +/- 10%. There have been no hospitalizations for congestive heart failure, and a decrease in medications required has been noted. For patients with cardiomyopathy and severe mitral regurgitation, mitral valve reconstruction as opposed to replacement can be accomplished with low operative and early mortality. Although longer term follow-up is mandatory, mitral valve reconstruction may allow new strategies for patients with end-stage cardiomyopathy and severe mitral regurgitation, yielding improvement in symptomatic status and survival.
We attempted to determine the accuracy and pitfalls of calculating the mitral regurgitant orifice area with the proximal isovelocity surface area method in a clinical series that included patients with valvular prolapse and eccentric jets.
The effective regurgitant orifice area, a measure of lesion severity of mitral regurgitation, can be calculated by the proximal isovelocity surface area method, the accuracy and pitfalls of which have not been established.
In 119 consecutive patients with isolated mitral regurgitation, effective regurgitant orifice area was measured by the proximal isovelocity surface area method and compared with measurements simultaneously obtained by quantitative Doppler and quantitative two-dimensional echocardiography.
The effective mitral regurgitant orifice area measured by the proximal isovelocity surface area method tended to be overestimated compared with that measured by quantitative Doppler and quantitative two-dimensional echocardiography (38 +/- 39 vs. 36 +/- 33 mm2 [p = 0.09] and 34 +/- 32 mm2 [p = 0.02], respectively). Overestimation was limited to patients with prolapse (61 +/- 43 vs. 56 +/- 35 mm2 [p = 0.05] and 54 +/- 34 mm2 [p = 0.014]) and was restricted to patients with nonoptimal flow convergence (n = 7; 137 +/- 35 vs. 84 +/- 34 mm2 [p = 0.002] and 79 +/- 33 mm2 [p = 0.002]). In patients with optimal flow convergence (n = 112), excellent correlations with both reference methods were obtained (r = 0.97, SEE 6 mm2 and r = 0.97, SEE 7 mm2, p < 0.0001).
In calculating the mitral effective regurgitant orifice area with the proximal isovelocity surface area method, the observed pitfall (overestimation due to nonoptimal flow convergence) is rare. Otherwise, the method is reliable and can be used clinically in large numbers of patients.
Color Doppler jet analysis is widely used to characterize the degree of mitral regurgitation (MR), but the validity of this approach in patients with ischemic or functional MR has not been established. It was hypothesized that color Doppler jet area overestimates the magnitude of MR of ischemic or functional origin. The severity of isolated MR in 170 patients was measured by using Doppler/echocardiography. Group 1 (n = 58) included patients with ischemic or functional MR, and group 2 (n = 112) included those with organic MR. The regurgitant jet area and 2 methods of quantitation (quantitative Doppler and quantitative 2-dimensional echocardiography) were measured simultaneously. In group 1, color jet area was larger (10.6 +/- 5.3 vs 8.2 +/- 5.3 cm2, p = 0.004) but corresponded to a smaller regurgitant volume and regurgitant fraction by quantitative Doppler (28 +/- 14 vs 55 +/- 46 ml, p = 0.0006, and 31 +/- 12% vs 38 +/- 20%, p = 0.02, respectively) and by quantitative 2-dimensional echocardiography (22 +/- 11 vs 49 +/- 40 ml, p < 0.0001, and 27 +/- 12% vs 36 +/- 20%, p = 0.005, respectively). Enlargement of the left-sided chambers was more marked in group 1. In ischemic/functional MR, the diagnosis of severe regurgitation by color Doppler (jet area > 8 cm2) was confirmed by quantitative methods (regurgitant fraction > or = 50%) in only 6% to 11% of patients, whereas it was confirmed in 60% to 73% of patients with organic MR (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Dilated cardiomyopathy is an important cause of morbidity and mortality among patients with congestive heart failure. Hemodynamic and prognostic characterization are critical in guiding selection of medical and surgical therapies.
A cohort of 102 patients with the clinical diagnosis of dilated cardiomyopathy who underwent echocardiographic examination between 1986 and 1990 was identified and followed up through July 1, 1991. Patients with moderate or severe symptoms had lower indices of systolic function and greater left atrial and right ventricular dilation. Mitral inflow Doppler signals were characterized by a restrictive left ventricular filling pattern. In multivariate logistic regression analysis, deceleration time, ejection fraction, and peak E velocity were independently associated with symptom status. Over a mean follow-up of 36 months, 35 patients died. Kaplan-Meier estimated survival at 1, 2, and 4 years was 84%, 73%, and 61%, respectively, and was significantly poorer than that of an age- and sex-matched population. The subgroup with an ejection fraction < 0.25 and deceleration time < 130 milliseconds had a 2-year survival of only 35%. The subgroup with ejection fraction < 0.25 and deceleration time > 130 milliseconds had an intermediate 2-year survival of 72%, whereas patients with an ejection fraction > or = 0.25 had 2-year survivals > or = 95% regardless of deceleration time. In multivariate analysis, ejection fraction and systolic blood pressure were independently predictive of subsequent mortality. Mitral deceleration time was significant in univariate analysis.
In patients with the clinical diagnosis of dilated cardiomyopathy, markers of diastolic dysfunction correlated strongly with congestive symptoms, whereas variables of systolic function were the strongest predictors of survival. Consideration of both ejection fraction and deceleration time allowed identification of subgroups with divergent long-term prognoses.
Data from cardiac catheterization at rest and during exercise in 57 patients with dilated cardiomyopathy (DCM) were analyzed to evaluate the bearing of mitral regurgitation (MR) detected by color Doppler echocardiography (CDE) on prognostically important invasive hemodynamic parameters and survival. The etiology of DCM was coronary artery disease in 21 patients and unproven ('idiopathic') in 36 patients. MR was detected by CDE in 34 patients (60%) with an agreement of 93% compared to left ventriculography. Mean age, etiology of DCM and duration of symptoms were similar in patients with and without MR, while patients with MR were in a higher NYHA class, had lower ejection fraction (LVEF) (25 +/- 13 vs. 35 +/- 17%; p < 0.02), larger left ventricular volumes (356 +/- 138 vs. 268 +/- 61 ml; p < 0.01) and higher left ventricular end-diastolic pressure (LVEDP) (21 +/- 9 vs. 13 +/- 7 mm Hg; p < 0.01). At rest, right-sided pressures were higher in patients with MR compared to patients without MR (pulmonary wedge pressure 20 +/- 9 vs. 10 +/- 3 mm Hg, mean pulmonary arterial pressure 30 +/- 11 vs. 20 +/- 8 mm Hg, mean right atrial pressure 9 +/- 4 vs. 4 +/- 2 mm Hg, all p < 0.001), but no significant differences were found in cardiac index (CI) or stroke index (SI).(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of this study was to determine the feasibility, relation to other methods and significance of the effective regurgitant orifice area measurement.
Assessment of the severity of valvular regurgitation (effective regurgitant orifice area) has not been implemented in clinical practice but can be made by Doppler echocardiography.
Effective regurgitant orifice area was calculated by Doppler echocardiography as the ratio of regurgitant volume/regurgitant jet time-velocity integral and compared with color flow Doppler mapping, angiography, surgical classification, regurgitant fraction and variables of volume overload.
In 210 consecutive patients examined prospectively, feasibility improved from the early to the late experience (65% to 95%). Effective regurgitant orifice area was 28 +/- 23 mm2 (mean +/- SD) for aortic regurgitation (32 patients), 22 +/- 13 mm2 for ischemic/functional mitral regurgitation (50 patients) and 41 +/- 32 mm2 for organic mitral regurgitation (82 patients). Significant correlations were found between effective regurgitant orifice and mitral jet area by color flow Doppler mapping (r = 0.68 and r = 0.63, p < 0.0001, respectively) and angiographic grade (r = 0.77, p = 0.0004). Effective regurgitant orifice area in surgically determined moderate and severe lesions was markedly different in mitral regurgitation (35 +/- 12 and 75 +/- 33 mm2, respectively, p = 0.009) and in aortic regurgitation (21 +/- 8 and 38 +/- 5 mm2, respectively, p = 0.08). Strong correlations were found between effective regurgitant orifice area and variables reflecting volume overload. A logarithmic regression was found between effective regurgitant orifice area and regurgitant fraction, underlining the complementarity of these indexes.
Calculation of effective regurgitant orifice area is a noninvasive Doppler development of an old hemodynamic concept, allowing assessment of the lesion severity of valvular regurgitation. Feasibility is excellent with experience. Effective regurgitant orifice area is an important and clinically significant index of regurgitation severity. It brings additive information to other quantitative indexes and its measurement should be implemented in the comprehensive assessment of valvular regurgitation.
Quantitation of valvular regurgitation remains a challenge. The accuracy of quantitative Doppler is controversial, and its ability to measure regurgitant volume is unknown; therefore, it is not widely used.
In 120 patients (20 without regurgitation, 19 with aortic regurgitation, and 81 with mitral regurgitation), the stroke volume through the mitral annulus and left ventricular outflow tract were measured using pulsed-wave Doppler concurrently with left ventricular stroke volume calculated using left ventricular volumes measured by two-dimensional echocardiography Simpson's biapical method. Regurgitant volume and fraction were thus computed using Doppler or ventricular methods. In normal patients there were good correlations between Doppler and left ventricular measurements of stroke volume. Doppler regurgitant volume and fraction were 4.4 +/- 4.4 mL and 5.3 +/- 4.5%, respectively. In patients with aortic regurgitation, there were good correlations between Doppler and left ventricular measurements of stroke volume, regurgitant volume, and regurgitant fraction (r = 0.97, r = 0.95, and r = 0.93, respectively; p < 0.0001). In patients with mitral regurgitation, despite good correlations between Doppler and ventricular methods for stroke volume, regurgitant volume, and regurgitant fraction (r = 0.94, r = 0.93, and r = 0.94, respectively; p < 0.001), these variables were overestimated by Doppler. However, in the last 54 patients compared with the first 27, overestimation decreased significantly for regurgitant volume (5 +/- 10 mL versus 18 +/- 27 mL, p < 0.05) and regurgitant fraction (3.3 +/- 6.7% versus 6.2 +/- 6.8%, p = 0.05).
Quantitative Doppler can be performed in large numbers of patients in a clinical laboratory. Its potential limitation was identified as overestimation of mitral regurgitation, which is overcome with increased experience. Its achieved accuracy in mitral and aortic regurgitation allows measurement not only of regurgitant fraction but most importantly of regurgitant volume.
This study was performed to assess whether the combination of multiple echocardiographic and Doppler variables can provide a reliable estimation of pulmonary artery wedge pressure in patients with chronic heart failure.
In patients with chronic heart failure a high pulmonary artery wedge pressure is associated with poor prognosis, more severe symptoms and low exercise tolerance. Several Doppler echocardiographic indexes have been shown to be related to pulmonary artery wedge pressure, but the dispersion of data has generally not allowed a quantitative assessment of this important variable.
Simultaneous Doppler echocardiographic examinations and right heart catheterizations were performed in 231 patients with chronic heart failure due to dilated cardiomyopathy. Mitral and pulmonary venous flow velocity variables, left atrial volumes, mitral regurgitation jet area and left ventricular ejection fraction were correlated with pulmonary artery wedge pressure by both single and multilinear regression analysis. The reliability of the obtained multilinear equations was then tested in a separate group of 60 patients.
By univariate analysis, the deceleration rate of early diastolic mitral flow and the systolic fraction of pulmonary venous flow showed the strongest correlations (r=0.78 and =-0.76, respectively). Stepwise regression analysis led to two multilinear equations for predicting pulmonary artery wedge pressure in the whole population: the first included only two-dimensional echocardiographic and mitral flow velocity variables (r=0.84) and the second also included pulmonary venous flow variables (r=0.87). The highest correlation was obtained (r=0.89) by a third equation in the 73 patients without significant mitral regurgitation. Correlation coefficients between estimated and measured pulmonary artery wedge pressure were 0.91 (SEE=2.7 mm Hg) and 0.97 (SEE=1.8 mm Hg) when the first and the second equation, respectively, were applied to the testing group.
These results indicate that, in patients with chronic heart failure due to dilated cardiomyopathy, pulmonary artery wedge pressure can be reliably estimated even when mitral regurgitation is present by combining Doppler echocardiographic variables of mitral and pulmonary venous flow.
To evaluate the relationship between the intensity of murmurs and severity of mitral and aortic regurgitation.
Consecutive patients with chronic isolated aortic (n = 40) or mitral (n = 170) regurgitation undergoing echocardiographic quantitation of regurgitation between 1990 and 1991 were studied. Regurgitant volume and fraction were measured using two simultaneous methods (quantitative Doppler echocardiography and quantitative two-dimensional echocardiography); the intensity of the regurgitant murmur (grade 0 to 6) was noted by physicians unaware of the study.
Correlations between murmur intensity and regurgitant volume and fraction were good in aortic regurgitation (r = .60 and r = .67, respectively; P < 0.001) and mitral regurgitation (r = .64 and r = .67, respectively; P < 0.001) but weaker (r = .47 and r = .45, respectively) in the subset of mitral regurgitation of ischemic or functional cause. Murmur intensity grades > or = 3 for aortic regurgitation and > or = 4 for mitral regurgitation predicted severe regurgitation (regurgitant fraction > or = 40%) in 71% and 91% of patients, respectively. Murmur grades < or = 1 for aortic regurgitation and < or = 2 for mitral regurgitation predicted "not severe" regurgitation in 100% and 88% of patients, respectively. Murmur grades 2 for aortic regurgitation and 3 for mitral regurgitation were not correlated to degree of regurgitation. The severity of regurgitation was the most powerful determinant of intensity of murmur.
Murmur intensity correlates well with the degree of chronic organic aortic and mitral regurgitation, and can be used as a predictor of regurgitation severity and as a simple guideline for diagnostic testing in these patients.
This study sought to analyze the determinants of pulmonary hypertension in patients with left ventricular dysfunction.
Pulmonary hypertension in patients with left ventricular dysfunction is a predictor of poor outcome. The independent role of cardiac functional abnormalities in the genesis of pulmonary hypertension is unclear.
In 102 consecutive patients with primary left ventricular dysfunction (ejection fraction < 50%), systolic pulmonary artery pressure was prospectively measured by Doppler echocardiography (using tricuspid regurgitant velocity), and left ventricular systolic and diastolic function, functional mitral regurgitation, cardiac output and left atrial volume were quantified.
Systolic pulmonary artery pressure was elevated in patients with left ventricular dysfunction (51 +/- 14 mm Hg [mean +/- SD]), but the range was wide (23 to 87 mm Hg). Of the numerous variables correlating significantly with systolic pulmonary artery pressure, the strongest were mitral deceleration time (r = -0.61, p = 0.0001; odds ratio of pulmonary pressure > or = 50 mm Hg [95% confidence interval] if < 150 ms, 48.8 [14.8 to 161]) and mitral effective regurgitant orifice (r = 0.50, p = 0.0001; odds ratio [95% confidence interval] if > or = 20 mm2, 5.9 [2.3 to 15.5]). In multivariate analysis, these two variables were the strongest predictors of systolic pulmonary artery pressure in association with age (p = 0.005). Ejection fraction or end-systolic volume was not an independent predictor of pulmonary artery pressure.
Pulmonary hypertension is frequent and highly variable in patients with left ventricular dysfunction. It is not independently related to the degree of left ventricular systolic dysfunction but is strongly associated with diastolic dysfunction (shorter mitral deceleration time) and the degree of functional mitral regurgitation (larger effective regurgitant orifice). These results emphasize the importance of assessing diastolic function and quantifying mitral regurgitation in patients with left ventricular dysfunction.
Mitral regurgitation (MR) may complicate acute myocardial infarction (MI). However, it is not known whether mild MR is an independent predictor of post-MI outcome.
The study cohort consisted of 727 Survival and Ventricular Enlargement Study patients who underwent cardiac catheterization, including left ventriculography, up to 16 days after MI. Left ventriculograms were analyzed for diastolic and systolic volumes, global left ventricular sphericity, extent of wall motion abnormality, and endocardial curvature. The presence of MR was related to the risk of developing a cardiovascular event during 3.5 years of follow-up. MR was present in 141 patients (19.4%). Severe (3+) MR was present in only 2 patients. Patients with MR were more likely to have a persistently occluded infarct artery (MR versus no MR, 27.3% versus 15.2%; P=.001). Although the ejection fractions were similar, MR patients had larger end-systolic and end-diastolic volumes and more spherical ventricles than patients without MR. Sphericity change from diastole to systole was also significantly reduced in MR patients. Patients with MR were more likely to experience cardiovascular mortality (29% versus 12%; P<.001), severe heart failure (24% versus 16%; P=.0153), and the combined end point of cardiovascular mortality, severe heart failure, or recurrent myocardial infarction (47% versus 29%; P<.001). The presence of MR was an independent predictor of cardiovascular mortality (relative risk, 2.00; 95% CI, 1.28 to 3.04).
Mild MR is an independent predictor of post-MI mortality. As such, it adds important information for risk stratification of post-MI patients.
Recent advances in three-dimensional (3D) echocardiography allow us to address uniquely 3D scientific questions, such as the mechanism of functional mitral regurgitation (MR) in patients with left ventricular (LV) dysfunction and its relation to the 3D geometry of mitral leaflet attachments. Competing hypotheses include global LV dysfunction with inadequate leaflet closing force versus geometric distortion of the mitral apparatus by LV dilatation, which increases leaflet tethering and restricts closure. Because geometric changes generally accompany dysfunction, these possibilities have been difficult to separate.
We created a model of global LV dysfunction by esmolol and phenylephrine infusion in six dogs. initially with LV expansion limited by increasing pericardial restraint and then with the pericardium opened. The mid-systolic 3D relations of the papillary muscle (PM) tips and mitral valve were reconstructed. Despite severe LV dysfunction (ejection fraction, 18+/-6%), only trace MR developed when pericardial restraint limited LV dilatation; with the pericardium opened, moderate MR accompanied LV dilatation (end-systolic volume, 44+/-5 mL versus 12+/-5 mL control, P<.001). Mitral regurgitant volume and orifice area did not correlate with LV ejection fraction and dP/dt (global function) but did correlate with changes in the tethering distance from the PMs to the anterior annulus derived from the 3D reconstructions, especially PM shifts in the posterior and mediolateral directions, as well as with annular area (P<.0005). By multiple regression, only changes in the PM-to-annulus distance independently predicted MR volume and orifice area (R2=.82 to .85, P=2x10(-7) to 6x10(-8)).
LV dysfunction without dilatation fails to produce important MR. Functional MR relates strongly to changes in the 3D geometry of the mitral valve attachments at the PM and annular levels, with practical implications for approaches that would restore a more favorable configuration.
Functional mitral regurgitation in patients with ischemic or dilated ventricles has been related to competing factors: altered tension on the leaflets due to displacement of their papillary muscle and annular attachments, which restricts leaflet closure, versus global ventricular dysfunction with reduced transmitral pressure to close the leaflets. In vivo, however, geometric changes accompany dysfunction, making it difficult to study these factors independently. Functional mitral regurgitation also paradoxically decreases in midsystole, despite peak transmitral driving pressure, suggesting a change in the force balance acting to create a regurgitant orifice, with rising transmitral pressure counteracting forces that restrict leaflet closure. In vivo, this mechanism cannot be tested independently of annular contraction that could also reduce midsystolic regurgitation.
An in vitro model was developed that allows independent variation of papillary muscle position, annular size, and transmitral pressure, with direct regurgitant flow rate measurement, to test the hypothesis that functional mitral regurgitation reflects an altered balance of forces acting on the leaflets. Hemodynamic and echocardiographic measurements of excised porcine valves were made under physiological pressures and flows. Apical and posterolateral papillary muscle displacement caused decreased leaflet mobility and apical leaflet tethering or tenting with regurgitation, as seen clinically. It reproduced the clinically observed midsystolic decrease in regurgitant flow and orifice area as transmitral pressure increased. Tethering delayed valve closure, increased the early systolic regurgitant volume before complete coaptation, and decreased the duration of coaptation. Annular dilatation increased regurgitation for any papillary muscle position, creating clinically important regurgitation; conversely, increased transmitral pressure decreased regurgitant orifice area for any geometric configuration.
The clinically observed tented-leaflet configuration and dynamic regurgitant orifice area variation can be reproduced in vitro by altering the three-dimensional relationship of the annular and papillary muscle attachments of the valve so as to increase leaflet tension. Increased transmitral pressure acting to close the leaflets decreases the regurgitant orifice area. These results are consistent with a mechanism in which an altered balance of tethering versus coapting forces acting on the leaflets creates the regurgitant orifice.
The purpose of this study was to quantify and characterize the regurgitant flow pattern and regurgitant orifice area in patients undergoing therapy for severe heart failure using contemporary echocardiographic techniques.
Mitral regurgitation may be dynamic in patients with heart failure and ultimately correlate with outcome in a group of patients.
Fourteen patients with severe heart failure felt to require hemodynamic monitoring for the optimization of medical therapy were enrolled. Two-dimensional and Doppler echocardiograms were performed before and following invasively guided therapy. Hemodynamics and standard echocardiographic dimensions were determined as well as regurgitant volume and regurgitant orifice area derived from color M-mode and Doppler measurements.
Invasively guided therapy for heart failure was associated with a reduction in weight, filling pressures of the left and right heart, systemic vascular resistance, and echocardiographic left atrial, left ventricular and mitral annular dimensions. The mitral regurgitant volume decreased from 47+/-27 ml before therapy to 14+/-14 ml after therapy; p < 0.001. While therapy for heart failure markedly attenuated the volume of regurgitation, the pattern of regurgitant flow across the mitral valve was not significantly altered. In contrast, there was no difference in the velocity time integral of the continuous-wave Doppler spectra of mitral regurgitation with therapy (128+/-23 cm to 123+/-25 cm, p = 0.23). In all patients, the regurgitant orifice area decreased with therapy from 0.55+/-0.38 cm2 to 0.21+/-0.20 cm2 (p < 0.001).
Pharmacologic reduction in filling pressure and systemic vascular resistance leads to a reduction in the dynamic mitral regurgitation of heart failure through a reduction in the regurgitant orifice area but not through a change in the gradient across the mitral valve. Reduction of the regurgitant orifice area is likely related to decreased left ventricular volumes and decreased annular distention.
A method is described for calculating tension and stress acting within the wall of the left ventricle during the cardiac cycle. This method is based upon ventricular pressure observations and measurements of left ventricular dimensions and wall thickness made from biplane angiocardiograms. To calculate wall tension and stress, it is assumed that the left ventricle can be represented as an ellipsoid of revolution with a relatively thin wall. The relative importance of ventricular pressure, volume, shape and wall thickness in determining the magnitude of wall tension and stress is illustrated and discussed.
Overestimation of severity of ischemic/functional mitral regurgitation by color Doppler jet area Sustained reduction in valvular regurgitation and atrial volumes with tailored vasodilator therapy in advanced congestive heart failure secondary to dilated (ischemic or idiopathic) cardiomyopathy
- Rb Mccully
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McCully RB, Enriquez-Sarano M, Tajik AJ, et al. Overestimation of severity of ischemic/functional mitral regurgitation by color Doppler jet area. Am J Cardiol. 1994;74:790 –793. 19. Hamilton MA, Stevenson LW, Child JS, et al. Sustained reduction in valvular regurgitation and atrial volumes with tailored vasodilator therapy in advanced congestive heart failure secondary to dilated (ischemic or idiopathic) cardiomyopathy. Am J Cardiol. 1991;67:259 –263.
Recommendations for quantitation of the left ventricle by two-dimensional echocardiography
American Society of Echocardiography Committee on Standards Subcommittee on Quantitation of Two-Dimensional Echocardiograms. Recommendations for quantitation of the left ventricle by two-dimensional
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