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Dynamic aspects of acute mitral regurgitation: effects of ventricular volume, pressure and contractility on the effective regurgitant orifice area
Abstract
The dynamics of acute mitral regurgitation were studied in six open-chest dogs in whom a portion of the anterior leaflet was excised. Phasic mitral and aortic flows were measured electromagnetically and left ventricular filling volume, regurgitant volume (RV) and forward stroke volume (SV) were calculated. The systolic pressure gradient (SPG) between the left ventricle (LV) and left atrium (LA) was obtained from high-fidelity pressure transducers. The effective mitral regurgitant orifice area (MRA) was calculated from the hydraulic equation of Gorlin. Volume infusion resulted in significant increases in both left atrial and left ventricular pressures; thus, the SPG was unchanged and the increase in RV was due primarily to the increase in MRA. Angiotensin infused to raise arterial pressure resulted in greater increments in left ventricular than left atrial pressure, so that SPG rose significantly. The increase in RV was due to increases in both MRA and SPG. Norepinephrine infusion increased systolic left ventricular pressure and SPG, while left ventricular end-diastolic pressure and left atrial pressure diminished. Despite a significant increase in SPG, RV did not increase, due to a substantial decrease in MRA. Thus, angiotensin and volume infusion induced a substantial increase in regurgitation due to the increase in MRA, while augmentation of contractility after norepinephrine infusion resulted in a decrease in regurgitation through reduction of MRA. These findings support the clinical view that maintaining a small LV with sustained myocardial contractility will reduce mitral regurgitation. Alternatively, left ventricular dilatation can enhance mitral regurgitation by increasing the effective regurgitant orifice independent of SPG.
... Their initial calculation was based on hydraulic principles assuming a fixed regurgitant orifice. Subsequently, Borgenhagen et al. (2) and others (3)(4)(5) showed that the ROA changes dynamically in response to loading conditions and varies with changes in ventricular size and mitral annular dimensions as well as within the cardiac cycle. Further studies of orifice area changes have been limited by the invasive nature of the measurements required until the development of the proximal flow convergence (PFC) technique, a noninvasive Doppler echocardiographic method that provides instantaneous mitral regurgitant flow rate and orifice area. ...
... This pattern had not been described previously and is of interest because of its potential to provide insights into the mechanism of functional MR and into potential therapeutic targets that would promote or lengthen the midsystolic decrease in orifice area, thereby decreasing the overall severity of regurgitation. Two explanations can be proposed for this pattern: 1) the regurgitant orifice area may vary in parallel with mitral annular area (MAA), which decreases to a minimum in midsystole and then increases in late systole with atrial filling (12); this would be consistent with early concepts relating orifice area to annular dimension (2)(3)(4)(5); dilation of the mitral annulus, in fact, has been implicated in the development of functional MR (13), tethering the leaflets apart to limit effective coaptation (14 -17); 2) another possibility is that ROA varies in response to phasic changes in the transmitral pressure (TMP), which may act to close the mitral leaflets more effectively when it reaches its peak in midsystole (18,19). ...
... The results of this study suggest that therapeutic interventions in patients with functional MR should ideally consider TMP in addition to changes in LV size and geometry. Traditional concepts have considered increasing afterload to have a detrimental effect on such MR, largely mediated through increases in LV size (2)(3)(4)(5), and vasodilator therapy to have a beneficial effect, also mediated through changes in LV volume. These effects, however, may potentially be attenuated in patients with aneurysmally dilated and scarred ventricles, which may not importantly change shape or size in response to therapy; in such patients, one could speculate that increased LV pressure with increased afterload could increase TMP and thus act to reduce MR. ...
OBJECTIVES We used the Doppler proximal flow convergence technique as a physiologic tool to explore the effects of the time courses of mitral annular area and transmitral pressure on dynamic changes in regurgitant orifice area. BACKGROUND In functional mitral regurgitation (MR), regurgitant flow rate and orifice area display a unique pattern, with peaks in early and late systole and a midsystolic decrease. Phasic changes in both mitral annular area and the transmitral pressure acting to close the leaflets, which equals left ventricular-left atrial pressure, have been proposed to explain this dynamic pattern.
... The integration of multiple parameters, including vena contracta width (VC), the effective regurgitant orifice area (EROA), the regurgitant volume (RV), and adjunctive signs are important for accurate assessment of MR severity [6]. Although functional MR is dynamic in nature [7,8], the effects of volume overload on MR severity quantitation have been less clearly identified. ...
... These pathologic changes are dependent on loading conditions. Secondary MR is, therefore, dynamic in nature [7]. The hemodynamic effects of exercise and various inotropic and vasodilator agents in patients with secondary MR have been studied [17,18]. ...
Background/aim:
Diagnosing and managing functional mitral regurgitation (MR) is often challenging and requires an integrated approach including a comprehensive echocardiographic examination. However, the effects of volume overload on the echocardiographic assessment of MR severity are uncertain. The purpose of this study was to weigh the effects of volume overload in the echocardiographic assessment of MR severity among patients with heart failure (HF).
Materials and methods:
Twenty-nine patients with decompensated HF, who had moderate or severe MR, were included in the present study. The volume status and the N-terminal pro-B-type natriuretic peptide (proBNP) levels were recorded and the echocardiographic parameters were assessed. After the conventional treatment for HF, the proBNP levels and the echocardiographic parameters were assessed again.
Results:
The mean age of the patients was 72 ± 9 years and the average hospitalization time was 10.9 ± 5.9 days. Between the beginning and the end of the treatment, there were significant reductions in the effective regurgitant orifice area (EROA) (0.36±0.09 cm2 to 0.29±0.09 cm2, p<0.001), vena contracta (VC) (p<0.001), the regurgitant volume (RV) (p< 0.001), and systolic pulmonary artery pressure (sPAP) (p< 0.001).
Conclusion:
This is the first study to investigate the relationship of changes in severity of MR with volume-load by monitoring the proBNP levels among patients with HF. The present results demonstrated that volume reduction, as evidenced by a decline in the proBNP levels, was accompanied by a marked reduction in the EROA, VC, and the RV among patients with left ventricular dysfunction.
... Treatment with vasodilators may worsen hypotension, necessitating the use of vasopressors and or mechanical circulatory support (MCS). It was previously thought that in MR, vasopressors needed to be avoided due to the increase in afterload and its potential to increase regurgitant flow and pulmonary venous pressure [41,42]. However, vasopressors such as dopamine and dobutamine may lower blood pressure [41]. ...
Acute ischaemic mitral regurgitation (IMR) is an increasingly rare and challenging complication following acute myocardial infarction. Despite recent technical advances in both surgical and percutaneous interventions, a poor prognosis is often associated with this challenging patient cohort. In this review, we revisit the diagnosis and typical echocardiographic features, and evaluate current surgical and percutaneous treatment options for patients with acute IMR.
... In a clinical situation of chronic mitral regurgitation, the volume-overloaded LA has to accommodate the excess in regurgitant volume by dilation in order to protect the pulmonary vasculature from high filling pressures [17,18]. As LA compliance is limited in acute MR, filling pressures increase and can result in pulmonary edema. ...
Aims
Progressive changes to left atrial (LA) structure and function following mitral regurgitation (MR) remain incompletely understood. This study aimed to demonstrate potential underlying mechanisms using experimental canine models and computer simulations.
Methods
A canine model of MR was created by cauterization of mitral chordae followed by radiofrequency ablation-induced left bundle-branch block (LBBB) after 4 weeks (MR-LBBB group). Animals with LBBB alone served as control. Echocardiography was performed at baseline, acutely after MR induction, and at 4 and 20 weeks, and correlated with histology and computer simulations.
Results
Acute MR augmented LA reservoir and contractile strain (40±4 to 53±6% and -11±5 to -22±9% respectively, p<0.05). LA fractional area change increased significantly (47±4 to 56±4%, p<0.05) while LA end-systolic area remained unchanged (7.2±1.1 versus 7.9±1.1 cm ² respectively, p = 0.08). LA strain ‘pseudonormalized’ after 4 weeks and decompensated at 20 weeks with both strains decreasing to 25±6% and -3±2% respectively (p<0.05) together with a progressive increase in LA end-systolic area (7.2±1.1 to 14.0±6.3 cm ² , p<0.05). In the LBBB-group, LA remodeling was less pronounced. Histology showed a trend towards increased interstitial fibrosis in the LA of the MR-LBBB group. Computer simulations indicated that the progressive changes in LA structure and function are a combination of progressive eccentric remodeling and fibrosis.
Conclusion
MR augmented LA strain acutely to supranormal values without significant LA dilation. However, over time, LA strain gradually decreases (pseudornormal and decompensated) with LA dilation. Histology and computer simulations indicated a correlation to a varying degree of LA eccentric remodeling and fibrosis.
... Several studies demonstrate that MR severity is dynamic [64][65][66]. Therefore, the results of chronic MR on LV and LA volumes and pulmonary artery pressure must be accounted for in a supplementary manner. ...
Both the European Society of Cardiology (ESC) and the American College of Cardiology (ACC/AHA) have recently released guidelines on the management of patients with secondary mitral regurgitation. This includes defining, classifying, and assessing the severity of secondary mitral regurgitation. These guidelines are also the first to incorporate the use of transcatheter edge-to-edge repair in decision-making based on recent studies. The review highlights the strengths and shortcomings of these studies and the applicability and generalisability of these results to assist in decision-making for the heart time. It also emphasises the importance of shared decision-making via the heart team. Echocardiography plays an important role in the assessment of these patients although these may be specifically for primary mitral insufficiency. The optimal guideline-directed medical therapy should be the first line of treatment followed by mechanical intervention. The choice of intervention is best directed by a specialist multidisciplinary team. Concomitant revascularization should be performed in a subgroup of patients with severe secondary mitral regurgitation given the role of adverse LV remodelling in propagation of the dynamic secondary MR. The guidelines need further confirmation from high-quality studies in the near future to decision-making towards either TEER, mitral valve replacement, or mitral valve repair with or without a subvalvular procedure.
... Indeed, atrial disease and remodeling form the basis of the atrial cardiopathy, which plays a critical role in the pathogenesis of AF (43). Third, LV volume and pressure were not measured directly in our study, which influence the amount of MR for a given lesion under different hemodynamic conditions (44). ...
Introduction
Mitral regurgitation (MR) is the most common valve abnormality in rheumatic heart disease (RHD) often associated with stenosis. Although the mechanism by which MR develops in RHD is primary, longstanding volume overload with left atrial (LA) remodeling may trigger the development of secondary MR, which can impact on the overall progression of MR. This study is aimed to assess the incidence and predictors of MR progression in patients with RHD.
Methods
Consecutive RHD patients with non-severe MR associated with any degree of mitral stenosis were selected. The primary endpoint was a progression of MR, which was defined as an increase of one grade in MR severity from baseline to the last follow-up echocardiogram. The risk of MR progression was estimated accounting for competing risks.
Results
The study included 539 patients, age of 46.2 ± 12 years and 83% were women. At a mean follow-up time of 4.2 years (interquartile range [IQR]: 1.2–6.9 years), 54 patients (10%) displayed MR progression with an overall incidence of 2.4 per 100 patient-years. Predictors of MR progression by the Cox model were age (adjusted hazard ratio [HR] 1.541, 95% CI 1.222–1.944), and LA volume (HR 1.137, 95% CI 1.054–1.226). By considering competing risk analysis, the direction of the association was similar for the rate (Cox model) and incidence (Fine-Gray model) of MR progression. In the model with LA volume, atrial fibrillation (AF) was no longer a predictor of MR progression. In the subgroup of patients in sinus rhythm, 59 had an onset of AF during follow-up, which was associated with progression of MR (HR 2.682; 95% CI 1.133–6.350).
Conclusions
In RHD patients with a full spectrum of MR severity, progression of MR occurs over time is predicted by age and LA volume. LA enlargement may play a role in the link between primary MR and secondary MR in patients with RHD.
... Reduced LV function can generate increased MR, which itself leads to worsening ventricular dilation (thus the maxim "MR begets MR"). Euvolemia should be maintained, as aggressive volume resuscitation may cause ventricular distension and worsening of MR. 51 At the same time, chronic MR patients may not tolerate abrupt drops in preload, because LV diastolic filling in the presence of eccentric hypertrophy depends on chronically increased volumes. ...
Mitral regurgitation (MR) is one of the most frequently encountered types of valvular heart disease in the United States. Patients with significant MR (moderate-to-severe or severe) undergoing noncardiac surgery have an increased risk of perioperative cardiovascular complications. MR can arise from a diverse array of causes that fall into 2 broad categories: primary (diseases intrinsic to the valvular apparatus) and secondary (diseases that disrupt normal valve function via effects on the left ventricle or mitral annulus). This article highlights key guideline updates from the American College of Cardiologists (ACC) and the American Heart Association (AHA) that inform decision-making for the anesthesiologist caring for a patient with MR undergoing noncardiac surgery. The pathophysiology and natural history of acute and chronic MR, staging of chronic primary and secondary MR, and considerations for timing of valvular corrective surgery are reviewed. These topics are then applied to a discussion of anesthetic management, including preoperative risk evaluation, anesthetic selection, hemodynamic goals, and intraoperative monitoring of the noncardiac surgical patient with MR.
... A retrospective study of two dogs given pimobendan chronically showed increased regurgitant volume (10) while a study of four dogs with experimentally induced mitral disruption showed decreased regurgitant volume (11), but another study of 19 preclinical DMVD dogs showed no changes in regurgitant volume (12). Other studies show evidence that positive inotropes decrease regurgitant fraction and effective regurgitant orifice area (EROA) in dogs with mitral disruption (13). However, to our knowledge pimobendan's effect on regurgitant volume has not been assessed in DCM. ...
Background: Pimobendan provides a significant survival benefit in dogs with cardiac disease, including degenerative mitral valve disease and dilated cardiomyopathy (DCM). Its positive inotropic effect is well-known, however, it has complex effects and the mechanisms behind the survival benefit are not fully characterized. Secondary hemodynamic effects may decrease mitral regurgitation (MR) in DCM, and the benefits of pimobendan may extend to improved cardiac relaxation and improved atrial function.
Hypothesis/Objectives: Our objective was to investigate the acute cardiac effects of pimobendan in dogs with a DCM phenotype. We hypothesized that pimobendan would increase left atrial (LA) contractility, reduce mitral regurgitation, improve diastolic function, and lower circulating NT-ProBNP levels.
Animals: Seven purpose-bred Beagles were studied from a research colony with tachycardia induced DCM phenotype.
Methods: The effects of pimobendan were studied under a placebo-controlled single-blinded cross-over design. In short, dogs underwent baseline and 3 h post-dose examinations 7 days apart with echocardiography and a blood draw. Dogs were randomized to receive oral placebo or 0.25 mg/kg pimobendan after their baseline exam. Investigators were blinded to treatments until all measurements were compiled.
Results: When treated with pimobendan, the dogs had significant increases in systolic function and decreases in MR, compared to when treated with placebo.
There were no detectable differences in left atrial measures, including LA size, LA emptying fraction, LA functional index or mitral A wave velocity. Heart rate decreased significantly with pimobendan compared to placebo. There was also a decrease in isovolumetric relaxation time normalized to heart rate. NT-proBNP levels had a high degree of variability.
Conclusions: Improved mitral regurgitation severity and improved lusitropic function may contribute to the reported survival benefit for dogs with cardiac disease administered pimobendan. Pimobendan did not overtly improve LA function as assessed by echocardiography, and NT-proBNP was not significantly changed with a single dose of this medication. Further studies are needed to better characterize LA effects with other imaging modalities, to better quantify the total improvement of MR severity, and to assess chronic use of pimobendan on diastolic function in DCM.
... Grading of MR severity can be significantly impacted by hemodynamic changes, particularly blood pressure. 114 Figure 14 shows an example of the dynamic nature of MR. Hemodynamic variation could be seen with conscious sedation (during TEE) but is particularly challenging in the operating room, brought about by anesthesia and vasoactive agents. ...
... The loading conditions in MR probably are favourable to LV ejection because LV preload is increased and LV afterload is decreased. However, altered loading conditions (i.e., elevated arterial stiffness) result in progressive, worsening regurgitation [24]. ...
Background: We examined the relative impact of arterial stiffness on the presence and/or severity of chronic mitral regurgitation (MR) in hypertensive patients. Methods: We prospectively enrolled 141 untreated hypertensive patients (mean age 56.6 ± 11.5 years): 94 with MR, 47 without MR. As a measure of arterial stiffness, pulse wave velocity (PWV) was assessed by applanation tonometry. Assessment of MR severity was obtained through calculation of effective regurgitant orifice area (EROA) and vena contracta by standard two-dimensional transthoracic echocardiography. Results: PWV appears to progressively increase according to the presence and severity of MR (no MR = 7.3 ± 1.1 m/s, mild MR = 7.9 ± 1.3 m/s, moderate MR = 9.0 ± 1.7 m/s, severe MR = 13.3 ± 4.1 m/s; P < 0.001 for all comparisons). EROA was positively correlated with age (P = 0.011), left atrial volume index (P = 0.023), PWV (P < 0.001) and augmentation index (P < 0.001), and negatively correlated with left ventricular ejection fraction (P = 0.002) and heart rate (HR) (P = 0.018). On stepwise multivariate logistic regression analysis, only PWV (OR = 2.87, 95% CI 1.750–4.738, P < 0.001) and HR (OR = 0.94, 95% CI 0.895–0.994, P = 0.02) appeared to be independent predictors of severe MR. Receiver operating characteristic curves showed that a cutoff of 9 m/s for PWV provided the best sensitivity/specificity for predicting both the presence of any degree of MR (sensitivity 73%, specificity 87%, AUC = 0.863; P < 0.001) and MR severity (sensitivity 100%, specificity 81%, AUC = 0.954; P < 0.001). Conclusion: Reduced arterial elasticity because of increased stiffness may be an important marker for the presence and severity of MR in hypertensive patients.
... 6,10 It is important to note that the evaluation of MR severity is significantly influenced by the LV loading conditions and the systemic blood pressure. 14 The assessment of the severity of MR with colour flow Doppler echocardiography is based on instantaneous peak flow rates and is therefore reliable only when there is little temporal variation of MR during the cardiac cycle. However, secondary MR is often dynamic, peaking in early and late systole and improving during mid systole when LV pressures are at their maximum. ...
Valvular heart disease (VHD) and heart failure (HF) are major health issues that are steadily increasing in prevalence in Western populations. VHD and HF frequently co-exist, which can complicate the accurate diagnosis of the severity of valve stenosis or regurgitation and affect decisions about therapeutic options. Transthoracic echocardiography is the first-line imaging modality to determine left ventricular (LV) systolic function, to grade valvular stenosis or regurgitation and to characterise the mechanism underlying valvular dysfunction. 3D transoesophageal echocardiography, cardiovascular magnetic resonance and cardiac CT are alternative imaging modalities that help in the diagnosis of patients with HF and VHD. The integration of multimodality cardiovascular imaging is important when deciding whether the patient should receive transcatheter aortic valve repair and replacement therapies. In this article, the use of multimodality imaging to diagnose and treat patients with VHD and HF is reviewed.
... This speculation about a potential mechanism of action in dogs with MR is supported by experimental findings in dogs with induced MR which suggest that reduced heart size and enhanced contractile function are associated with a reduction in mitral regurgitant orifice area and therefore reduced MR. 21,22 The observed reduction in heart size appeared to be maintained over the duration of the study with the average heart size, as indicated by the AUC for the VHS, of dogs in the pimobendan group being smaller compared to dogs in the placebo group. ...
Background:
Changes in clinical variables associated with the administration of pimobendan to dogs with preclinical myxomatous mitral valve disease (MMVD) and cardiomegaly have not been described.
Objectives:
To investigate the effect of pimobendan on clinical variables and the relationship between a change in heart size and the time to congestive heart failure (CHF) or cardiac-related death (CRD) in dogs with MMVD and cardiomegaly. To determine whether pimobendan-treated dogs differ from dogs receiving placebo at onset of CHF.
Animals:
Three hundred and fifty-four dogs with MMVD and cardiomegaly.
Materials and methods:
Prospective, blinded study with dogs randomized (ratio 1:1) to pimobendan (0.4-0.6 mg/kg/d) or placebo. Clinical, laboratory, and heart-size variables in both groups were measured and compared at different time points (day 35 and onset of CHF) and over the study duration. Relationships between short-term changes in echocardiographic variables and time to CHF or CRD were explored.
Results:
At day 35, heart size had reduced in the pimobendan group: median change in (Δ) LVIDDN -0.06 (IQR: -0.15 to +0.02), P < 0.0001, and LA:Ao -0.08 (IQR: -0.23 to +0.03), P < 0.0001. Reduction in heart size was associated with increased time to CHF or CRD. Hazard ratio for a 0.1 increase in ΔLVIDDN was 1.26, P = 0.0003. Hazard ratio for a 0.1 increase in ΔLA:Ao was 1.14, P = 0.0002. At onset of CHF, groups were similar.
Conclusions and clinical importance:
Pimobendan treatment reduces heart size. Reduced heart size is associated with improved outcome. At the onset of CHF, dogs treated with pimobendan were indistinguishable from those receiving placebo.
... [7] The IMR has dynamic characteristics. [13,14] The dynamic characteristics of MR can be appreciated during an exercise Doppler echocardiogram. [15] The degree of MR at rest is unrelated to exercise-induced changes in effective regurgitant orifiace area (EROA) or regurgitant volume. ...
Ischemic mitral regurgitation (IMR) is a frequent complication of left ventricular (LV) global or regional pathological remodeling due to chronic coronary artery disease. It is not a valve disease but represents the valvular consequences of increased tethering forces and reduced closing forces. IMR is defined as mitral regurgitation caused by chronic changes of LV structure and function due to ischemic heart disease and it worsens the prognosis. In this review, we discuss on etiology, pathophysiology, and mechanisms of IMR, its classification, evaluation, and therapeutic corrective methods of IMR.
... Grading of MR severity can be significantly impacted by hemodynamic changes, particularly blood pressure. 114 Figure 14 shows an example of the dynamic nature of MR. Hemodynamic variation could be seen with conscious sedation (during TEE) but is particularly challenging in the operating room, brought about by anesthesia and vasoactive agents. ...
... Several factors, including LV size, extent of emptying, mitral annular diameter, papillary muscle function, and left atrial size, have been implicated. 9,[25][26][27] Experimental and clinical studies have also shown that the severity of functional MR often varied over time as a result of dynamic changes in the mitral regurgitant orifice, changes in ventricular-atrial pressure gradients, or both. 24 -27 For instance, the severity of functional MR has been shown to increase during isometric exercise and to decrease during dobutamine and nitroglycerin infusion. ...
Background— Functional mitral regurgitation (MR) is common in patients with heart failure and left ventricular (LV) dysfunction, and its severity may vary over time, depending primarily on the loading conditions. Because dynamic changes in the severity of functional MR may affect forward stroke volume, we hypothesized that exercise-induced changes in MR severity influence the stroke volume response of patients with LV dysfunction to exercise, and hence their exercise capacity.
Methods and Results— Heart failure patients (n=25; mean age 53±12 years) with LV dysfunction underwent dynamic bicycle exercise at steady-state levels of 30%, 60%, and 90% of predetermined peak V̇ o 2 . During each exercise level, right heart pressures, cardiac output, V̇ o 2 , and MR severity were measured simultaneously. During exercise, MR severity, as evaluated by the ratio of MR jet over left atrium area, increased from 15±8% to 33±15%. Peak V̇ o 2 , exercise-induced changes in stroke volume, and those in capillary wedge pressure correlated with the changes in MR ( r =−0.55, −0.87, and 0.62, respectively, P <0.01). The changes in MR severity also correlated with those in end-diastolic ( r =−0.75, P <0.01) and end-systolic ( r =−0.72, P <0.01) sphericity indexes and those in the coaptation distance ( r =0.86, P <0.01).
Conclusions— Our data indicate that in patients with LV dysfunction, exercise-induced changes in MR severity limit the stroke volume adaptation during exercise and therefore contribute to limitation of exercise capacity.
The mitral valve apparatus is a complex structure that requires harmonious interplay of several key components to function properly. As such, diseases of the mitral valve can present a significant challenge for clinicians to diagnose and manage. Innovation in cardiac imaging techniques, transcatheter based interventions and study of clinical outcomes has transformed the care available for patients with mitral valve disorders. In this chapter, a case-based review of the optimal imaging approach to patients being evaluated for transcatheter mitral valve intervention will be presented. More specifically, imaging considerations for the following interventions will be reviewed:
Transcatheter edge to edge repair for mitral regurgitation
Percutaneous balloon mitral valvuloplasty in mitral stenosis
Transcatheter mitral valve in valve
The purpose of this study was to investigate the effects of loading conditions and left ventricular (LV) contractility on mitral annular dynamics. In 10 anesthetized pigs, eight piezoelectric transducers were implanted equidistantly around the mitral annulus. High-fidelity catheters measured left ventricular pressures and the slope of the end-systolic pressure-volume relationship (Ees ) determined LV contractility. Adjustments of pre- and afterload were done by constriction of the inferior caval vein and occlusion of the descending aorta. Mitral annulus area indexed to body surface area (MAAi ), annular circularity index (ACI), and non-planarity angle (NPA) were calculated by computational analysis. MAAi was more dynamic in response to loading interventions than ACI and NPA. However, MAAi maximal cyclical reduction (-Δr) and average deformational velocity (- v ¯ $$ \overline{v} $$ ) did not change accordingly (p = 0.31 and p = 0.22). Reduced Ees was associated to attenuation in MAAi -Δr and MAAi - v ¯ $$ \overline{v} $$ (r2 = 0.744; p = 0.001 and r2 = 0.467; p = 0.029). In conclusion, increased cardiac load and reduced LV contractility may cause deterioration of mitral annular dynamics, likely impairing coaptation and increasing susceptibility to valvular incompetence.
Introduction/objectives:
To evaluate regurgitant fraction (RF) using Simpson's method of discs to estimate total stroke volume (RFSMOD_TSV) and using Motion-mode to estimate total stroke volume (RFM-modeTSV) in dogs with subclinical myxomatous mitral valve disease (MMVD). We also sought to evaluate the effects of pimobendan on RF, and to determine the reproducibility of RFSMOD_TSV and RFM-modeTSV.
Animals, materials, and methods:
Echocardiography was performed on 57 dogs with MMVD (30 stage B1 and 27 stage B2). Ten dogs received pimobendan for 7-10 days and had a second echocardiogram. Nine dogs underwent six repeated echocardiographic examinations by two operators on three nonconsecutive days within one week for reproducibility analysis.
Results:
Both RFSMOD_TSV and RFM-modeTSV exhibited a curvilinear relationship with left atrium-to-aortic root ratio. Both RFSMOD_TSV and RFM-modeTSV varied considerably within stage B1 (minimum-maximum: -9.1%-58.2% and -35.7%-66.2%, respectively) and B2 (13.6%-76.2% and 20.1%-85.7%, respectively). Method comparison showed RFSMOD_TSV and RFM-modeTSV were not interchangeable with proportional bias. Pimobendan significantly reduced RFSMOD_TSV (-32.0 ± 23.3%) and RFM-modeTSV (-19.2 ± 10.9%) within the same dog and relative to controls. Good inter-day and between-operator reproducibility was observed for RFSMOD_TSV and RFM-modeTSV based on intraclass correlation coefficients 0.86-0.90 and 0.83-0.90, respectively. Reproducibility coefficients were 19.6-24.1% and 24.1-27.0%, respectively.
Conclusions:
Use of RF using the total stroke volume method to aid the assessment of dogs with subclinical MMVD might be of clinical value. However, further study is warranted. Based on response to pimobendan and reproducibility analysis, RF SMOD_TSV might be a more reliable technique to quantify RF.
Background
We report the case of a 93-year-old patient with normal left ventricular function and severe mitral annulus calcification, with mild mitral steno-insufficiency.
Case Presentation
She had developed creeping drugs-induced renal toxicity that is generally totally overlooked, due mainly to statins, a proton pump inhibitor, and aspirin. The Na and fluid retention, along with hypertension that ensued, although not severe, caused acute heart failure (sub-pulmonary edema) by worsening the mitral insufficiency. This occurred due to a less efficient calcific mitral annulus contraction during systole and an increasing mitral transvalvular gradient, as the transvalvular mitral gradient has an exponential relation to flow. After the suspension of the nephrotoxic drugs and starting intravenous furosemide, she rapidly improved. At 6 months follow-up, she is stable, in an NYHA 1-2 functional class, despite the only partial recovery of the renal function.
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.
Secondary (functional) mitral regurgitation (SMR) most commonly arises secondary to left ventricular (LV) dilation/dysfunction. The concept of disproportionately severe SMR was proposed to help explain the different results of two randomised trials of transcatheter edge-to-edge mitral valve repair (TEER) versus medical therapy. This concept is based on the fact that effective regurgitant orifice area (EROA) depends on LV end-diastolic volume (LVEDV), ejection fraction, regurgitant fraction and the velocity-time integral of SMR. This review focuses on the haemodynamic framework underlying the concept and the myths and misconceptions arising from it. Each component of EROA/LVEDV is prone to measurement error which can result in misclassification of individual patients. Moreover, EROA is typically measured at peak systole rather than its mean value over the duration of MR. This can result in physiologically impossible values of EROA or regurgitant volume. Although the EROA/LVEDV ratio (1) emphasises that grading MR severity needs to consider LV size and function and (2) helps explain the different outcomes between COAPT and MITRAFR, there are important factors that are not included. Among these are left atrial compliance, LV pressure and ejection fraction, pulmonary hypertension, right ventricular function and tricuspid regurgitation. Because medical therapy can reduce LV volumes and improve both LV function and SMR severity, the key to patient selection is forced titration of neurohormonal antagonists to the target doses that have been proven in clinical trials (along with cardiac resynchronisation when appropriate). Patients who continue to have symptomatic severe SMR after doing so should be considered for TEER.
Mitral regurgitation (MR) is a complex valve lesion that can pose significant management challenges. This Expert Consensus Decision Pathway emphasizes that recognition of MR should prompt an assessment of its etiology, mechanism, and severity, as well as consideration of the indications for treatment. The document is a focused update of the 2017 ACC Expert Consensus Decision Pathway on the Management of Mitral Regurgitation, with some sections updated and others added in light of the publication of new trial data related to secondary MR, among other developments. A structured approach to evaluation based on clinical findings, accurate echocardiographic imaging, and, when necessary, adjunctive testing, can help clarify decision making. Treatment goals include timely intervention by an experienced multidisciplinary heart team to prevent left ventricular dysfunction, heart failure, reduced quality of life, and premature death.
Mitral valve disease is the most common valvular disorder worldwide. Mitral stenosis rates have been declining, but mitral regurgitation remains the most common valvular disease in the United States. Medical therapy has a limited role in the treatment of mitral valve disorders, and surgery with either valve repair or replacement remains the mainstay of treatment. A thorough understanding of the complex mitral valve apparatus, pathophysiology of the valve, echocardiographic findings, and grading classification of regurgitation and stenosis are all essential to guiding optimal patient management and, ultimately, surgical care.
Mitral regurgitation (MR) is a major cause of cardiovascular morbidity and mortality. MR is classified as primary (organic) if it is due to an intrinsic valve abnormality, or secondary (functional) if the etiology is because of remodeling of left ventricular geometry and/or valve annulus. Transthoracic echocardiography (TTE) is the initial modality for MR evaluation. Parameters used for the assessment of MR include valve structure, cardiac remodeling, and color and spectral Doppler. Quantitative measurements include effective regurgitant orifice area, regurgitant volume, and regurgitant fraction. Knowledge of advantages and limitations of echo-Doppler parameters is essential for accurate results. An integrative approach is recommended in overall grading of MR as mild, moderate, or severe since singular parameters may be affected by several factors. When the mechanism and/or grade of MR is unclear from the TTE or is discrepant with the clinical scenario, further evaluation with transesophageal echocardiography or cardiac magnetic resonance imaging is recommended, the latter emerging as a powerful MR quantitation tool.
The preanesthetic database should include the medical history and physical examination, with particular attention to cardiac and pulmonary auscultation, inspection of the jugular veins, and palpation of peripheral arterial pulses. Commonly considered diagnostics include electrocardiography (ECG), thoracic radiography, echocardiography, and non-invasive blood pressure measurement. Recently, the use of cardiac-specific blood-based markers such as N-terminal pro-B-type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnl) as part of the preanesthetic work-up in animals with suspected cardiac disease has been contemplated. Echo should be performed by individuals not only proficient in image acquisition but also with an adequate familiarity of the pathophysiology of the most common cardiac diseases. This chapter also talks about congenital defects, volume overload conditions, pressure overload, diastolic dysfunction-associated diseases, and arrhythmias. Pharmacological support may be required if hypotension is severe and does not respond to fluid therapy or changes in anesthetic depth.
Im Gegensatz zur Mitralstenose ist die Ätiologie der Mitralinsuffizienz sehr komplex. Dieses hat u. a. seine Ursache darin, daß sehr unterschiedliche Strukturen des komplexen Mitralklappenapparates an der Entwicklung dieses Klappenfehlers beteiligt sein können, allerdings in sehr variabler Ausprägung. Eine Regurgitation an der Mitralklappe kann entstehen durch:
narbige Schrumpfung der Segel,
Klappenperforation,
traumatischen Abriß eines Klappensegels,
myxomatose Umwandlung von Klappensegeln,
angeborene Spaltbildung der Mitralklappe,
Abriß eines Sehnenfadens 1. Ordnung,
Verlängerung von Sehnenfäden durch myxomatose Umwandlung,
Nekrose oder narbige Umwandlung eines Papillarmuskels,
Papillarmuskelabriß,
Sphinkterverlust des Anulus fibrosus bei reduzierter Myokardkontraktilität oder absoluter Arrhythmie,
Lateralverlagerung der Papillarmuskeln bei Dilatation des linken Ventrikels, Aneurysma oder Asynergie.
A 68-year-old man is referred to his family doctor for dyspnea and fatigue for ordinary activities; symptoms arose 3 months before. At the beginning, dyspnea was mild and was present only after a moderate to intense physical activity. In the last 2 weeks, the symptoms worsened until dyspnea was evident during moderate physical activity (fast walking or after few steps of stairs) with even one episode of orthopnea at night that resolved after 30 min. No chest pain at rest or during exertion was referred; there were no syncope or dizziness and no palpitations.
Maximal positive dp/dt and maximal negative dp/dt of left ventricular pressure are important parameters for assessing left ventricular systolic (maximal positive dp/dt) and diastolic (maximal negative dp/dt) function [1]. However, these parameters require high fidelity pressure recordings with the accompanying risk of an invasive procedure. A noninvasive method for assessment of maximal dp/dt and maximal negative dp/dt would, therefore, be of great value.
The left atrium is a muscular contractile chamber located upstream of the left ventricle which serves as a reservoir for storing blood during left ventricular contraction, as a conduit for blood from the pulmonary veins to the left ventricle during early ventricular filling and, also, as a booster pump to complete left ventricular filling.
This chapter presents the background, challenges, strategic mapping, high-risk markers, high-risk predictors and investigations for mitral regurgitation (MR). It also discusses the primary, secondary and acute mitral regurgitation. MR is categorized as chronic or acute with etiology divided into primary/degenerative or secondary/functional MR (due to dilation or dysfunction of the LV). MR causes long-term volume overload and depending on the etiology will lead to irreversible myocardial damage. Transthoracic echocardiography (TTE) is the primary imaging tool used for detection of MR. The predictors of high long-term morbidity and mortality include: pulmonary hypertension (HTN), atrial fibrillation (AF), and LV dysfunction, heart failure (HF), liver disease, renal failure, morbid obesity, RV failure, active smoking and cognitive disorders. In patients with normal blood pressure and LV function, vasodilators provide no benefit and may possibly worsen the severity of primary regurgitation as the pathology is myxomatous degeneration with valvular redundancy.
Im Gegensatz zur Mitralstenose ist die Ätiologie der Mitralinsuffizienz sehr komplex. Dieses hat u. a. seine Ursache darin, daß sehr unterschiedliche Strukturen des komplexen Mitralklappenapparates an der Entwicklung dieses Klappenfehlers beteiligt sein können, allerdings in sehr variabler Ausprägung. So kann eine Regurgitation an der Mitralklappe entstehen durch:
1.
narbige Schrumpfung der Segel,
2.
Klappenperforation,
3.
traumatischen Abriß eines Klappensegels,
4.
myxomatöse Umwandlung von Klappensegeln,
5.
angeborene Spaltbildung der Mitralklappe,
6.
Abriß eines Sehnenfadens 1. Ordnung,
7.
Verlängerung von Sehnenfäden durch myxomatöse Umwandlung,
8.
Nekrose oder narbige Umwandlung eines Papillarmuskels,
9.
Papillarmuskelabriß,
10.
Sphincterverlust des Anulus fibrosus bei reduzierter Myokardkontraktilität oder absoluter Arrhythmie,
11.
Lateralverlagerung der Papillarmuskeln bei Dilatation des linken Ventrikels, Aneurysma oder Asynergie.
In conclusion, mitral reconstruction via an annuloplasty ring effectively corrects mitral regurgitation in cardiomyopathy patients and is a safe procedure in a high-risk population with an acceptable operative mortality rate. Not only has survival in these patients improved but also functional status has changed remarkably. The effects of this procedure in patients with severe myocardial dysfunction may be attributed to a decrease in the regurgitant orifice area, improvement in the efficiency of each contraction with better effective forward flow, an increase in coronary flow reserve, and reversal of some the alterations in the neurohormonal changes seen in heart failure. These changes all contribute to restoration of the normal left ventricular geometric relationship. While longer-term follow-up is necessary with a greater number of patients, we are encouraged by these results and feel that mitral reconstruction offers a new strategy for end-stage cardiomyopathy.
Valvular heart disease is an important clinical problem in women as a number of congenital and acquired diseases affecting the cardiac valves occur with greater frequency in women. Women also have differences in physiognomy and physiology that influence the clinical presentation, diagnostic approach, therapeutic options, and results of therapy. Women, on average, tend to be smaller than men. This not only applies to their external dimensions, but also to the dimensions of the cardiovascular system. For example, the heart of a normal woman weighs on average approximately 100 g less than men1 (Robbins, Pathology, 3rd ed. W.B. Saunders Company, Philadelphia, 1967, p. 512). They experience differences in cardiovascular remodeling in response to the hemodynamic alterations that result from valvular dysfunction, physiologic changes that accompany a normal pregnancy and the pathologic effects of pregnancy-related complications can deleteriously accelerate valve-related hemodynamic alterations and symptoms of valve dysfunction. In this chapter, we will define those areas of valvular heart disease than directly applies to women, and identify those gender-related issues in the diagnosis, evaluation, and treatment of valve disease.
Valvular heart disease (VHD), although not as common as coronary disease, heart failure, or hypertension, is an important, and challenging, clinical entity. It is of interest for the following reasons: substantial advances have been made in the understanding of its pathophysiology; important changes in patient characteristics and aetiologies have occurred over recent years; diagnosis is now largely dominated by non-invasive imaging, especially echocardiography which has become the standard to evaluate valve structure and function; and, finally, treatment has not only developed through the continuing progress in prosthetic valve technology, but also has been re-orientated by the development of conservative surgical techniques and the development of interventional cardiology....
Heart failure is not a disease but a complex clinical syndrome representing the end-stage of a number of different cardiac diseases. It can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. It has been defined as a reduction in cardiac function such that cardiac output is reduced relative to the metabolic demands of the body and is associated with failure of compensating mechanisms.
Mitral valve regurgitation is one of the most important and frequent valve diseases in the western hemisphere. Primary mitral valve regurgitation is due to pathological alterations of the valve structure itself, whereas secondary mitral valve regurgitation is due to pathology of the left ventricle which ultimately leads to deterioration of mitral valve functioning and mitral regurgitation. The diagnostic pathway requires various cardiovascular examinations. Central diagnostic tool resembles echocardiography which provides besides visual impressions semi quantitative and quantitative parameters. Treatment options in patients with mitral valve regurgitation are based on interdisciplinary discussion between cardiologists and heart surgeons in the heart team. Besides the conservative treatment including medical and device heart failure therapy, surgical and interventional procedures are to be discussed in order to reduce mitral valve regurgitation. The decision making is greatly influenced by the nature of mitral valve regurgitation and by the concomitant comorbidities.
The function of the mitral valve is dependent on the precise interaction of cusps, chordae, ventricular base, and the posterior ventricular wall. For closure to take place with or without atrial contraction, a vortex forms behind the anterior cusp and moves it posteriorly, and the ventricular muscle starts to develop tension. With this the ventricular pressure rises, reversing the diastolic forward flow of blood through the orifice. Closure occurs after systole has started, just before the aortic valve opens. The normal annulus narrows, bringing the posterior cusp nearer to the anterior cusp and the posterior left ventricular wall shortens allowing the cusps to rise to the plane of the atrioventricular ring. A small puff of regurgitation occurs as the cusps close. Most of this is blood displaced by the cusps as their contact progresses from a touching of the free edges to contact over a substantial area [2, 3].
This volume unites anatomists, pathologists, cardiologists, surgeons and physiologists, in an attempt to define the causes and to clarify the diagnosis of ischemic mitral incompetence; and then to discuss the medical and surgical approaches to solving the problem. The ability to diagnose mitral incompetence, of any origin, has been enhanced by recent developments in ultrasound technology: 2D-echocardiography, pulsed-Doppler measurement of local velocity, and color-coded flow mapping. This proceedings volume contains important applications of these methods for pre-, intra-, and post-operative examination of mitral regurgitant flow patterns. Our understanding and interpretation of the measured flow patterns is enhanced by an understanding of the physiology of flow, both antegrade and retrograde, across the mitral valve.
Hemodynamic effects of mitral regurgitation (MR) are dependent on multiple factors including the chronicity of the regurgitation, orifice size, etiology, and loading conditions. Although the MitraClip procedure is very safe, significant hemodynamic changes can occur intraprocedurally, early and late postprocedure. Assessment and management of these hemodynamic changes can be complex, although most patients remain clinically stable throughout the procedure. This chapter reviews the hemodynamic effects of MR in the acute and chronic setting, the intra- and periprocedural effects of the MitraClip, as well as the role of various drugs used in anesthesia.
Transesophageal echocardiography has emerged recently as a powerful cardiac imaging tool. The strengths and limitations of transesophageal echocardiography are reviewed. The clinical use of transesophageal echocardiography in aortic dissection, endocarditis, mitral valve disease, prosthetic heart valves, stroke, and miscellaneous other conditions is discussed. (C) Copyright 1994 Southern Society for Clinical Investigation
Objectives. We used color Doppler flow mapping to determine whether vena contracta width (VCW) is a load-independent measure of the severity of mitral regurgitation.
Background. VCW has been proposed to be a relatively load-independent measure of mitral regurgitation severity in flow models using a fixed orifice. However, in patients with mitral regurgitation, VCW may not be load independent because of a dynamic regurgitant orifice.
Methods. VCW, effective regurgitant orifice area and regurgitant volume were measured by quantitative Doppler mapping in 31 patients with chronic mitral regurgitation at baseline and during nitroprusside infusion. Patients with rheumatic heart disease, annular calcification or endocarditis were considered to have a fixed regurgitant orifice, whereas patients with mitral valve prolapse, dilated cardiomyopathy or ischemia were considered to have a dynamic regurgitant orifice.
Results. Systolic blood pressure (148 ± 27 to 115 ± 25 mm Hg) and end-systolic wall stress (121 ± 50 to 89 ± 36) decreased with nitroprusside (p < 0.05). Although nitroprusside did not significantly change mean values for VCW (0.5 ± 0.2 to 0.5 ± 0.2 cm), regurgitant volume (69 ± 47 to 69 ± 56 ml) or effective regurgitant orifice area (0.5 ± 0.4 to 0.5 ± 0.6 cm2), individual patients exhibited marked directional variability. Specifically, VCW decreased in 16 patients (improved mitral regurgitation), remained unchanged in 7 patients and increased in 8 patients (worsened mitral regurgitation) with nitroprusside. Also, the VCW response to nitroprusside was concordant with changes in effective regurgitant orifice area and regurgitant volume, and was not different between dynamic and fixed orifice groups.
Conclusions. Contrary to the results from in vitro studies, VCW is not load independent in patients with mitral regurgitation caused by dynamic changes in the regurgitant orifice. The origin of mitral regurgitation does not predict accurately whether the regurgitant orifice is fixed or dynamic. Finally, short-term vasodilation with nitroprusside may significantly worsen the severity of mitral regurgitation in some patients.
Using transthoracic three-dimensional (3D) echo regional volume analysis combined with low-dose dobutamine to investigate the effects on regional volume, mitral configuration and functional mitral regurgitation (FMR).
Fifty-six patients with ischemic cardiomyopathy (ICM) were included in this study. The effective regurgitant orifice area (EROA) of FMR secondary to ICM with depressed left ventricular ejection fraction was compared with mitral tenting area and coaptation height (CH) before and after low-dose dobutamine (10 μg/kg per min). Using 3-DQ software we measured and calculated regional stroke-volumes (rSV), the ratio of the rSV to the whole left ventricular stroke volume (rgSVratio) in all 17 segments and the average rgSVratio of 4 anterior-PM attached segments (rgSVratio-aver anter-PM), 4 posterior-PM attached segments (rgSVratio-aver post-PM), 8 PMs attached segments (rgSVratio-aver PMs) and all 17 segments before and after dobutamine.
Compared with the resting condition, the SVr and rgSVratio on the basal and mid segments of anterior, lateral, inferior, and posterior walls were increased after dobutamine infusion (P < 0.05). EROA at rest was associated with tenting area, CH and rgSVratio-aver of PMs and the reduction in EROA caused by dobutamine was associated with reductions in tenting area, CH and increases in rgSVratio-aver of PMs. Tenting area was associated with rgSVratio-aver of PMs and reduction caused by dobutamine was associated with increases in rgSVratio-aver of PMs.
The FMR decreasing during low-dose dobutamine is quantitatively associated with the regional LV volume change of attached PMs. Real time transthoracic three-dimensional echocardiography may provide a simple and noninvasive approach to assess regional LV time-volume characteristic during FMR.
The unimpeded, forward flow of blood across the mitral orifice is contingent upon a coordinated interaction between the mitral annulus, the mitral valve leaflets, the chordae tendineae, and the papillary muscles. An understanding of the functional anatomy and physiology of each of these components of the "mitral complex" is clinically important for derangement of any part may produce obstruction to blood flow or allow mitral regurgitation. The differential diagnosis then of mitral stenosis and mitral regurgitation can be functionally analyzed in terms of diseases of the mitral annulus, diseases of the mitral valve leaflets, diseases of the chordae tendineae, and diseases of the papillary muscles. By this consideration of selective involvement of the mitral complex, certain physical signs, such as the late systolic murmur that may occur in papillary muscle dysfunction, the "murmur on top of the head" heard with a ruptured chordae tendineae to the anteromedial mitral leaflet, the chordal snap of a redundant chordae tendineae, or the atrial gallop of an acutely ruptured chordae tendineae, can be sought for in an attempt to differentiate clinically the possible etiology of the disease and its anatomic area of involvement. This correlation of physical signs with the functional anatomy helps to provide an additional scientific basis to the physical examination.
The sudden development of a harsh apical systolic murmur in a patient with a recent myocardial infarct is usually considered to indicate rupture of a papillary muscle or perforation of the interventricular septum.1,2 the differential diagnosis of a loud precordial systolic murmur of sudden onset may be difficult and to describe a syndrome whereby such a murmur may occur secondary to mechanical dysfunction of a papillary muscle.
Illustrative Patients
Patient 1.
—An 85-year-old white male, previously in good health, was admitted to hospital with severe crushing substernal pain which he had had for several hours. His blood pressure was 135/75 mm Hg, and his pulse rate was 88 per minute and regular. The lungs were clear on auscultation. The heart was not enlarged, and there were no murmurs or gallop sounds. The electrocardiogram on admission showed an acute anteroseptal myocardial infarct. The serum glutamic oxaloacetic transaminase (SGOT) was 165
Multiple measurements of left ventricular volumes, ejection fractions, and circulatory pressures were made under conditions of varied outflow resistance in five intact anesthetized dogs by using a biplane videoangiographic recording system which displays simultaneously two roentgen images on the same television screen, records the images on video tape, and requires low radiation levels and small amounts of contrast medium. Aortic pressure was controlled by intra-aortic infusion of angiotensin or acetylcholine. With spontaneous sinus rhythm and normal aortic pressure, end-diastolic volume averaged 35 ml (2.3 ml/kg), and ejection fraction averaged 47% of end-diastolic volume. When aortic pressure was increased, average end-diastolic volumes increased to 53 ml and ejection fractions decreased to 29%. Conversely, when aortic pressure was decreased, average ejection fraction increased to 73%, although changes in stroke volume were usually not large under these conditions. Concomitant large changes in the shape of the left ventricular cavity were also observed. Similar changes were observed when heart rate was maintained constant by electrical pacing of the atria and ventricles with a constant atrial-ventricular stimulus interval. The variability in left ventricular volume and ejection fraction observed in the same animal during different circulatory states may account in part for the differences in values for these variables reported by different investigators.
Summary The normal anatomy of the canine mitral valve has been described. It has been compared with that of human and other mammalian mitral valves. An attempt has been made to correlate anatomy with function, and the implications of the findings for the design of prostheses have been discussed.
The normal anatomy of the canine mitral valve has been described. It has been compared with that of human and other mammalian mitral valves. An attempt has been made to correlate anatomy with function, and the implications of the findings for the design of prostheses have been discussed.
This article has attempted to summarize the current status of the therapeutic use of vasodilator drugs in acute and chronic heart failure. It is apparent from the increasing number of publications in this area that this alternative to more standard forms of therapy is likely to find a permanent and important place in the management of patients with heart disease. It should also be apparent that ideal drugs for the therapy of chronic heart failure are not yet available. Nevertheless, it is probable that such drugs will emerge and become at least as important as the routine use of digitalis in such patients.
Acute mitral regurgitation was produced in six open chest dogs by excising a portion of the anterior valve leaflet. Electromagnetic flow probes were placed in the left atrium around the mitral anulus and in the ascending aorta to determine phasic left ventricular filling volume, regurgitant volume and stroke volume. The systolic pressure gradient was calculated from simultaneously measured high fidelity left atrial and left ventricular pressures. The effective mitral regurgitant orifice area was calculated from Gorlin's hydraulic equation. Infusion of nitroprusside resulted in a significant reduction in mitral regurgitation. No significant change occurred in the systolic pressure gradient between the left ventricle and the left atrium because both peak left ventricular pressure and left atrial pressure were reduced. The reduction of mitral regurgitation was largely due to reduction in the size of the mitral regurgitant orifice. Reduction of ventricular volume rather than the traditional concept of reduction of impedance of left ventricular ejection may explain the effects of vasodilators in reducing mitral regurgitation.
Acute mitral regurgitation (MR) was produced in 12 dogs by closed chest partial valvulectomy and the relative contributions of MR pressure gradient (MRG), the time for regurgitant flow (VSI), and the MR orifice area (MRA) to mitral regurgitant volume (MRV) assessed. Aortic and left atrial pressures, biplane left ventricular (LV) angiography, forward flow and mitral regurgitant flow (MRF) were measured following MR induction and following augmentation of left ventricular end-diastolic volume (EDV), increased aortic resistance (angiotensin), and in the presence of increased ventricular contractility (calcium or epinephrine). Mitral regurgitation orifice area was determined by calculation and the diameters of the mitral anulus and subvalvular areas measured angiographically. Angiotensin and volume infusion induced a substantial increase in MRF which was largely dependent on an increase in MRA but not MRG, while augmentation of contractility decreased MRF accompanied by a decrease in MRA, relatively independent of MRG. Left ventricular size and shape are major determinants of MRA and resultant MRF in acute mitral regurgitation. These findings may help to explain the effects of such factors as ventricular loading and volume on the clinical course of mitral regurgitation in man.
Eight patients with mixed mitral stenosis and regurgitation underwent hemodynamic and angiographic study prior to mitral valve replacement. The stenotic orifice of the mitral valve was calculated employing the total left ventricular stroke volume by cineangiography as the numerator of the Gorlin Formula. Excellent agreement with the measured orifice of the mitral valve was obtained using a value of 37.9 (0.85 X 44.5) for the constant in the Gorlin formula as recommended by Cohen and Gorlin. Recalculation of this constant independently by our data yielded a value that was almost identical. Regurgitant flows and orifice sizes were calculated for each patient using the same constant as for calculation of the stenotic orifices.
We examined the hemodynamic response to afterload reduction by sodium nitroprusside in 7 patients with severe mitral regurgitation of purely valvular origin. Lowering of systemic vascular resistance was associated with major reductions in pulmonary capillary mean (29 +/- 2 to 13 +/- 1 mm Hg) and left ventricular end diastolic (20 +/- 3 to 9 +/- 1 mm Hg) pressures, while substantial increases were noted in cardiac index (2.2 +/- 0.5 to 3.1 +/- 0.4 litres/min per m2 body surface area) and forward stroke volume (23 +/- 4 to 34 +/- 4 ml/beat/m2 body surface area). Angiographic calculations showed significant decreases in regurgitant volume (73 +/- 19 to 55 +/- 12 ml/beat/m2 body surface area) and regurgitant fraction (0.70 +/- 0.07 to 0.57 +/- 0.06). No significant change occurred in left ventricular ejection fraction or heart rate, suggesting that the improved cardiac function was not due to a reflex increase in adrenergic stimulation. These observations support the concept that afterload reduction may be therapeutic in severe mitral regurgitation by reducing impedance to forward left ventricular output, thereby promoting greater forward and small regurgitant fractions of the total stroke volume.
The function of the papillary muscles to restrain the mitral valves is obvious. However, the dynamic nature of this function is not always appreciated. Failure of one or both papillary muscles to shorten during the ejection phase of ventricular systole, fibrosis, and atrophy of a papillary muscle or centrifugal migration of the papillary muscles due to left ventricular dilatation result in mitral incompetence. Depending upon the etiology of the papillary muscle dysfunction, apical systolic murmurs of varying characteristics may be heard. In general, a noncontracting papillary muscle in a normal-sized heart is associated with a murmur which is late in onset and crescendo-decrescendo in quality, whereas in the dilated heart the murmur is early, beginning with the first heart sound, and may be decrescendo, plateau, or crescendo-decrescendo in quality. Obviously, the murmurs of papillary muscle dysfunction may vary considerably depending upon the nature of the dysfunction and time course of activation of the muscle and other portions of the ventricular musculature. Associated electrocardiographic abnormalities may also occur.
The diagnosis of papillary muscle dysfunction in the presence of coronary disease makes it necessary to rule out the more obvious and destructive causes of mitral regurgitation. The combination of a systolic murmur, the presence of angina, and the history of a myocardial infarction make up the major features of the clinical syndrome. Artrial gallop (S4) and diastolic filling gallop (S3) are fairly common. The chest film and EEG are rarely, if ever, diagnostic. At the time of cardiac catheterization, elevated left ventricular end diastolic pressure, widespread coronary artery disease with frequent involvement of the right coronary artery, and systolic ejection abnormalities of the left ventricle are usually present. The therapeutic problem revolves around the question of which is the major lesion - the haemodynamic effect of mitral regurgitation or the intrinsic state of the myocardium.
In order to evaluate the circulatory action of vasodilator therapy in patients with significant mitral regurgitation, sodium nitroprusside was infused IV in 14 patients who had mitral regurgitation due to a variety of causes. In 13 of these patients, valvular insufficiency had been present for several years. The mean arterial pressure fall from 88 ± 1.2 to 71 ± 2.1 mm Hg was accompanied by a significant decrease in pulmonary artery pressure (from 27.4 ± 2.7 to 19.1 ± 2.4 mm Hg), pulmonary artery wedge v wave (from 31.7 ± 3.3 to 17.0 ± 1.9 mm Hg), and left ventricular and diastolic pressure (from 16.7 ± 1.6 to 9.3 ± 1.2 mm Hg). In 10 patients significant decreases in angiographic end diastolic volumes (from 196 ± 10 to 177 ± 10 ml) and end systolic volumes (from 90 ± 10 to 77 ± 9 ml) were accompanied by slight decreases in the total stroke volume and slight increases in the ejection fraction. The improved forward stroke volume index (from 27 ± 3.0 to 33 ± 2.1 ml) was due to a very significant reduction in the regurgitant fraction (from 57 ± 6 to 42 ± 6%). Nitroprusside, therefore, has beneficial hemodynamic effects in patients with chronic mitral regurgitation.
The objective of this study is to describe the mechanism of production of the first heart sound (S1). The temporal relation between the major components of S1 and (1) cessation of flow across the mitral valve, (2) closure of the valve, and (3) time of peak rate of rise of left ventricular pressure (peak LV dP/dt), were investigated in open-chest dogs. Phasic flow across the mitral valve was recorded by a supraannular electromagnetic flow probe, and timing of valve closure was determined by synchronized cinefluorogram of the motion of the valve cusps after they were made radio opaque. Closure of the mitral valve did not occur at the crossing point of atrial and ventricular pressures (at the beginning of systole), but 20-40 msec later due to inertia of mitral flow. The first major component of the first sound coincided with two simultaneous events: cessation of mitral flow and closure of the valve. It did not show a fixed temporal relationship to time of peak dP/dt.
To assess the potential beneficial effects of vasodilator agents in patients with severe mitral regurgitation, sodium nitroprusside was administered intravenously at a rate of 16 to 100 μg/min in eight patients with clinically significant mitral regurgitation presumably due to dysfunction of the subvalvar apparatus. In all patients there was a decrease in the magnitude of the peak 'V' wave (from 50±4.5 to 19±2.9 mm Hg) and in left ventricular filling pressure (33±1.8 to 16±1.4 mm Hg), together with a decreased intensity of the apical pansystolic murmur. There was a significant increase in forward cardiac index (2.2±3.5 to 3.3±.47 liter/min/M2) and forward stroke volume index (23±4.4 to 36±6.6 ml/M2) along with a reduction in systemic vascular resistance (1802±331 to 1102±241 dynes/sec/cm-5). In the five patients in whom the therapy was continued, relief of symptoms of pulmonary venous congestion occurred. In the four patients in whom left ventricular volumes were determined angiographically, the observed increase in forward stroke volume was due to a reduction in the regurgitant fraction. These findings suggest that the use of vasodilator agents like nitroprusside can achieve the major objectives of treatment of patients with mitral regurgitation: an increase in forward stroke output, a reduction in regurgitant volume and a decrease in pulmonary venous pressure.
The mitral complex is a functional entity composed of the annulus, valve leaflets, chordae, and papillary muscles. The mechanical properties of the complex are dependent on the unique structural relations of the collagen in the leaflets and chordae. In the chordae the collagen is arranged in avascular columns. These columns interdigitate between muscle fibers in the papillary muscles, and the collagen is anchored to the myofiber membrane by microfibrils. In the leaflet the chordae are continuous with the dense fibrous tissue, forming a sheet of collagen which merges with the annulus. Within the leaflet there are cardiac muscle fibers in direct continuity with left atrial muscle. Contraction of isolated valve preparations can be initiated by electrical stimulation and is preceded by a propagated depolarization. Action potentials from cells in the middle third of the leaflet have a slow upstroke velocity, prominent plateau, and a characteristic positive afterpotential. Valve muscle electromechanical properties are markedly altered by 1 x 10-7M acetylcholine; this concentration has little effect on working left atrial muscle. In preparations containing portions of the left atrium and valve leaflet, the excitation wave spreads into the leaflet after electrical stimulation of the atrial muscle. This suggests that the accompanying contractile event may occur in situ before the initiation of systole.
A cylindrical ultrasonic transducer on a catheter tip lodged in the cleft between the free wall of the right ventricle and the interventricular septum provides an easily measured echo from the posteroinferior left ventricular epicardial surface. The sonic path represents a diameter of the left ventricle at approximately its largest cross-sectional area. Experiments in six dogs demonstrated that measurements by ultrasound agree within ±6% with simultaneous radiographic measurements of left ventricular diameter. Procedures designed to alter left ventricular volume were employed in 14 dogs to clarify the physiologic meaningfulness of the left ventricular diameter measured by ultrasound. Both end-diastolic and end-systolic diameter increased with anoxia, with sudden injections of saline into the left ventricle, after propranolol, and after inflation of a balloon in the thoracic aorta. These diameters decreased with isoproterenol, with increased heart rate, and after inflation of a balloon in the inferior vena cava. The present technique provides accurate and physiologically meaningful estimates of left ventricular diameter. Ventricular diameter measurements obtained during cardiac catheterization should permit assessment of ventricular distensibility and of ventricular function.
The effects on myocardial oxygen consumption and mechanics of acute, simulated aortic and mitral regurgitation were studied in open-chest, anesthetized dogs to determine how changes in the mechanical performance of the ventricle alter oxygen consumption. When regurgitation was induced acutely with effective stroke volume (total stroke volume less regurgitant volume) and heart rate held constant, left ventricular end-diastolic volume, total stroke volume, the ejection fraction, left ventricular wall tension, and the extent of shortening of the contractile element and the circumferential fibers all increased. With volumes of regurgitation approaching effective systemic blood flow, oxygen consumption increased only moderately, despite the increases in tension and shortening. When valvular regurgitation was induced while peak ventricular wall tension was held relatively constant, stroke volume doubled and the extent of both contractile element and circumferential fiber shortening increased. Contractile element work in generating tension was unchanged; that which led to fiber shortening increased substantially. Myocardial oxygen consumption did not increase significantly. Thus, marked increases in the efficiency of the contractile elements and myocardial fibers occurred. The low energy cost per unit of work expended in shortening as opposed to that used for tension development therefore allows the excess stroke volume of valvular regurgitation to be maintained at only a small added oxygen cost to the ventricle.
The anterior leaflet of the mitral valve of the dog contains blood vessels, nerve fibers, and cardiac muscle in addition to elastic fibers and collagen. When studied in a myograph, the electrically stimulated mitral valve actively developed tension and shortened. Active tension was found to be a function of initial length of the valve and was increased by norepinephrine and decreased by acetylcholine. The presence of neuronally releasable norepinephrine stores in the valve was indicated by responsiveness to tyramine. The negative inotropic response of the mitral valve to acetylcholine was consistent with an atrial origin of the tissue. Possible functional roles for mitral valve muscle and the potential significance of its neural control are discussed.
A canine preparation was devised in which aortic regurgitant flow could be acutely produced, metered and controllably varied. Aortic regurgitant flows in excess of the dog's resting cardiac output resulted in a marked decrease of effective cardiac output, a substantial rise of peripheral resistance and left ventricular end-diastolic pressure, and a marked depression of the left ventricular function curve, with little change in the mean left atrial pressure. When mitral regurgitation was added to aortic regurgitation, effective cardiac output, stroke work and left ventricular end-diastolic pressure fell, while left atrial pressure rose.
The mitral complex Clinical manifestations of papillary muscle dysfunction
- Mr Silverman
- Jw Hurst
- Np Depasquale
- Phillips
Silverman MR, Hurst JW: The mitral complex. Am Heart J 76: 399, 1968 3. Burch GE, DePasquale NP, Phillips JH: Clinical manifestations of papillary muscle dysfunction. Arch Intern Med 112: 112, 1963
Analysis and interpretation of the normal mitral valve flow curve
- E L Yellin
- S Laniado
- C S Peskin
- Rwm Frater
Yellin EL, Laniado S, Peskin CS, Frater RWM: Analysis and
interpretation of the normal mitral valve flow curve. In The
Mitral Valve: A Pluridisciplinary Approach, edited by Kalmanson D. Acton, Mass, Publishing Sciences Group Inc, 1976, pp
163-172
Analysis and interpretation of the normal mitral valve flow curve. In The Mitral Valve: A Pluridisciplinary Approach, edited by Kalmanson D. Acton, Mass
- E L Yellin
- S Laniado
- C S Peskin
- Rwm Frater
- Yellin EL