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Ventricular remodeling and mitral valve modifications in dilated cardiomyopathy: New insights from anatomic study
Abstract
The purpose of this study was to analyze the behavior of the mitral valve ring and the left ventricle in dilated cardiomyopathy.
We analyzed 68 fixed adult human hearts, divided into 48 hearts with dilated cardiomyopathy of ischemic or idiopathic origin and 20 hearts free of pathologic heart conditions. Digital images of the mitral ring perimeter, attachment of the anterior and posterior leaflets, and fibrous and muscular portions were collected. We also measured the internal perimeter of the left ventricle, the distance from the septum to the anterior and posterior papillary muscles, the distance between the papillary muscles, and the extension of interventricular septum.
The analysis of the results showed proportional distribution of the ring's fibrous portion (r2 = 0.98) and muscular portion (r2 = 0.99) according to the degree of mitral valve dilation. Linear regression revealed that the perimeters of anterior and posterior leaflet attachments (r2 = 0.96 and r2 = 0.98, respectively) also had a proportional relation. We did not observe proportionality between the degree of dilation of the mitral ring and the left ventricle. It was observed that dilation of the left ventricle takes place globally in its segments.
Differently from what was thought, in ischemic or idiopathic dilated cardiomyopathy, dilation of mitral ring is proportional and does not exclusively affect the posterior portion. The degree of left ventricular dilation does not determine the degree of dilation of the mitral ring because they are independent processes. These observations shed new light on the techniques used to correct mitral valve insufficiency in dilated cardiomyopathy.
... Several authors have hypothesized that dilated chambers tended to have a spherical shape. [1][2][3]5,[18][19][20] This hypothesis is based on Laplace's law. It postulates that the increase of internal tension against ventricular walls results in a dilated spherical chamber. ...
... Spherical shape and proportionality hypotheses Dilated specimens were not spherical Dilated chambers shape was not spherical as suggested by some authors. [1][2][3]5,[18][19][20] All the observed SSIs were <70% of the expected one when considering the spherical shape hypothesis. Despite under 'geometric' language, we can declare that there is a tendency to a more spherical shape in both basal and apical regions; but these tendencies were not similar. ...
... It was followed by basal and finally by apical segments, mainly in the idiopathic group, corroborating the hypothesis of other authors. 7,20 We could hypothesize that this resistance of apical segment to dilatation, when compared with basal and equatorial regions, is due to its intrinsic arrangement of muscular bands. Apical bands arrangement composes a more complex network than that in equatorial and basal regions. ...
Aims:
Some authors have hypothesized that left ventricular chamber dilatation in ischaemic and idiopathic cardiomyopathies results in spherical transformation. Aiming to characterize how this transformation occurs, a study was performed by comparing normal and dilated specimens regarding sphericity and proportionality in left heart chambers. It is important to provide data for the development of therapeutic strategies in these diseases.
Methods and results:
An anatomical study was performed by comparing normal (n = 10), ischaemic (n = 15), and idiopathic (n = 18) dilated human cardiomyopathic specimens regarding left ventricular chambers and their segmental proportionality to normal hearts. It was performed by capturing and processing images with proper software in three different levels of left ventricular chamber (basal, equatorial, and apical). These obtained data were analysed based on sphericity and proportionality by two dedicated indexes. Spherical shape: Calculated segmental indexes showed that dilated specimens were not spherical because they were smaller than as expected for a spherical shape (all values were <70% of a perfect sphere). Proportionality: There was no difference between basal index perimeters among groups, but apical index was lower in dilated specimens than in normal hearts, and so dilatation was not proportional to normal hearts.
Conclusions:
Left ventricular chambers of anatomical specimens with dilated cardiomyopathies did not display a spherical shape and were not proportional to normal hearts.
... The annulus is generally saddled in shape taking a kidney-like shape in systole and a round shape at diastole. However, it is anatomically divided into two distinct parts; an anterior and posterior portion with the former considered to be non-distensible found between two fibrous bodies while the latter accounts for about 2/3 of the mitral valve orifice and is considered to be easily prone to distention and dilatation with LAM and other diseases affecting the mitral valve and the left heart [4,5] (Figure 1). The two leaflets are also described as anterior and posterior with the anterior leaflet being wider with a shorter base while the posterior leaflet is narrower but with a much broader attachment. ...
... anterior and posterior], chordae tendineae rupture or elongation and left ventricular abnormalities produced during the course of forward and backwards movement into the left ventricle and back to the left atrium during systole and diastole results in mitral valve regurgitation[1,4,7,11] . ...
... It is known that mechanical loading on the mitral valve (MV) tissue plays an important role in myxomatous degeneration, the most common cause of organic MR (Pedersen et al. 2007). In addition, mitral annular dilation, the main geometric factor that contributes in functional MR (Agricola et al. 2004;Trichon and O'Connor 2002;Hueb et al. 2002), has a direct correlation with mechanical over-tension caused by dilated cardiomyopathy on the MV tissue (Rausch et al. 2013;Padala et al. 2009). However, the mechanism under which tissue deterioration and rupture are developed has not been investigated. ...
... The decreasing trends observed in fracture toughness values represent the effect of induced fatigue on the mechanical properties of the MV tissue. In similar studies, the effect of fatigue on the fracture toughness and elastic properties of porcine coronary and aortic tissue has been reported (Chu et al. 2012;Gilpin 2005). Based on Lemaître's theory, the fatigue effect on fracture toughness and elastic modulus is governed by a damage accumulation process in the material (Lemaître 1996). ...
Sudden failure and rupture of the tissue is a rare but serious short-term complication after the mitral valve surgical repair. Excessive cyclic loading on the suture line of the repair can progressively damage the surrounding tissue and finally cause tissue rupture. Moreover, mechanical over-tension, which occurs in a diseased mitral valve, gradually leads to tissue floppiness, mitral annular dilation, and leaflet rupture. In this work, the rupture mechanics of mitral valve is studied by characterizing the fracture toughness exhaustion of healthy tissue. Results of this study show that fracture toughness of the posterior mitral valve is lower than its anterior counterpart, indicating that posterior tissue is more prone to failure. Moreover, the decrease in fracture toughness by increasing the number of fatigue cycles shows that excessive mechanical loading leads to progressive failure and rupture of mitral valve tissue within a damage accumulative process.
... In chronic ischemic MR fibrous perimeter increases. 37 This corresponds to the inter-trigone distance. Generally, it is said that intertrigonal distance is part of the fibrous skeleton of the heart and therefore is fixed and does not dilate. ...
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.
... Similar to the septal annulus, the fibrous portion of the mitral annulus has traditionally been considered a static part that does not dilate in functional mitral regurgitation. However, it was revealed that the fibrous part of the mitral annulus was proportionately dilated in patients with cardiomyopathy (24) and in animal models of biventricular failure (25). Therefore, it is not unreasonable to expect that the septal annulus of the tricuspid valve would dilate in FTR and a dilated RV. ...
Background
This study aimed to investigate the course of tricuspid annulus dilation in functional tricuspid regurgitation with varied severities by direct intraoperative assessment.
Methods
A total of 317 patients who underwent left heart surgery and concomitant tricuspid repair were divided into three groups according to the severity of the functional tricuspid regurgitation (mild, moderate and severe). Demographic and echocardiographic data were collected. The length of each tricuspid annulus segment was measured intraoperatively. The risk factors for preoperative severe functional tricuspid regurgitation and its postoperative recurrence were identified, and the impact of each tricuspid annulus segment on postoperative recurrence was compared.
Results
In the course of tricuspid annulus dilation, the posterior annulus dilated 17% (group 1: 33.31 ± 6.94 mm vs. group 2: 35.56 ± 7.63 vs. group 3: 38.98 ± 8.70, p < 0.01), the anterior annulus dilated 13.4% (group 1: 36.71 ± 6.30 mm vs. group 2: 38.21 ± 8.35 vs. group 3: 41.63 ± 9.20, p < 0.01), and the septal annulus dilated 11.4% (group 1: 38.11 ± 5.28 mm vs. group 2: 39.76 ± 6.90 vs. group 3: 42.46 ± 7.50, p < 0.01). Tricuspid annulus circumference index ( p < 0.01) independently correlated with preoperative severe tricuspid regurgitation and postoperative recurrence. When patients were grouped based on the length of each segment, the septal annulus demonstrated significantly higher sensitivity ( p < 0.001) to postoperative recurrence than the anterior ( p = 0.085) or posterior annulus ( p = 0.262).
Conclusions
This study revealed that each segment of tricuspid annulus could dilate in functional tricuspid regurgitation and highlighted the potential benefits of septal annulus plication in tricuspid annuloplasty, which may aid in the development of a methodology for prosthetic ring annuloplasty.
... Methods for sizing vary widely even among commercial rings, with improper sizing carrying the potential for serious complications (17) . Prior pathologic studies showed that the normal adult mitral annular circumference should be around 10 cm, with a ratio of 1:2 between the anterior intertrigonal part and the posterior portion of the annulus (18,19) . Moreover, cardiac size and mitral annular size were previously shown not to always correlate with body surface area (20,21) . ...
... In human hearts with ischemic and nonischemic dilated cardiomyopathy, Hueb et al., 1 in a study aimed to analyze annular modifications, found that, compared with cardiomyopathy, by 24% if ischemic and by 50% if nonischemic. The degree of antemortem MR was not reported. ...
In secondary mitral regurgitation, the concept that the mitral valve (MV) is an innocent bystander, has been challenged by many studies in the last decades. The MV is a living structure with intrinsic plasticity that reacts to changes in stretch or in mechanical stress activating biohumoral mechanisms that have, as purpose, the adaptation of the valve to the new environment. If the adaptation is balanced, the leaflets increase both surface and length and the chordae tendineae lengthen: the result is a valve with different characteristics, but able to avoid or to limit the regurgitation. However, if the adaptation is unbalanced, the leaflets and the chords do not change their size, but become stiffer and rigid, with moderate or severe regurgitation. These changes are mediated mainly by a cytokine, the transforming growth factor‐β (TGF‐β), which is able to promote the changes that the MV needs to adapt to a new hemodynamic environment. In general, mild TGF‐β activation facilitates leaflet growth, excessive TGF‐β activation, as after myocardial infarction, results in profibrotic changes in the leaflets, with increased thickness and stiffness. The MV is then a plastic organism, that reacts to the external stimuli, trying to maintain its physiologic integrity. This review has the goal to unveil the secret life of the MV, to understand which stimuli can trigger its plasticity, and to explain why the equation “large heart = moderate/severe mitral regurgitation” and “small heart = no/mild mitral regurgitation” does not work into the clinical practice.
... In human hearts with ischemic and non-ischemic dilated cardiomyopathy, Hueb et al. 1 , in a study aimed to analyze annular modifications, found that, compared with cardiomyopathy, by 24% if ischemic and by 50% if non-ischemic. The degree of ante-mortem MR was not reported. ...
... First, dilatation of the mitral valve annulus occurs primarily in the posterior aspect of the valve. Although studies show that there is some enlargement of the anterior aspect of the mitral valve in patients with functional mitral valve regurgitation [25], this is relatively small and unimportant in most patients with degenerative mitral valve pathology [26]. Thus, the portion of the annulus that needs to be reduced extends posteriorly from the right to the left fibrous trigones. ...
Mitral valve repair for patients with degenerative or functional mitral valve regurgitation improves symptoms and prognosis, and several techniques have been described. Important principles in operation are simplicity, reproducibility, and durability of repair. At Mayo Clinic, we have operated on more than 6000 patients with degenerative mitral valve disease and valve prolapse, and this review details our approach to mitral valve repair, including robotic and minimally invasive techniques. Most patients with isolated leaflet prolapse can be managed with leaflet plication or triangular resection, and chordal replacement is reserved for repair of anterior leaflet prolapse. Posterior annuloplasty with a standard-sized flexible band is used to reduce annular circumference and improve leaflet coaptation. With these methods, early risk of mortality for mitral valve repair is low in the current era (< 1%), and rate of recurrent valve leakage is 1.5 per 100 patient-years during the first year post-repair and 0.9 per 100 patient-years thereafter. This paper also briefly summarizes important considerations for patients with mitral valve regurgitation and severe calcification, perforations due to endocarditis, and rheumatic heart disease.
... Partial banding proponents believe minimal dilation exists between the trigones despite ventricular dilation. This observation differs from de Oliviera's observation that annular dilation was proportional in ischaemic and non-ischaemic dilated hearts [23]. Rigid rather than flexible bands or rings are preferred in ischaemic cardiomyopathy [24] because they pull the lateral wall medially and fix it in a systolic position. ...
Mitral regurgitation (MR) occurs when any of the valve and ventricular mitral apparatus components are disturbed. As MR progresses, left ventricular remodelling occurs, ultimately causing heart failure when the enlarging left ventricle (LV) loses its conical shape and becomes globular. Heart failure and lethal ventricular arrhythmias may develop if the left ventricular end-systolic volume index exceeds 55 ml/m2. These adverse changes persist despite satisfactory correction of the annular component of MR. Our goal was to describe this process and summarize evolving interventions that reduce the volume of the left ventricle and rebuild its elliptical shape. This 'valve/ventricle' approach addresses the spherical ventricular culprit and offsets the limits of treating MR by correcting only its annular component.
... Given the outstanding results of open valve repair, surgery has remain the criterion standard for most cases of symptomatic valvular heart disease. [3][4][5][13][14][15][16][17][18][19][20][21] In the near term, percutaneous valve intervention will probably have two indications, as follows: ...
... Finally, dilatation of the mitral annulus was always believed to occur in its posterior segment, the anterior segment being relatively protected from enlargement, but there is recent evidence that the anterior annulus can also dilate. (12) Correction of the anterior leaflet prolapse, as initially proposed by ...
Prosthetic valve replacement in young patients carries increased morbidity and mortality, even with recent types and models of prostheses. Fortunately, rheumatic mitral regurgitation in this young population group is amenable to repair, although the results are less favourable than those observed with other types of mitral valve disease and in older populations. A better knowledge of the pathology and evolution of repair techniques has improved results. Hence mitral valve repair is still worthwhile, even in rheumatic pathology and, the percentage of valves repaired, increases with the experience and the will of the surgeon to preserve the valve. Mitral valve replacement can only be justified when good repair is not feasible. It is vital that the surgeon has adequate experience which can only be gained by exposure to enough patients with this condition. Most of these patients are in developing countries and hampered by socio-economic conditions – which means 1st World surgeons get limited required exposure.
... Согласно рекомендациям ACC/AHA [14,16], выполнимость такой пластики у асимптомных пациентов при ДСТ должна быть не менее 90%, а при ФЭД стремиться к 100% случаев ввиду общепризнанных преимуществ клапаносохраняющих операций перед заменой клапана: значительное улучшение функции ЛЖ, более низкий риск развития тромбоэмболии и осложнений связанных с приемом антикоагулянтов и эндокардита оперированного клапана, а также увеличение свободы от всех клапаносвязанных осложнений. В последующем преимущества клапаносохраняющих методик были подтверждены превосходными результатами отдаленных наблюдений, что сделало реконструкцию МК -операцией выбора при коррекции МН [1,2,[17][18][19][20]. ...
Recently, the main cause of mortality and disability in the world are cardiovascular diseases. By the data from autopsies, valve defects have 4-7% prevalence, and most common are mitral valve defects. Valve prolapse is caused by in-born defect of connective tissue development. Reconstruction surgery continue becoming more common in mitral regurgitation (MR) correction and is more preferable than the valve replacement. Regardless the long history of successful management of MR, official data from most world cardiosurgery centers shows than reconstruction operations are done just in 10-20% cases. Issues on the improvement of the management of patients with connective tissue dysplasia are still open. There is enough literature on laboratory and experimental studies showing benefits and disadvantages of one or other methods, but there are no large clinical trials with sufficient evidence, to confirm or stronly deny differences in clinical outcomes depending on the selection of one or other method.
... [2][3][4][5][6] The principal mechanism underlying the development of IMR is related to tethering of the mitral valve (MV), resulting from ischemic LV remodeling and distortion. 2,[7][8][9][10] Currently, MV repair or MV replacement with or without concomitant coronary artery bypass graft (CABG) surgery is performed for the operative management of IMR, and it is unclear which patients do better with MV replacement versus repair. 11 An important limitation of MV ring repair for IMR is the significant recurrence rates of MR after ring annuloplasty. ...
Background:
In ischemic mitral regurgitation (IMR), ring annuloplasty is associated with a significant rate of recurrent MR. Ring size is based on intertrigonal distance without consideration of left ventricular (LV) size. However, LV size is an important determinant of mitral valve (MV) leaflet tethering before and after repair. We aimed to determine whether LV-MV ring mismatch (mismatch of LV size relative to ring size) is associated with recurrent MR in patients with IMR after restrictive ring annuloplasty.
Methods:
Patients with moderate or severe IMR from the 2 Cardiothoracic Surgical Trials Network IMR trials who received MV repair were examined at 1 year after surgery. Baseline LV size was assessed by LV end-diastolic dimension and LV end-systolic dimension (LVESd). LV-MV ring mismatch was calculated as the ratio of LV to ring size (LV end-diastolic dimension/ring size and LVESd/ring size).
Results:
At 1 year after ring annuloplasty, 45 of 214 patients with MV repair (21%) had moderate or greater MR. In univariable logistic regression analysis, larger LVESd (P=0.02) and LVESd/ring size (P=0.007) were associated with recurrent MR. In multivariable models adjusted for age, sex, baseline LV ejection fraction, and severe IMR, only LVESd/ring size (odd ratio per 0.5 increase, 2.20; 95% confidence interval, 1.05-4.62; P=0.038) remained significantly associated with 1-year MR recurrence.
Conclusions:
LV-MV ring size mismatch is associated with increased risk of MR recurrence. This finding may be helpful in guiding choice of ring size to prevent recurrent MR in patients undergoing MV repair and in identifying patients who may benefit from MV repair with additional subvalvular intervention or MV replacement rather than repair alone.
Clinical trial registration:
URL:http://clinicaltrials.gov. Unique identifiers: NCT00806988 and NCT00807040.
... Although the insertion of the anterior leaflet has been considered inextensible for several years, an anatomical study demonstrated that this assumption is not completely true; in fact, Hueb et al. measured MV annular perimeter, anterior leaflet (AL) insertion and posterior leaflet (PL) insertion both in patients who died for any reasons but heart disease and in patients who died for end-stage cardiomyopathy. [25] The annular perimeter increased of 15 mm between normal and end-stage cardiomyopathy (from 88.0 mm to 103.0 mm), PL insertion increased of 12.3 mm (from 50.1 mm to 62.4 mm). Although AL insertion increase of just 2.7 mm (from 37.9 mm to 40.6 mm), the fibrous portion increased of 7.2 mm (from 19.0 mm to 26.2 mm) but the muscular portion even decreased of 4.5 mm (from 18.9 mm to 14.4 mm). ...
... MR due to ischemic heart disease can arise as a direct complication of a myocardial infarct, e.g., due to papillary muscle dysfunction or rupture, or as a consequence of left ventricular remodeling secondary to a myocardial infarct (41). Remodeling of the left ventricle results in apical and inferior displacement of the papillary muscles and tethering of the mitral leaflets, failure of coaptation and hence MR ( Figure 9) (42,43). This is of particular significance in patients who have had a posterior infarction since remodeling may result in an asymmetric restriction of the posterior leaflet in systole (44,45). ...
The mitral valve is the most commonly diseased heart valve and the prevalence of mitral valve disease increases proportionally with age. Echocardiography is the primary diagnostic imaging modality used in the assessment of patients with mitral valve disease. It is a noninvasive method which provides accurate anatomic and functional information regarding the mitral valve and can identify the mechanism of mitral valve pathology. This is especially useful as it may guide surgical repair. This is increasingly relevant given the growing trend of patients undergoing mitral valve repair. Collaboration between cardiac surgeons and echocardiographers is critical in the evaluation of mitral valve disease and for identification of complex valvular lesions that require advanced surgical skill to repair. This article will provide an overview of transthoracic and transesophageal assessment of common mitral valve pathology that aims to aid surgical decision making.
... It is widely accepted that dilatation occurs essentially in the posterior segment of the annulus, although there is some evidence that it may also occur in the anterior segment, especially in dilated cardiomyopathy. 5 It is still subject to some degree of speculation whether dilatation is only a functional phenomenon or the result of direct involvement by the rheumatic process, as the annulus does not appear to retain the normal capacity of changing its shape during the cardiac cycle. ...
In developing countries, rheumatic fever and carditis still constitutes a major public health problem. Patients have special characteristics that differ from those with rheumatic mitral valve disease we still see in developed countries. They are usually young, poor, uneducated, and have low compliance to prophylaxis / therapy. In addition, they usually have great difficulty in accessing medical care. In these situations, the rate of complications associated to valve replacement is significantly increased. Alternatively, mitral valve repair is now known to achieve better long-term results in this pathology, but this was not widely recognized three or four decades ago, when first reports showed worse results after repair of rheumatic regurgitation than with degenerative valves. This has been reported by several groups in developing countries in different continents, with high incidence of repairs and excellent long term results. It is, therefore, becoming increasingly clear that, although, the results may not compare to those obtained with degenerative pathology, repair of rheumatic valves, when feasible, is the procedure of choice, especially in these underprivileged populations.
... However, no large trials comparing the relative efficacy of these devices have been performed, and the choice of which mitral valve annuloplasty ring should be used for IMR continues to be controversial. Recently, clinical and experimental evidence has indicated that fixing the septal-lateral dimension is a very important aspect towards maintaining mitral valve competence (18,19) as the intertrigone area dilates (20,21), the pattern of annular dilation and tethering of the mitral leaflets is asymmetric in patients with ischemic LV remodeling, with the tethering being predominant at the medial aspect (3,4). Thus, it could be concluded that the ideal ring for annuloplasty in IMR would be a specifically shaped rigid ring, aimed at reducing the septal-lateral dimension and, in particular, the P3 region (the site of the most extensive tethering). ...
The Carpentier-McCarthy-Adams IMR ETlogix annuloplasty ring was specifically designed to treat ischemic mitral regurgitation (IMR) associated with asymmetric mitral annular dilation and leaflet tethering. The study aim was to review, retrospectively, the results of mitral annuloplasty with this asymmetric ring in a representative number of patients.
Between January 2005 and July 2012, the IMR ETlogix ring was implanted in 190 consecutive patients (mean age 69.5 +/- 7.6 years) with grade > or =2+ IMR (graded from 0 to 3+). Preoperatively, 37 patients (19.5%) were in NYHA class IV, and 73 (38.4%) suffered from unstable angina. The operative risk according to the European System for Cardiac Operative Risk Evaluation II was 15.6 +/- 14.5%. Using two- dimensional echocardiography, postoperative changes in mitral annular diameter (MAD) and tenting height (TH) of the mitral valve in four-chamber, two-chamber and long-axis views, were assessed at mid-systole.
Thirty-eight patients (20.0%) received one or more concomitant major cardiac surgical procedure(s) other than, or in addition to, coronary artery bypass grafting or tricuspid valve annuloplasty. Nineteen (10.0%) hospital deaths occurred, and one patient underwent immediate reoperation for residual MR. During the follow up (mean 4.8 +/- 2.1 years) there were 26 cardiac deaths, 14 non-cardiac deaths, and three mitral valve replacements. The seven-year actuarial survival, freedom from grade > or =2+ MR and reoperation were 62.0%, 93.1% and 97.6%, respectively. Renal impairment (p = 0.012) and extracardiac arteriopathy (p = 0.047) were predictors of death; bilateral internal thoracic artery grafting was a protective factor (p = 0.033). Heart failure symptoms were improved (p <0.01). Left ventricular reverse remodeling was achieved in 50.6% of patients. The MAD and TH were each decreased in all three echocardiographic views (p < 0.001), the reductions being greater in the long-axis view.
By restoring the mitral apparatus geometry and competence, asymmetric annuloplasty with the IMR ETlogix ring provides good mid-term outcomes and helps left ventricular reverse remodeling in IMR.
... Furthermore, the septal portion of the mitral annulus has traditionally been considered a static portion of the mitral apparatus that did not remodel in states of pathology. Recent data have questioned this surgical dogma, revealing that fibrous portion of the mitral annulus dilates in patients with cardiomyopathy [19] and in animal models of biventricular failure [20]. As such, it is not unreasonable to expect that the septal region of the TA would dilate under either pressure or volume overload of the RV. ...
OBJECTIVES Pulmonary hypertension (PHT) is associated with tricuspid annular dilatation, but the effect of acute increase of pulmonary
pressure on three-dimensional (3D) tricuspid annular dynamics and shape is unknown. Better understanding of tricuspid annular
dynamics may lead to improved and more durable surgical reparative techniques.
Rheumatic heart disease remains a major health problem in developing countries. It is the most important sequel of rheumatic fever and occurs in about 30% of patients with rheumatic fever (1).
Rheumatic mitral valves shows a different set of lesions by comparison with degenerative valves, because of the characteristic inflammatory process, which results in thickening of the leaflets and other components of the mitral valve apparatus, of variable degrees, and distorts and impairs the movements of the valve. So, the disease appears here in two forms - stenosis and regurgitation, or a combination of both (2).
Valvular Heart Disease VHD is a common aetiology of pulmonary hypertension. Assessment of the presence and severity of Pulmonary hypertension thus has an important role in the risk stratification and therapeutic management of VHD (3).
The pathophysiology of PH in VHD thus involves progressive structural alteration of the pulmonary vascular bed mediated by the potent vasoconstrictor endothelin-1. An increase in pulmonary-arterial vasoconstriction and systolic PAP results into RV dilation and hypertrophy. The RV failure is associated with tricuspid annulus dilation and an increase in tricuspid regurgitation severity, which further acerbates RV dysfunction. At the decompensated phase, systolic PAP can decrease despite the increase in pulmonary vascular resistance, due to the fall in RV stroke volume related to advanced RV failure (4).
The right ventricle has long been neglected, yet it is RV function that is strongly associated with clinical outcomes in many conditions. There are, however, limited data regarding the normal dimensions of the right ventricle, in part because of its complex shape. The echocardiographic evaluation of the RV is more challenging than that of the left ventricle. The main difficulties encountered may be explained by 1) the complex shape of the RV, 2) heavy apical trabeculations of the RV, which limits endocardial surface recognition, and 3) the marked load dependence of several indices of RV function. As a result, many physicians rely on visual estimation to assess RV size and function (5).
Functional tricuspid regurgitation (FTR) is thought to arise due to annular dilation and alteration of right ventricular (RV) geometry in the presence of normal leaflets, yet mitral leaflets have been shown to remodel significantly in functional mitral regurgitation. We set out to evaluate tricuspid valve anterior leaflet deformations in ovine FTR. Eleven animals (FTR group) underwent implantation of a pacemaker with high rate pacing to induce biventricular dysfunction and at least moderate TR. Subsequently, both FTR (n=11) and Control (n=12) animals underwent implantation of 6 sonomicrometry crystals around the tricuspid annulus, 4 on the anterior leaflet, and 14 on RV epicardium. Tricuspid valve geometry and anterior leaflet strains were calculated from crystal coordinates. Left ventricular ejection fraction and RV fractional area change were significantly lower in FTR animals versus Control. Tricuspid annular area, septo-lateral diameter, RV pressures were all significantly greater in the FTR group. Mean TR grade (+0-3) was 0.7±0.5 in Control and 2.4±0.5 in FTR (p=<0.001). The anterior leaflet area and length increased significantly. Global radial leaflet strain was significantly lower in FTR mostly driven by decreased free edge leaflet strain. Global circumferential anterior leaflet strain was also significantly lower in FTR with more remarkable reduction in the belly region. Rapid ventricular pacing in sheep resulted in a clinically pertinent model of RV and annular dilation with FTR and leaflet enlargement. Both circumferential and radial anterior leaflet strains were significantly reduced with FTR. Functional TR may be associated with alteration of leaflet mechanical properties.
Secondary, or functional, mitral regurgitation (MR) occurs with impaired coaptation of structurally normal valve leaflets due to abnormal structure and/or function of the left ventricle (LV). A leading cause of functional mitral regurgitation is ischemic cardiomyopathy, resulting in left ventricular dysfunction and subsequent congestive heart failure (CHF) and ischemic mitral regurgitation (IMR). The value of surgical or transcatheter correction of IMR remains controversial, since the underlying pathology of IMR is attributed to a dysfunctional left ventricle. However, even mild IMR has been shown to be harmful to CHF patients, as IMR is both a surrogate of advanced CHF and an independent contributor to CHF morbidity and mortality. While observational and randomized studies have examined surgical treatment of IMR with conflicting outcomes, additional well-designed randomized controlled trials should be performed to further clarify the optimal treatment for IMR. Additionally, close attention should be paid to the quality of interventions performed, as durable reduction in IMR provides the best hope of a positive clinical outcome. This review focuses on the pathophysiology of IMR, current evidence regarding surgical and transcatheter interventions, and future directions in management of IMR.
In the past decades, more than 40 mitral valve annuloplasty rings of various shapes and consistency were marketed for mitral regurgitation (MR), although the effect of ring type on clinical outcome remains unclear. Our objective was to review the literature and apply a simplification method to make rings of different shapes and rigidity more comparable. We studied relevant literature from MEDLINE and EMBASE databases related to clinical studies as well as animal and finite element models. Annuloplasty rings were clustered into 3 groups as follows: rigid (R), flexible (F), and semirigid (S). Only clinical articles regarding degenerative (DEG) or ischemic/dilated cardiomyopathy (ICM) MR were included and stratified into these groups. A total of 37 rings were clustered into R, F, and S subgroups. Clinical studies with a mean follow-up of less than 1 year and a reported mean etiology of valve incompetence of less than 60% were excluded from the analysis. Forty-one publications were included. Preimplant and postimplant end points were New York Heart Association class, left ventricular ejection fraction (LVEF), left ventricular end-systolic dimension (LVESD), and left ventricular end-diastolic dimension (LVEDD). Statistical analysis included paired-samples t test and analysis of variance with post hoc Bonferroni correction. P < 0.05 indicated statistical difference. Mean ± SD follow-up was 38.6 ± 27 and 29.7 ± 13.2 months for DEG and ICM, respectively. In DEG, LVEF remained unchanged, and LVESD decreased in all subgroups. In our analysis, LVEDD decreased only in F and R, and S did not change; however, the 4 individual studies showed a significant decline. In ICM, New York Heart Association class improved in all subgroups, and LVEF increased. Moreover, LVESD and LVEDD decreased only in F and S; R was underpowered (1 study). No statistical difference among R, F, and S in either ICM or DEG could be detected for all end points. Overall, owing to underpowered data sets derived from limited available publications, major statistical differences in clinical outcome between ring types could not be substantiated. Essential end points such as recurrent MR and survival were incomparable. In conclusion, ring morphology and consistency do not seem to play a major clinical role in mitral valve repair based on the present literature. Hence, until demonstrated otherwise, surgeons may choose their ring upon their judgment, tailored to specific patient needs.
Vortical blood flow in the human left ventricular (LV) inflow initiates from the mitral valve (MV) and evolves within the LV during diastolic E-filling. Hence, vortical flow links MV and LV hemodynamics. This study sought to elucidate and quantitatively characterize the in vivo 3D dynamics of LV vortical flow over E-filling and relation to MV-LV hemodynamic coupling using 4D Flow MRI flow field. 34 healthy volunteers and 5 example patients underwent 4D Flow MRI. Vortical blood flow evolution was mapped in the LV over E-wave using enstrophy density. A new dimensionless profile PMV-LV was derived as a function of both MV vortex formation time (VFT) and LV volumetric enstrophy density. Results reveal that 3D vortical flow evolution in the healthy LV follows a bi-phasic behavior with a vortical growth phase followed by a vortical decay phase. In healthy LVs studied, the PMV-LV profile showed that the vortical growth and decay phases are characterized by a vortical growth time T_growth= 1.23+/-0.25, growth rate {\alpha}=0.80+/-0.17, decay time T_decay= 0.96+/-0.39 and decay rate \b{eta}=-1.02+/-0.49. Distinctly altered parameters were found in the pilot patients studied. The derived PMV-LV profile quantitatively characterizes MV-LV hemodynamic coupling by vortical flow dynamics. Results herein unravel new insights into cardiac physiology and could enable a novel standardized methodology to study MV-LV hemodynamic coupling and association to cardiac function in health and disease.
In industrialized countries, mitral regurgitation (MR) ranks second among valve diseases, after aortic stenosis, and affects 9.3% of the population over 75 years of age. Inadequate systolic coaptation of the mitral valve leaflets, in addition to changes in the pressure gradient between the atrium and left ventricle, is the cause of mitral valve regurgitation. MR, however, is the result of various etiological causes and regurgitation mechanisms. Therefore, it is possible to classify MR based on the etiological causes (acute and chronic), regurgitation mechanisms (according to Carpentier’s functional classification), and pathophysiology (degenerative/organic or functional causes).
Functional ischaemic mitral regurgitation carries an adverse prognosis. Survival is worse compared to those without mitral regurgitation; increasing severity of mitral regurgitation is associated with progressively worse survival. It is primarily a disease of the left ventricle, occurring following myocardial infarction and ischaemia; remodelling and dilatation of the left ventricle pulls or restricts the mitral valve leaflets preventing them from coapting adequately and resulting in mitral regurgitation. Changes in mitral annular geometry and motion; mitral leaflet geometry and motion; papillary muscle geometry, function and viability; and left ventricular geometry, function and viability also occur in functional ischaemic mitral regurgitation.
Surgical treatment of ischemic mitral regurgitation with reduction ring annuloplasty is the current standard of practice, yet recurrence in a third of patients limits the benefit of this approach. In an effort to improve outcomes, attention has turned to understanding the contribution of leaflet tethering in this disease process. Subvalvular techniques to alleviate leaflet restriction have been shown to be safe, and in the appropriate patient population decrease recurrence of ischemic mitral regurgitation when combined with reduction annuloplasty. We describe our preferred technique of posterior papillary muscle repositioning. Further understanding of the preoperative parameters that predict recurrence, and deployment of concomitant subvalvular repair techniques in this subset of patients will be the next important breakthrough in the surgical treatment of ischemic mitral regurgitation.
Functional ischemic mitral regurgitation is most commonly repaired by mitral annuloplasty. Important surgical principles must be followed when repairing ischaemic mitral valves by annuloplasty to ensure a durable long term repair. When these principles are followed, a durable, long term repair is achievable. Recent randomized controlled trials have given insights into the groups of patients who would benefit most from concomitant mitral annuloplasty and coronary artery bypass graft surgery. Risk factors for recurrent mitral regurgitation following mitral annuloplasty have been identified; these patients may require additional adjunctive repair procedures or a mitral valve replacement.
Aims:
Transcatheter mitral valve replacement (TMVR) is an emerging technology with the potential to treat patients with mitral regurgitation at excessive risk for mitral valve surgery. Geometrical measurements of the mitral valvular complex may have implications for the design of TMVR devices and for patient selection. This study sought to quantify the dynamic geometry of the mitral valvular complex in patients with significant functional mitral regurgitation (FMR) using multi-slice computed tomography (MSCT).
Methods and results:
MSCT images were acquired in 32 patients with symptomatic, significant FMR. Two independent observers analysed image sets using a dedicated software package and a standard measurement methodology. In patients with FMR, the mean mitral annulus intercommissural and aorto-mural diameters were, respectively, 41.5±5.2 mm and 38.7±5.9 mm in systole, and were 41.5±4.4 mm and 40.0±4.7 mm in diastole. In patients without MR, the diameters were, respectively, 33.6±5.1 mm and 28.8±8.0 mm in systole, and 36.2±4.5 mm and 31.6±7.9 mm in diastole. The obstacle-free zone below the mitral annulus averaged more than 20.0 mm and varied by less than 1 mm between systole and diastole, which is not statistically significant. The aorto-mitral angle was 129.7±10.5° in systole and 131.0±9.4° in diastole.
Conclusions:
The mitral annulus is larger in dimension, more circular, and less dynamic in patients with FMR. The obstacle-free zone below the mitral annulus is relatively constant during the cardiac cycle. Measurements of the mitral valvular apparatus vary considerably between patients, which suggests that tridimensional imaging will play an important role in the sizing of TMVR devices.
Population ageing, the high prevalence of hypertension, obesity and diabetes and especially the very high incidence of ischaemic heart disease, make advanced chronic heart failure (HF) an epidemic and extremely serious public health problem in the developed world. Spain, a country with a relatively low incidence of ischaemic heart disease, has about 40,000 new cases of myocardial infarction annually.
After its introduction in the early 90s, the edge-to-edge (EE) technique has been used in patients with mitral regurgitation (MR) due to different etiologies and mechanisms. More than 20 years after its introduction, it is now clear that the best indications for the EE repair are represented by bileaflet prolapse (facing segments), segmental anterior leaflet prolapse/flail and commissural prolapse/flail. In addition this technique does have an important role also in functional mitral regurgitation, and as a “rescue” procedure in case of suboptimal conventional mitral reconstruction (“rescue” EE). Finally it has been used for the prevention/treatment of SAM. In this chapter the results of the EE repair in the most common indications described above will be outlined and discussed.
Congestive heart failure (CHF) has become an international heath care problem and it is one of the world’s leading causes of hospitalization and mortality. In the United States alone, 4.9 million people (2.3 % of total population) are suffering from heart failure with 550,000 new cases diagnosed each year. Hospital discharge for CHF increased from 377,000 in 1979 to 970,000 in 2002, an increase of 157 %. Estimated health expenditures amount to $ 25.3 billion in 2005 [1]. In spite of these, only 2,100 of the 53,000 patients who die annually are offered transplantation, which many consider to be the standard treatment for selected patients with severe CHF and end-stage heart disease. Transplantation is severely limited by the paucity of donor availability and enormous cost. The inapplicability in the older patient or those with comorbid medical conditions as well as relatively fixed donor pool suggest that transplantation will likely never have a major epidemiological impact [2]. Treatment with mechanical circulatory support devices dances on the horns of the same dilemma. Consequently, despite improvements with medical management, 1 year, 3 year and 5-year survival after hospitalization from CHF have been reported at approximately 80–60 %, 50 % and 40–20 % respectively, which is worse than that of most cancers [3–7].
Physicians who are involved in heart failure treatment are regularly confronted with patients who present with functional mitral regurgitation (MR), occurring in a setting of ischaemic or non-ischaemic cardiomyopathy. For these patients, the current guidelines do not offer clear treatment algorithms, and mitral valve surgery is often not advised. This is however not a proper representation of the currently available literature on this topic, and may lead to patients not being evaluated for an intervention from which they may benefit. This chapter deals with the surgical perspective of functional mitral regurgitation. Topics covered are pathophysiology (with its implications for surgical techniques and annuloplasty ring choice), patient assessment and a critical appraisal of the outcome of different surgical approaches. While the focus lies on the results of undersized restrictive annuloplasty, various additional techniques are discussed in order to provide a tailored medico-surgical approach to this difficult subset of patients.
Secondary mitral regurgitation (SMR) is defined as an insufficiency of the mitral valve, due to an abnormal function of normal valve leaflets, related to impaired left ventricular (LV) function (Lancellotti et al., Eur J Echocardiogr 11(4):307–32, 2010). Some authors consider it to be a ventricular disease with a “valvular phenotype” (Komeda et al., Circ J 73(Suppl A):A23–8, 2009).
SMR can be caused either by ischemic heart disease (with or without LV dilatation), or non-ischemic dilated cardiomiopathy (Marwick et al., Heart 95(20):1711–8, 2009). It has also been described in patients with right ventricular pacing, due to secondary LV dyssynchrony (Barold and Ovsyshcher, Pacing Clin Electrophysiol 28(5):357–60, 2005), or on maintenance dialysis due to end-stage chronic kidney disease (Cirit et al., Nephrol Dial Transplant 13(2):389–92, 1998). Therefore, SMR can result from a heterogeneous group of etiologies, with particular aspects regarding pathophysiology, clinical presentation, and prognosis.
After a myocardial infarction, SMR has been reported to occur with an incidence ranging from 20–25 % (Lamas et al., Circulation 96(3):827–33, 1997) up to 40–50 % of patients, (Bursi et al., Circulation 111(3):295–301, 2005; Perezde Isla et al., Eur Heart J 27(22):2655–60, 2006). Despite the fact that SMR has an independent adverse prognostic value, even when the severity is only mild and there are no signs of congestive heart failure (Lamas et al., Circulation 96(3):827–33, 1997; Lancellotti et al., Circulation 108(14):1713–7, 2003; St John Sutton et al., Circulation 96(10):3294–9, 1997; Agricola et al., J Am Soc Echocardiogr 24(12):1376–82, 2011), morbidity and mortality are related to SMR severity (Grigioni et al., Circulation 103(13):1759–64, 2001; Amigoni et al., Eur Heart J 28(3):326–33, 2007).
Progressive LV remodeling encountered in dilated cardiomiopathy, independent on its etiology, leads to SMR despite anatomically normal mitral valve leaflets (Yiu et al., Circulation 102(12):1400–6, 2000; Trichon et al., Circulation 108(Suppl 1):II103–10, 2003). In these patients, SMR is a multifactorial condition (Donal et al., Eur J Echocardiogr 10(1):133–8, 2009) associated with poor hemodynamics and adverse clinical prognosis (Grigioni et al., Circulation 103(13):1759–64, 2001; Robbins et al., Am J Cardiol 91(3):360–2, 2003).
The pathophysiology of SMR is at present quite well established, and particular clinical interest is directed towards finding a tailored therapeutic strategy for each particular case (Anyanwu et al., Curr Treat Options Cardiovasc Med 10(6):529–37, 2008). Therefore, it is generally recommended a comprehensive assessment of the mechanism of SMR and its classification before planning the surgical intervention, in order to tailor it on the specific characteristics of each patient. However, despite the multitude of therapeutic strategies developed to correct SMR (Fattouch et al., J Thorac Cardiovasc Surg 138(2):278–85, 2009; Fattouch et al., J Thorac Cardiovasc Surg 143(4 Suppl):S38–42, 2012; Fattouch et al., J Thorac Cardiovasc Surg 143(6):1352–5, 2012; Vassileva et al., Eur J Cardiothorac Surgery 39(3):295–303, 2011; Magne et al., J Am Coll Cardiol 51(17):1692–701, 2008; Braun et al., Ann Thorac Surg 85(2):430–6, 2008), post-intervention recurrence of MR still has a high incidence (Magne et al., Circulation 120(11 Suppl):S104–11, 2009).
Disappointing results seen with mitral valve replacement for functional regurgitation led surgeons to attempt valve repair to preserve left ventricular geometry. Secondary regurgitation is due to left ventricular pathology which often distorts the mitral annulus (Schmitto et al., Cardiol Rev 18(6):285–291, 2010). Bolling and colleagues first popularized mitral valve repair using an undersized mitral annuloplasty in the 1990s to address this pathology (Bach and Bolling, Am Heart J 129(6):1165–1170, 1995; Bolling et al., J Thorac Cardiovasc Surg 109(4):676–682, 1995; Bolling et al., J Thorac Cardiovasc Surg 115(2):381–386, 1998). Although Bolling’s initial cases were done using a down-sized fl exible band, practically every other method of annuloplasty has been employed, ranging from suture methods, pericardium, flexible rings and bands, semirigid bands, complete symmetrical rings and specially shaped rings. Although, choice of ring has been historically driven by surgeon preference, critical examination of pathophysiological principles and clinical data allow formulation of certain concepts regarding optimal ring choice for treatment of secondary mitral valve regurgitation.
In ischemic cardiomyopathy with large left ventricular aneurysms, ventricular size increases in response to the surface area of infracted scarred myocardium. This dilatation of contractile myocardium is a compensatory hemodynamic response to maintain an effective forward stroke volume and can be seen as an extension of the Frank-Starling mechanism.
IntroductionSurgical treatment of MR inpatients with severe LV dysfunctionIschemic MRIMR surgeryTricuspid valve surgeryAortic valve surgery in Patients with LV dysfunctionWhy is valve surgery safer today for patients with LV dysfunction and heart failure?Conclusion
References
Mitral valve repair is the treatment of choice for severe degenerative mitral regurgitation providing better freedom from cardiac events, quality of life and long-term survival compared with mitral valve replacement. Increasing numbers of asymptomatic patients are therefore referred for mitral repair. With refinements of the surgical techniques, long-term results have further improve in the last decade. Certainly experience is crucial in determining the likelihood of success and atients with a mitral valve deemed reparable should be referred to centers with high volume and extensive experience in this field. In this article the current role of mitral valve repair in dege erative mitral regurgitation (MR) will be outlined. Moreover some important concepts regarding indication and techniques of mitral repair in the more challenging setting of secondary (functional) mitral regurgitation will be presented and discussed.
Mitral and aortic valves are coupled via fibrous tissue. This coupling is considered to be important for cardiac function before and after mitral valve surgery. The relationship between mitral-aortic coupling and different types of mitral regurgitation (MR) is not completely understood.
Real-time three-dimensional transesophageal echocardiography (RT3D-TEE) was performed in 133 subjects: 30 normal subjects, 15 patients with Carpentier type I MR (annular dilatation and congenital cleft), 40 type II (mitral valve prolapse), 20 type IIIa (rheumatic) and 28 type IIIb (ischemic mitral regurgitation). Custom software was used to track mitral (MA) and aortic annuli (AoA) in 3D space throughout cardiac cycle, allowing measurement of changes in mitral and aortic valve morphology. Normal mitral-aortic coupling is characterized by reciprocal changes in the annular areas throughout cardiac cycle, with systolic reduction of the angle between the two annular planes. In Carpentier type II patients, not only MA but also AoA areas were increased (P < 0.05 vs normal), but the reciprocal pattern of mitral-aortic coupling was preserved. In both type I IMR and IIIb patients, MA and AoA areas were both increased (P < 0.05 vs normal) and the reciprocal behavior of mitral-aortic coupling was lost. Only MA area was increased in type IIIa patients. The extent of mitral-aortic angle reduction during systole was diminished in all 4 Carpentier groups (P < 0.05 vs normal).
Mitral valve diseases may affect normal mitral-aortic coupling and aortic valve function. Different patterns of abnormal mitral-aortic coupling are associated with different Carpentier types of MR.
The increasing popularity of mitral valve repair and current interest in replacement with a mitral homograft or heterograft warrant a new look at the normal functional anatomy of the system. We conducted a detailed review of the anatomic structure of both the intact and excised mitral apparatus of porcine and human species. The following intact structural dimensions were measured: total annular length, anterior and posterior annular length. Excised measurements included: total annular length, anterior and posterior annular lengths, leaflet edge lengths, leaflet heights, and anterolateral and posteromedial commissural heights. Leaflet area was calculated from planimetric measurements. Chordal lengths were measured and distribution recorded. The majority of leaflet measurements were not statistically different between groups. For both groups, the measured annular length increased significantly upon valve excision. In both groups, the posterior leaflet area was significantly larger than the anterior leaflet area, and the area of each leaflet alone was significantly greater than the calculated orifice area. Chordal length was not significantly different between groups, however, distribution varied slightly with the ratio of origins to insertions being 8:1 (porcine) and 5:1 (human). The results are consistent with previous studies of the human mitral valve. This study showed little difference between human and porcine data, and the porcine valve was identified as an appropriate model for further investigation of the mitral valve system.(ABSTRACT TRUNCATED AT 250 WORDS)
The mitral anulus is a dynamic structure that undergoes alterations in size and shape throughout the cardiac cycle, contracting during systole. Numerous reports have shown this systolic orifice reduction to be due chiefly to posterior annular contraction, whereas the anterior perimeter was unchanged. Segmental motion of the mitral anulus from true in vivo three-dimensional data, however, has not been described. We used radiopaque markers and simultaneous biplane videofluoroscopy to measure the lengths of mitral anular segments in seven closed-chest, sedated dogs. Eight markers were placed equidistant from each other around the mitral anulus, As viewed from the left atrium, segment 1 began at the posteromedial commissure, and the remaining segments were numbered sequentially clockwise around the anulus (that is, the posterior mitral anulus encompassed segments 1 to 4 and the anterior anulus encompassed segments 5 to 8). Marker image coordinates obtained from two orthogonal views 7 to 12 days after implantation were merged to construct three-dimensional marker coordinates at end-diastole and end-systole. From end-diastole to end-systole, mean annular area decreased by 11% +/- 8% (5.5 +/- 0.9 cm2 to 4.9 +/- 0.8 cm2, p = 0.005) and perimeter by 5% +/- 4% (8.8 +/- 0.7 cm to 8.3 +/- 0.7 cm, p < 0.01). Mitral annular segmental percent systolic shortening (negative values indicate lengthening) were as follows (mean +/- standard deviation): segment 1, 7% +/- 9%; segment 2, 8% +/- 10%; segment 3, 16% +/- 6%; segment 4, 10% +/- 7%; segment 5, -4% +/- 5%, segment 6, -7% +/-7%; segment 7, 3% +/- 2%; and segment 8, 6% +/- 5%. With the exception of segment 1, all posterior (2 to 4) and two anterior (7 and 8) mitral annular segments contracted significantly (p < or = vs zero, paired t test). Two anterior annular segments (5 and 6, regions overlapping aortic-mitral continuity), however, unexpectedly lengthened during left ventricular systole. We conclude that the anterior mitral anulus may be a much more dynamic component of the mitral apparatus that previously thought. Such heterogeneous dynamic annular motion should be taken into account when various mitral valve reparative techniques are being designed.
RESUMO : Foram estudados 101 pacientes submetidos a plástica da valva mitral em seis anos, com seguimento de 100%. Entre eles, 36 eram do sexo masculino e 65 do sexo feminino, com idade variando de dois a 62 anos (M = 28 ± 16,4). Desses, 57 (56,4%) foram submetidos apenas a abordagem valvar mitral. Os demais foram submetidos a procedimentos associados, como plástica tricúspide (9,9%), revascula-rização do miocárdio (4,0%), entre outros. Não foi registrado óbito imediato. O índice de mortalidade tardia foi de 2% (AVC hemorrágico após cinco anos e septicemia), no primeiro ano. As complicações não fatais foram representadas pela endocardite evidenciada em dois pacientes (2%), sendo tratados e curados, e um paciente com reestenose mitral pós-plástica por reagudização da doença reumática. O estudo atuarial revelou um índice de 79,0 ± 17,7% de sobrevida, um total de 76,3 ± 17,8% de pacientes livres de complica-ções, 80,0 ± 17,9% de reoperações, 100,0% livres de tromboembolismo. Os resultados ecodoplercardio-gráficos registraram que 89% dos pacientes evoluíram com ausência de insuficiência. Dos 11 % restantes, 7,4% apresentram insuficiência mitral discreta, 2,4% moderada e 2% importante. De acordo com a classifi-cação da NYHA, os pacientes das classes III (83,8%) e IV (16,2%) passaram para as classes I (33,3%), II (60,6%), III (4,1%) e IV (2%). Os autores concluem que o anel de pericárdiO flexível conforma-se perfeita-mente com o anel valvar, não produz hemólise e se endoteliza completamente a médio prazo. DESCRITORES: valva mitral, plastia; próteses valvulares cardíacas, biológicas, cirurgia.
Functional mitral regurgitation is frequently observed in the setting of left ventricular dyfunction. This finding is a marker of poor outcome in patients with either ischemic or dilated cardiomyopathy.
The mechanism accounting for this phenomenon is an altered balance of tethering versus coapting forces acting on the mitral valves in the failing heart.
Tethering forces represent an anomalous tension on the mitral valves due to displacement of mitral valve attachments secondary to increased left ventricular chamber sphericity associated with systolic ventricular dysfunction. On the other hand, coapting forces are weak and unable to counteract the abnormal tension acting on the mitral valve, which restricts closure and leads to regurgitation.
Vasodilators and inotropic drugs are effective in the management of functional mitral regurgitation. Although partial left ventriculectomy or Batista’s procedure is still investigational, this new technique seems to provide an optimal control of functional mitral regurgitation and improve functional capacity and survival of some patients with heart failure.
To confirm or deny the thesis that mitral anular dilatation is a cause of mitral regurgitation, this anulus was measured In 102 patients, 24 of whom had normal hearts and 78 of whom had dilated left ventricles, some associated with mitral regurgitation, others not. The circumference of the mitral anulus in the 24 patients] with normal hearts averaged 9 cm (range 7 to 11 cm); In 24 patients with idiopathic cardiomyopathy of the ventricular dilated type, both with (12 patients) and without (12 patients) mild to moderate regurgitation, 11 cm (range 10 to 14 cm); and in 31 patients with severe mitral regurgitation, 12 cm (range 8 to 18 cm). Among the latter 31 patients with severe mitral regurgitation, the anuius was only mildly dilated in the 15 with rheumatic disease (average 11 cm) and in the six with ruptured chordae tendineae on previously normal valves (average 10 cm); in contrast, in the 10 patients with floppy mitral valves with or without the Marfan syndrome the mitral anulus was greatly dilated (average 15.5 cm). Thus, only in patients with floppy valves with or without the Marfan syndrome or both does anular dilatation by itself appear great enough to cause mitral regurgitation. It appears, therefore, that dilatation of the mitral anulus is a rare cause of mitral regurgitation and that abnormality of the fibrous skeleton of the heart is necessary for the mitral anulus to dilate enough to cause mitral regurgitation.
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.
A comparative anatomical study of the mitral ring and the 2 major mitral cusps of 12 adult mammals, including man, has been made. Two 25 mm thick sections of 2 adult human thoraces were cut to show the position and orientation of the adult mitral valve as it lies in the chest of the cadaver. Thin sections of hearts and valves were prepared so that the structure and basal attachments of the cusps could be examined microscopically. In most human hearts there is no distinctive, well-defined fibrous thickening or ring at the basal attachment of the aortic (anterior) mitral cusp; the mitral 'ring' is therefore considered to be usually incomplete anteriorly. This is consistent with the findings in the hearts of all other mammals examined. The posterior part of the ring is interposed between the myocardium of left atrium and left ventricle and corresponds to the region of the attachment of the mural (posterior) cusp of the mitral valve. In most mammals, including man, this part of the ring is a well-defined band of collagen: in a few mammals, including the sheep, the ring is represented by a thin lamina of loose collagen. The relation of the free wall of the left ventricle to the posterior part of the ring is of functional significance as it is the ventricular myocardium that is responsible for the major changes in the circumference of the ring occurring posteriorly during the cardiac cycle. In the ruminant ungulates, the sheep and ox, the aortic (anterior) mitral cusp has an attachment that is common to it and the related cusps of the aortic valve. Each cusp has two zones whose structure is an expression of their function. There is in each cusp a distal 'appositional' zone whose substance is formed of a loose meshwork of collagen fibres. In the fresh heart it is soft to touch and comes into apposition with a corresponding zone on the opposing cusp during closure of the valve. The proximal part of the cusp is called the 'free' zone which does not come into contact with the opposing cusp. The characteristic feature of the free zone is the presence of a stratum of denser collagen, the lamina fibrosa. The denseness of the collagen in the lamina varies considerably in different animals. In some mammals, including man, there is usually a ridge of demarcation between the appositional and free zones; this, when present, represents the 'line of closure' of the valve. The amount of left atrial muscle in the mitral valve cusps varies considerably in different mammals. Because of the great variation in the structure, attachments, relative size, and mobility of the 2 major mitral cusps in different animals, it is considered that there are basic differences in the mitral valves of different mammals.
A new, totally flexible ring for atrioventricular annuloplasty is described. The technique for its insertion closely follows the principles of Carpentier's selective annulus reconstruction [4]. Ninety-nine such rings have been inserted (47 in the mitral and 52 in the triscuspid position); 45 valves were simultaneously replaced. There were 6 (4 hospital and 2 late) deaths. The thromboembolic incidence was 4.8%. No instances of dehiscence or late ring deterioration have been detected. Thirty-four patients have been recatheterized, 19 of them with mitral rings. The mitral gradients and angiographic findings show the correct functioning of the implanted ring. It is concluded that use of this flexible ring, which adapts to the continuous changes of the normal mitral annulus, produces a more physiological type of valve operation.
To confirm or deny the thesis that mitral anular dilatation is a cause of mitral regurgitation, this anulus was measured in 102 patients, 24 of whom had normal hearts and 78 of whom had dilated left ventricles, some associated with mitral regurgitation, others not. The circumference of the mitral anulus in the 24 patients with normal hearts averaged 9 cm (range 7 to 11 cm); in 24 patients with idiopathic cardiomyopathy of the ventricular dilated type, both with (12 patients) and without (12 patients) mild to moderate regurgitation, 11 cm (range 10 to 14 cm); and in 31 patients with severe mitral regurgitation, 12 cm (range 8 to 18 cm). Among the latter 31 patients with severe mitral regurgitation, the anulus was only mildly dilated in the 15 with rheumatic disease (average 11 cm) and in the six with ruptured chordae tendinease on previously normal valves (average 10 cm); in contrast, in the 10 patients with floppy mitral valves with or without the Marfan syndrome the mitral anulus was greatly dilated (average 15.5 cm). Thus, only in patients with floppy valves with or without the Marfan syndrome or both does anular dilatation by itself appear great enough to cause mitral regurgitation. It appears, therefore, that dilatation of the mitral anulus is a rare cause of mitral regurgitation and that abnormality of the fibrous skeleton of the heart is necessary for the mitral anulus to dilate enough to cause mitral regurgitation.
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.
Since the introduction of the annuloplasty ring, many attempts have been made to obtain a flexible ring that preserves the physiological motion of the mitral annulus. We experimented with a new technique using autologous pericardium to construct a more flexible ring. Twenty patients underwent mitral valve repair for degenerative disease and were treated by a posterior pericardial annuloplasty and the usual valvuloplasty procedures. A long strip of pericardium was prepared, marked with metal clips and rolled up in a tubular fashion with the serosal surface on the outside. The pericardial tube was apposed on the posterior annulus just beyond the commissures. No patient required early or late reoperation. Doppler analysis showed good valve function: 18 patients had no or mild, and 2 had moderate regurgitation. Transmitral flow indexes were nearly normal (MVA = 3.7 +/- 0.4 cm2; flow velocity peak = 1.06 +/- 0.2 m/s). Fluoroscopic examination was employed for assessing annular motion using the metal clips as radiopaque markers. Planimetry of the hemiarea showed a mild narrowing (mean 8.5% +/- 6.4%) of annular size during ventricular systole. There was a trend toward a systolic reduction of the anteroposterior diameter of the annulus. These findings demonstrate that the mitral orifice preserves its flexible properties after this type of annuloplasty. Posterior pericardial annuloplasty seems to be a physiological correction of annular dilatation in patients with degenerative disease.
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.
To assess the role of dilatation of the mitral valve ring in the genesis of mitral regurgitation in patients with dilated left ventricles, cross-sectional echocardiography (CE) was performed on 23 normal subjects (group 1), 11 patients with congestive cardiomyopathy who had mitral regurgitation (group 2), and 11 patients with congestive cardiomyopathy and no mitral regurgitation (group 3). By performing CE in the long axis, the maximum antero-posterior diameter of MVR in diastole (Dd), the smallest diameter in systole (Ds), and left ventricular end-diastolic dimension (LVED) were measured. Percentage of shortening of MVR in systole (delta D%) and ratio Dd/LVED were calculated. The LVED, Dd, and Ds were significantly higher than normal in Group 2 and Group 3 patients, while delta D% and Dd/LVED were significantly lower. Dd was within normal limits in eight patients in Groups 2 and 3, four of whom had mitral regurgitation. We conclude that dilatation of the mitral annulus occurs only in some patients with dilated cardiomyopathy, and it does not occur in proportion with the degree of dilatation of the left ventricle. Mitral regurgitation, which occurs in association with left ventricular dilatation, may be due to a mechanism independent of mitral ring dilatation, such as loss of sphincteric action of the annulus or malalignment of the papillary muscles.
The mitral valve has a nonplanar shape and a sphincter action. Pathologic dilatation occurs along the posterior annulus. To preserve the physiologic function and correct annular dilatation, we developed an annuloplasty system that is universally flexible and produces a measured plication of the posterior annulus (Cosgrove-Edwards Annuloplasty System).
The results of 150 consecutive mitral valve repairs using this system were analyzed. Mean age was 58 +/- 13 years; 59% were men. The cause of the valve disease was degenerative in 75% of the patients, rheumatic in 13%, ischemic in 8%, and infectious in 4%. Associated procedures were performed in 61 patients (41%).
Echocardiographic mitral regurgitation decreased from 3.7 +/- 0.6 before repair to 0.2 +/- 0.4 after repair (p < 0.0001). There were no hospital deaths and no cases of hemodynamically significant systolic anterior motion or other annuloplasty-related complications. Follow-up was 100% complete at a mean of 3.1 +/- 3.6 months. There were three late deaths, three transient ischemic attacks, and one episode of endocarditis. Five patients (3.3%) have undergone reoperation for recurrent mitral insufficiency; no reoperations were related to the annuloplasty system. At a mean of 9 months, three-dimensional reconstruction of the mitral annulus from multiple echocardiographic images confirmed the nonplanar shape and sphincter mechanism of the annulus. Annular orifice area decreased 19% during the cardiac cycle from a mean of 10.3 cm2 in diastole to 8.6 cm2 in systole.
This annuloplasty system is effective for repair of insufficiency secondary to all causes, preserves physiologic annulus function, and is associated with a low incidence of valve-related complication.
One hundred and twenty-nine patients underwent posterior mitral annuloplasty with a Gore-Tex tube for mitral regurgitation between January 1982 and June 1991. The hospital mortality was 1.5% (CL = 0.5%-2.5%). The overall survival of hospital survivors was 96.5% +/- 2.7% at five and 86.2% +/- 7.6% at nine years, freedom from cardiac death was 99.1% +/- 0.9% and 95.2% +/- 3.9%, respectively. The actuarial freedom from embolism was 96.1% +/- 2.3% at five and 88.5% +/- 5.5% at nine years. The freedom from endocarditis (one patient) was 100% and 92.6 +/- 7.1%, respectively. Reoperation was necessary in six cases between one and 72 months after the operation (mean 38.5 +/- 30.5 months). The etiology of the valvular insufficiency was rheumatic in all reoperated cases. The freedom from reoperation was 94.1% +/- 3.2% at five and 87.2% +/- 5.6% at nine years. There was no mortality at reoperation. Of the 117 patients alive at the end of follow up and not requiring reintervention, 113 (96.6%) showed good functional improvement and were in NYHA functional class I or II. We conclude that both the immediate and long-term results of reconstructive surgery using the technique of inserting a half-ring on the posterior mitral annulus compare favorably with those obtained using other annuloplasty methods.
Although the ideal technique is still controversial, mitral valve reconstruction for mitral insufficiency usually includes an annuloplasty. From August 1985 to June 1993, 126 cases of pure, acquired mitral insufficiency were repaired by means of a posterior annuloplasty. Whatever the etiology, all types of mitral insufficiency allowing a mitral reconstruction were included. The annuloplasty, performed with a flexible linear reducer, was associated with valvular (62%) and subvalvular (11%) repairs. An associated surgical procedure was necessary in 62% of the patients. Operative mortality was 2.4%, and follow-up (mean 29 months) was complete for all survivors. Five-year survival was 90%. Five-year complication-free rate for emboli was 91%. Only one patient at 12 months underwent reoperation to treat recurrent mitral insufficiency. Ninety-seven patients were in New York Heart Association Class I or II. Follow-up echocardiographic studies on 75% of eligible patients showed a free rate for significant regurgitation of 99%. Mean valve area was estimated at 2.88 +/- 0.85 cm2. These findings suggest that the flexible linear reducer seems to be a reliable device and a valid alternative for annuloplasty.
This clinical study was undertaken to evaluate the Duran flexible ring and the Carpentier rigid ring in terms of mitral annulus motion, transmitral flow and left ventricular function. Twenty-six patients (11 receiving rigid rings and 15, flexible rings) with normal sinus rhythm and with no or only trivial mitral valve regurgitation after surgical repair were selected. Angiograms demonstrated no significant differences in left ventricular systolic function between the two groups of patients. The area of the mitral annulus with the flexible ring significantly changed during the cardiac cycle. There were significant differences in the left ventricular fractional shortening (rigid ring, 35.8%; flexible ring, 43.4%) and in the peak velocity (rigid ring, 222 cm/s; flexible ring, 186 cm/s) at peak exercise. These data suggest that the flexible ring interferes less with the normal movements of the mitral annulus during the cardiac cycle, and that, under exercise conditions, it performs better than the rigid ring. We therefore conclude that mitral valve reconstruction using the Duran flexible ring is advantageous in patients with mitral regurgitation due to degenerative disease and sinus rhythm.
The purpose of this study was to document the various causes of dilated cardiomyopathy in a large group of adult patients with congestive heart failure.
Previous reports of the causes of dilated cardiomyopathy have usually been case reports of a single specific etiology or review articles. The frequency of any single specific heart muscle disease is largely unknown.
We evaluated 673 patients referred for congestive heart failure due to dilated cardiomyopathy. The evaluation included medical history, physical examination, routine blood chemistry and hematologic measurements, electrocardiography and echocardiography. Thyroid function tests, antinuclear antibody tests and urinary vanillylmandelic acid and metanephrine levels were also obtained. Endomyocardial biopsy with right heart catheterization was performed in every patient. Coronary arteriography was performed in patients who had at least two standard cardiovascular risk factors or a history suggestive of myocardial ischemia. The cases were retrospectively reviewed, and a final cause for dilated cardiomyopathy was listed for each patient.
The most common causes of dilated cardiomyopathy were idiopathic origin (47%), idiopathic myocarditis (12%) and coronary artery disease (11%). The other identifiable causes of dilated cardiomyopathy made up 31% of the total cases.
Idiopathic dilated cardiomyopathy is a common cause of congestive heart failure. Specific heart muscle diseases occur with much less frequency.
A static morphometric study of the outflow chamber of the left ventricle (OCLV) was investigated in a series of 10 formalin-fixed hearts. A spatial reconstruction of the shape and the volume of the OCLV was carried out by means of a Somaton Plus TR4 Tomodensitometer (Siemens). The technic allows evaluation of the surface of the aortic and the mitral orifices and visualization of the three-dimensional OCLV and LV morphology, as well as calculation of their volumes. The limits of the technic in the dynamic study of the OCLV are presented.
This study was undertaken to clarify the mechanisms of mitral regurgitation (MR) in dilated hearts.
In all, 68 patients with dilated heart and MR, including 26 patients with dilated cardiomyopathy (DCM), 24 with prior anterior myocardial infarction (A-MI), and 18 with prior posteroinferior myocardial infarction (I-MI), as well as 25 normal subjects were examined by transesophageal two-dimensional and color Doppler echocardiography.
The maximum area of the MR signal in the DCM group correlated positively with the anteroposterior diameter of the mitral annulus at late systole. Although the coaptation edge length of the anterior and posterior mitral leaflets appeared shorter in dilated hearts than in the hearts of controls, a significant difference did not exist. The length of the coaptation edge correlated negatively with the maximum area of the MR signal in all dilated hearts, and characteristic systolic displacement of the coaptation point of both mitral leaflets occurred. The MI groups demonstrated anterior and posterior displacement in the direction of the short axis of the left ventricle in the A-MI and I-MI groups, respectively. However, the DCM group demonstrated inferior displacement toward the long axis of the left ventricle; its magnitude correlated positively with the maximum area of the MR signal.
A major cause of MR in dilated hearts is mitral malcoaptation due to displacement of the coaptation point of the mitral leaflets along the long or short axis of the left ventricle. This is caused by left ventricular enlargement and/or asynergy of the left ventricular wall, rather than by a decrease in mitral coaptation edge length due to mitral annular dilation.
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.
Severe mitral regurgitation is a frequent complication of end-stage cardiomyopathy that contributes to heart failure and predicts a poor survival. We studied the intermediate-term outcome of mitral reconstruction in 48 patients who had cardiomyopathy with severe mitral regurgitation and were operated on between June 1993 and June 1997.
Ages ranged from 33 to 79 years (63 +/- 6 years) with left ventricular ejection fractions of 8% to 25% (16% +/- 3%). All patients were receiving maximal drug therapy and were in New York Heart Association class III-IV with severe, refractory 4+ mitral regurgitation. Operatively, all 48 had undersized flexible annuloplasty rings inserted, 7 had coronary bypass grafts for incidental disease, 11 had prior bypass grafts, and 11 also had tricuspid valve repair.
One operative death occurred as a result of right ventricular failure. Postoperative transesophageal echocardiography revealed mild mitral regurgitation in 7 patients and no mitral regurgitation in 41. There were 10 late deaths, 2 to 47 months after mitral reconstruction. The 1- and 2-year actuarial survivals have been 82% and 71%. At a mean follow-up of 22 months, the number of hospitalizations for heart failure has decreased, and 1 patient has had heart transplantation. Significantly, New York Heart Association class improved from 3.9 +/- 0.3 before the operation to 2.0 +/- 0.6 after the operation. Twenty-four months after the operation, left ventricular volume and sphericity have decreased, whereas ejection fraction and cardiac output have increased.
Whether this favorable modification of left ventricular function and geometry will persist remains unknown. However, mitral repair for cardiomyopathy with mitral regurgitation allows new strategies for these patients.
The application of the flexible Duran mitral annuloplasty ring in the treatment of various mitral valvular diseases is a physiologically appealing method of surgical repair. However, accurate identification of the trigonal structures, which is crucial in selecting the proper ring size, cannot always be made with certainty. A method is proposed to calculate the intertrigonal distance (ITD) from the aortic diameter.
Using digital calipers, the linear intertrigonal distance was measured in human homograft (n = 10) and sheep (n = 10) aortic root specimens. The aortic diameter was obtained from the circumference of the pressurized aortic root. A conversion factor was acquired for each specimen by dividing the aortic diameter with the measured ITD. A single constant conversion factor, which closely approximated the mean of the conversion factors in both groups, was then applied broadly to derive the ITD by calculation from the aortic diameter, which is known. The validity of using this constant conversion factor was tested by comparing the degree of variation of the calculated ITD from the direct measurements of the ITD.
The mean of the conversion factors was 0.79 and 0.80 in the human and the sheep roots, respectively. The value 0.80 was used as the constant conversion factor in both groups for calculating the ITD. A paired comparison t-test in each group showed the difference between the calculated intertrigonal distance and the direct measurements of the ITD to be insignificant, validating the use of 0.80 as a constant conversion factor.
The results of the study suggest that the conversion factor of 0.80 can be reliably used to obtain a calculated value of the intertrigonal distance; this method has the potential to aid the surgeon in determining the intertrigonal distance and the proper ring size.
Mitral annulus dilatation has been identified as an important factor in functional mitral regurgitation (FMR). However, the pathophysiologic interaction of annular dilatation and papillary muscle (PM) displacement in FMR, which occurs clinically in left ventricular (LV) dilatation, is still not well understood. It is difficult to separate these competing factors in vivo, leading to confusion in identifying the real role of the annular dilatation in FMR and its interaction with PM displacement.
To better understand the competing factors, an in vitro model was developed with a D-shaped adjustable mitral annulus that could be changed from 5.5 cm2 to 13.0 cm2 during experiments, independent of varying PM positions. Six excised normal porcine mitral valves were mounted in a left ventricular model with the adjustable annulus device and tested in a physiologic pulsatile flow system under normal cardiac output and left ventricular pressure (5.0 l/min, 120 mmHg). Papillary muscles were placed in normal and then displaced to an apical posterolateral position, to simulate pathological conditions seen clinically. Regurgitation was measured directly by a flow probe and the mitral valve geometry and leaflet coaptation were recorded by video camera through the model's atrium window. In addition, 2D echocardiography was used to evaluate leaflet coaptation and color Doppler flow mapping to detect the regurgitant flow field.
The results showed that in normal PM position, the mitral regurgitant was consistently at low level until the annulus was enlarged to 1.75 times the normal size, at which time it increased sharply. Papillary muscle apical posterolateral displacement, which simulates a dilated LV, caused regurgitation to occur earlier (1.5 times the normal annulus size), and had an increased regurgitant volume (p < 0.05). The leaflet gaps were first observed at the commissural areas of the valves, consistent with the location of regurgitant jets detected by color Doppler flow mapping. Asymmetric PM displacement created more regurgitation than both the symmetric PM tethering (p = 0.063) and normal PM position (p < 0.01). The regurgitant jets were observed at the same commissural side as the PM displacement, even without significant enlargement of the annulus.
This in vitro study provides insight into the interaction between annular dilatation and PM displacement on FMR. The resulting effects and their overall similarity to clinical observation could help further understand the mechanism of FMR and provide additional information to improve future therapeutic strategies.
Functional mitral regurgitation is frequently observed in the setting of left ventricular dyfunction. This finding is a marker of poor outcome in patients with either ischemic or dilated cardiomyopathy. The mechanism accounting for this phenomenon is an altered balance of tethering versus coapting forces acting on the mitral valves in the failing heart. Tethering forces represent an anomalous tension on the mitral valves due to displacement of mitral valve attachments secondary to increased left ventricular chamber sphericity associated with systolic ventricular dysfunction. On the other hand, coapting forces are weak and unable to counteract the abnormal tension acting on the mitral valve, which restricts closure and leads to regurgitation. Vasodilators and inotropic drugs are effective in the management of functional mitral regurgitation. Although partial left ventriculectomy or Batista's procedure is still investigational, this new technique seems to provide an optimal control of functional mitral regurgitation and improve functional capacity and survival of some patients with heart failure.
Mitral annuloplasty with a flexible linear reducer Posterior pericardial annuloplasty: a physiological correction
- L Camilleri
- M Filaire
- A Repossini
- B Legault
- V Eder
- Fleury
- Jp
Camilleri L, Filaire M, Repossini A, Legault B, Eder V, Fleury JP, et al. Mitral annuloplasty with a flexible linear reducer. J Card Surg. 1995;10:99-103. 21. Salati M, Scrofani R, Santoli C. Posterior pericardial annuloplasty: a physiological correction? Eur J Cardiothorac Surg.
Remodelamento ventricular esquerdo em cardiomiopatias de diferentes etiologias na sua forma dilatada: estudo morfológico comparativo em peças anatômicas [dissertation]
- Simão Filho
Simão Filho C. Remodelamento ventricular esquerdo em cardiomiopatias de diferentes etiologias na sua forma dilatada: estudo morfológico comparativo em peças anatômicas [dissertation]. São Paulo: Medical School, São Paulo Univ.; 1998.
- Dm Braile
- Rv Ardito
- Gh Pinto
- Jl Santos
- M Zaiantchick
- Dr Souza
Braile DM, Ardito RV, Pinto GH, Santos JL, Zaiantchick M, Souza
DR. Plástica mitral. Rev Bras Circ Cardiovasc. 1990;5:86-98.
La valvuloplastie reconstitutive: une douvelle technique de valvuloplastie mitrale
- Carpentier
Integrated mechanism for functional mitral regurgitation: leaflet restriction versus coapting force: in vitro studies
- He