Systolic Papillary Muscle Dyssynchrony Predicts Recurrence of Mitral Regurgitation in Patients with Ischemic Cardiomyopathy (ICM) Undergoing Mitral Valve Repair

Objective: We investigated the impact of papillary muscle dyssynchrony (DYS‐PAP) in predicting recurrent mitral regurgitation (MR) in patients with ischemic cardiomyopathy (ICM) undergoing undersized mitral ring annuloplasty (UMRA). Methods: One hundred forty‐four ICM patients (left ventricular ejection fraction <35%) in sinus rhythm undergoing UMRA between January 2001 and December 2010 at three Institutions (University Hospital, Maastricht, The Netherlands; Careggi Hospital, Florence, Italy; Civic Hospital, Brescia, Italy) were recruited. The primary endpoint was the recurrence of MR at the latest echocardiographic study defined as insufficiency ≥2+ in patients with no/trivial MR at discharge. The assessment of DYS‐PAP was performed by applying two‐dimensional (2D) speckle‐tracking imaging. Results: In patients with MR recurrence, DYS‐PAP significantly worsened (84.1 ± 8.8 msec vs.65.4 ± 8.8 msec at baseline, P < 0.001) whereas in patients with no MR recurrence, DYS‐PAP did not vary (22.3 ± 5.3 msec vs. 25.9 ± 7.2 msec at baseline, P = 0.8). Recurrent MR was positively correlated with preoperative DYS‐PAP (P < 0.001), baseline anterior mitral leaflet tethering angle α (P < 0.001) and tethering symmetry index α/β before surgery (P < 0.001). There was no significant correlation between MR recurrence and other echocardiographic parameters. Logistic regression analysis revealed that baseline values of DYS‐PAP (OR: 5.4 [95% CI: 3.1–7.7], P < 0.001), α (OR: 5.0 [2.6–6.7], P < 0.001), and α/β (OR: 3.9 [2.5–5.7], p < 0.001) were predictors of recurrent MR. A DYS‐PAP value ≥ 58 msec predicted recurrence of MR with 100% sensitivity and 83% specificity (area under the curve [AUC]: 0.92 [0.7–1], P < 0.001). Conclusions: A DYS‐PAP cutoff value of 58 msec is useful to identify patients in whom UMRA is likely to fail. That way decision making in ischemic functional MR might be facilitated.     

二尖瓣替换术保留瓣下结构对维护术后早期左心室几何形态的重要性

目的 比较、分析33例慢性二尖瓣返流病例分别行传统的二尖瓣替换术(MVR)(组1,n=11例)、保留后叶腱索的MVR(组2,n=11例)和保留前、后叶腱索的MVR(组3,n=11例)术后早期左心室几何形态的变化.方法应用超声心动技术测量术前、术后10天左心房内径(LAD),左心室短轴舒张末、收缩末内径(LVEDD,LVESD)和左心室长轴舒张末、收缩末纵径(LVEDL,LVESL)的变化.结果 术前三组间无显著性差异.术后三组LAD均较术前明显缩小(分别为P<0.01,P<0.01和P<0.05),三组间无显著性差异.三组LVEDD均明显回缩(分别为P<0.01,P<0.01和P<0.05);LVESD也缩小,但仅组3与术前比较呈显著性差异(P<0.05)组1 LVEDL和LVESL均明显增加(P<0.05);组2无明显改变;组3明显缩短(分别为P<0.05和<0.01),且与组1比较呈显著性差异(P<0.05).结论 保留瓣下结构的MVR(P-MVR)矫治慢性二尖瓣返流对术后早期左心室几何形态具有维护作用,尤其体现在防止左心室长轴的纵向扩张.MVR时保留前、后叶腱索对左心室几何形态的维护更为完善,在防止左心室长轴纵向扩张的同时,促进左心室长、短轴的缩短.     

Functional Ischemic Mitral Regurgitation in Anterior Ventricular Remodeling: Results of Surgical Ventricular Restoration with and Without Mitral Repair

Ischemic functional mitral regurgitation following ischemic cardiomyopathy is a secondary phenomenon to ventricular dilation, and therapeutic approaches to this complication are not uniform. Solutions to improve mitral function include either mitral repair or observing the effects of coronary revascularization and/or ventricular rebuilding during surgical ventricular restoration (SVR).The present study of 108 patients (comprising 18% of our 588 SVR population) reports the effects of mitral repair following SVR and CABG by comparing geometric, functional, hemodynamic and outcome changes to SVR patients without mitral repair. The degree of mitral regurgitation went from 2.9 ± 1.2 before to 0.7 ± 0.7 after SVR and mitral repair. SVR improved EF from 29 ± 7% to 34 ± 10% p 0.001; reduced end diastolic volume from 243 ± 74 to 163 ± 53 ml and end systolic volume from 170 ± 63 to 107 ± 41 ml, p 0.000. Ventricular size and shape geometric measurements improved in all patients, either with and without mitral repair. SVR improved tenting and papillary muscle width between muscle heads in all patients, but alterations in mitral annular size improved only following mitral repair.Preoperative mitral regurgitation occurred in patients with larger ventricular volume and lower ejection fraction and was an independent predictor of operative mortality risk.     

Worsening of Left Ventricular End-Systolic Volume and Mitral Regurgitation without Increase in Left Ventricular Dyssynchrony on Acute Interruption of Cardiac Resynchronization Therapy

Background: Responders to cardiac resynchronization therapy (CRT) have greater left ventricular (LV) dyssynchrony than nonresponders prior to CRT. Aim: We conducted this study to see whether the long term responders have more worsening of LV dyssynchrony and LV function on acute interruption of CRT. Materials and Methods: We identified 22 responders and 13 nonresponders who received CRT as per standard criteria for 23.73 ± 7.9 months (median 24.5 months). We assessed the acute change in LV function, mitral regurgitation (MR) and compared LV dyssynchrony in CRT on and off modes. Results: On turning off CRT, there was no significant worsening of LV dyssynchrony in both responders and nonresponders. The dyssynchrony measurements by SPWMD, TDI and 3D echocardiography did not correlate significantly. LVESV increased (p = 0.02) and MR (p = 0.01) worsened in CRT-off mode in responders only without significant change in LVEF or LV dimensions. Discussion and Conclusion: In long-term responders to CRT, there is alteration in the function of remodeled LV with acute interruption of CRT, without significant worsening of LV dyssynchrony. The role of different echocardiographic parameters in the assessment of LV dyssynchrony remains controversial. Even after long-term CRT reversely remodels the LV, the therapy needs to be continued uninterrupted for sustained benefits.     

Ruptured Mitral Valve Aneurysm: An Uncommon Cause of Acute Dyspnoea

The mitral valve aneurysm is a rare disease that is usually induced by infective endocarditis. While the mechanism of the development of this lesion is unclear, complications such as perforation can occur and lead to significant mitral regurgitation. We describe a patient presented with ruptured aneurysm of anterior mitral leaflet resulting in acute severe mitral regurgitation that was confirmed by transthoracic and transesophageal echocardiography. Early detection and prompt intervention are important to prevent the complications of valvular aneurysms, which include rupture, embolism, and endocarditis. This report emphasizes the role of echocardiography in evaluating the mitral valve aneurysms and its complications. (Echocardiography 2010;27:E119‐E121)     

Role of Papillary Muscle Dysfunction in the Pathogenesis of Mitral Regurgitation in Myocardial Infarction:

To elucidate the pathogenesis of mitral regurgitation (MR) after myocardial infarction (MI), the incidence of papillary muscle dysfunction (PMD), mitral annular size, and the extent of wall-motion abnormalities were examined in 81 patients with previous MI by two-dimensional echocardiography and real-time two-dimensional Doppler flow imaging. The prevalence of pathological MR was lower in patients with anterior MI (36%) than in those with inferior (65%) or anterior and inferior MI (88%) (P < 0.01 vs anterior MI group). The incidence of PMD in patients with MR in the anterior MI group (15%) was lower than that in the inferior (50%, P < 0.01) or anterior and inferior MI group (43%, P < 0.05). The mitral annular dimension in patients with MR was significantly greater than in those without MR, but it was similar among the three groups. The extent of wall-motion abnormality correlated significantly with the area of MR jet in the anterior MI group (y = 3.1x + 15.5, r = 0.52, P < 0.01) and in the inferior MI group (y = 8.3x + 32.7, r = 0.57, P < 0.01). However, the slope of this relationship was significantly steeper in the inferior MI group than in the anterior MI group (P < 0.05). These results indicated that the degree of MR with inferior MI was greater than with anterior MI for a given MI area. PMD may play an important role in the higher prevalence and greater degree of MR in inferior MI.     

Left Ventricular Shape Deformation and Mitral Valve Prolapse in Chronic Pulmonary Hypertension

Mitral valve prolapse (MVP) has been described in patients with right ventricular pressure or volume overload. The frequency of this phenomenon and its relationship to left ventricular shape and mitral valve annulus size, as well as its reversibility in chronic pulmonary hypertension, are poorly understood. We have observed an increased frequency of MVP in a patient population with chronic thromboembolic pulmonary hypertension that often resolves after thromboendarterectomy and reduction of pulmonary hypertension. To further evaluate the relationship between MVP and left ventricular shape in pulmonary hypertension, we studied 51 consecutive patients undergoing surgery for thromboembolic pulmonary hypertension. Echocardiographic features including interventricular septal position, as measured by an eccentricity index, left ventricular size, and several mitral valve annulus dimensions were evaluated prior to surgery and during the postoperative hospitalization period. The pulmonary artery systolic pressure was elevated for all patients prior to surgery, 87 ± 21 mmHg (mean ± SD). Twelve patients (23.5%) had MVP before surgery, which resolved in ten patients postoperatively. In addition, one patient whose pulmonary hypertension improved little, developed MVP postoperatively. Those patients with MVP had a greater pulmonary artery pressure preoperatively than those without MVP (102 ±19 vs 84 ±21 mmHg). The eccentricity index for those patients with MVP (1.68±0.2) was greater than for those with no MVP (1.53 ± 0.37). No significant differences were noted between groups with MVP and without MVP according to all mitral annulus dimensions or left ventricular chamber areas. Postoperatively, eccentricity index decreased significantly in both those with MVP and without MVP (1.29 ± 0.18 and 1.20 ± 0.15, respectively) as did pulmonary artery systolic pressure (67± 22 and 47 ± 13 mmHg, respectively). Mitral valve prolapse in chronic pulmonary hypertension occurs frequently and is noted particularly in those patients with the most severe pulmonary hypertension. It appears that deformation of the left ventricle is associated with echocardiographic MVP and that reduction of pulmonary hypertension reverses this deformation and allows for resolution of MVP.     

Mitral Valve Adaptation to Isolated Annular Dilation: Insights Into the Mechanism of Atrial Functional Mitral Regurgitation

Objectives

This study hypothesized that compensatory mitral leaflet area (MLA) adaptation occurs in patients with persistent atrial fibrillation (AF) without left ventricular (LV) dysfunction but has limitations that augment mitral regurgitation (MR). The study also explored whether asymmetrical annular dilation is matched by relative leaflet enlargement.

Temporal Changes in Interpapillary Muscle Dynamics as an Active Indicator of Mitral Valve and Left Ventricular Interaction in Ischemic Mitral Regurgitation

Background

Regional subpapillary myocardial hypokinesis may impair lateral reduction in the interpapillary muscle distance (IPMD) from diastole to systole, and adversely affect mitral valve geometry and tethering.

Objectives

The goal of this study was to investigate the impact of impaired lateral shortening in the interpapillary muscle distance on mitral valve geometry and function in ischemic heart disease.

Methods

To quantify ventricular size/shape, regional myocardial contraction, lateral shortening of the IPMD, mitral valve geometry, and severity of mitral regurgitation, 67 patients with ischemic heart disease underwent cardiac magnetic resonance imaging, and a correlation analysis of measured parameters was performed. The impact of reduced IPMD shortening on mitral valve (dys)function was confirmed in swine and in a physiological computational mitral valve model.

Results

Lateral shortening of the IPMD from diastole to systole was severely reduced in patients with moderate/severe ischemic mitral regurgitation (9.6 ± 2.8 mm), but preserved in mild IMR (11.5 ± 3.4 mm). Left ventricular size and ejection fraction did not differ between the groups. In swine with subpapillary infarction and impaired IPMD, mitral regurgitation was evident within 1 week, compared to those pigs with a nonpapillary infarction and preserved IPMD. In the controlled computational valve model, IPMD had the maximal impact on regurgitation, and was exacerbated with additional annular dilation.

Conclusions

By using cardiac magnetic resonance imaging in humans, we demonstrated that it is the impairment of lateral shortening between the papillary muscles, and not passive ventricular size, that governs the severity of mitral regurgitation. Loss of lateral shortening of IPMD tethers the leaflet edges and impairs their systolic closure, resulting in mitral regurgitation, even in small ventricles. Understanding the lateral dynamics of ventricular-valve interactions could aid the development of new repair techniques for ischemic mitral regurgitation.