Development Of Severe Mitral Regurgitation Research Articles

Mitral Valve Aneurysm in Mitral Valve Endocarditis: A Case Report

Mitral valve aneurysm (MVA) is an ominous complication of infective endocarditis (IE), with worse outcomes seen among patients with preexisting valvular disease or intravenous drug use. Valve aneurysms can perforate or lead to rupture of the chordae tendineae, with the consequent development of severe mitral regurgitation and acute pulmonary edema. We present a case of a 54-year-old woman with hypertension, obesity, diabetes mellitus, hyperlipidemia, chronic obstructive pulmonary disease, peptic ulcer disease, obstructive sleep apnea, gastroesophageal reflux disease, intravenous drug abuse and bipolar disorder who developed MVA one month after being discharged for IE. Decline in the clinical status of patients with IE is a troubling sign that may indicate an IE complication such as MVA. Physicians should diligently monitor patients with IE for changes in signs and symptoms, as early recognition and surgical intervention are key to prevent further morbidity and mortality.

LARGE VENTRICULAR SEPTAL DEFECT CAUSED BY AN ACUTE INFERIOR ST ELEVATION MYOCARDIAL INFARCTION

SESSION TITLE: Monday Abstract Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Septal rupture is an uncommon, but fatal, complication of myocardial infarction (MI) which usually occurs 3-5 days after an acute MI, however, in rare instances it may develop within the first 24 hours or as late as 2 weeks. It is associated with a tremendously high mortality rate (41-80%) which has been unchanged during the last few decades [1]. We hereby report one such rare instance when this complication occurred within 48 hours following MI. CASE PRESENTATION: A 59 year old male with a history of coronary artery disease status post percutaneous coronary intervention in 2011 presented to the emergency room with chest pain for 1 hour prior to admission. Initial electrocardiogram showed acute inferior ST elevation MI. Emergent cardiac catheterization showed occlusion of the right coronary artery and a drug eluting stent was placed. The patient was transferred to intensive care unit for close monitoring, however, 5 hours later he developed sudden increasing shortness of breath. Physical examination revealed a new systolic murmur and an echocardiogram was performed showing a large ventricular septal defect (VSD) (Image-1). Overnight he developed atrial fibrillation and became hemodynamically unstable with a systolic blood pressure in the 60's. He was then cardioverted without success and amiodarone was bolused followed by a continuous infusion. The decision was made for emergent coronary artery bypass grafting and repair of the VSD the next day. The defect was successfully closed with a Dacron patch after timely and prompt correction of atrial fibrillation. DISCUSSION: There are 3 life threatening complications of acute MI which include rupture of the left ventricular free wall, rupture of the interventricular septum and development of severe mitral regurgitation. One study compared 225 patients who had a first MI and experienced one of the mechanical complications to 1012 patients without complications to analyze the reason behind these complications. They reported that delayed hospitalization (>24hours), excessive in-hospital physical activity and recurrent ischemia as some of the risk factors for rupture [2]. Early retrospective studies noted lower mortality rates in patients undergoing surgical repair > 6 weeks after infarction than those who went in earlier, however these studies had selection bias as patients with normal ejection fraction and smaller defects survived to become low risk surgical candidates [3]. Hence, optimal approach varies with the clinical presentation. In patients like ours who develop cardiogenic shock, death is inevitable without urgent surgical intervention. CONCLUSIONS: This case is an unusual scenario where this fatal complication occurred within 48 hours following MI even after prompt revascularization. It is unique because it was further complicated with atrial fibrillation, which can further reduce survival probability, yet he survived and defied the odds. Reference #1: Saplaouras A1, Sakellaropoulou A1, Mililis P1, Bazoukis G1, Kolokathis AM1, Konstantinidou E1, Anagnostou A1, Panagopoulou N1, Vlachos K1, Lakoumentas I1, Sideris A1. Ventricular septal rupture following myocardial infarction: A potentially fatal complication. Clin Case Rep. 2019 Jan 9;7(2):397-400 Reference #2: Figueras J, Cortadellas J, Calvo F, Soler-Soler J. Relevance of delayed hospital admission on development of cardiac rupture during acute myocardial infarction: study in 225 patients with free wall, septal or papillary muscle rupture. J Am Coll Cardiol 1998; 32:135. Reference #3: Daggett WM, Guyton RA, Mundth ED, et al. Surgery for post-myocardial infarct ventricular septal defect. Ann Surg 1977; 186:260 DISCLOSURES: No relevant relationships by John Mikhail, source=Web Response No relevant relationships by Mohammed Shariff, source=Web Response

Safety and efficacy of percutaneous balloon mitral valvotomy in severe mitral stenosis with moderate mitral regurgitation – A prospective study

BackgroundPercutaneous balloon mitral valvotomy (PBMV) is generally considered as a contraindication in patients with mitral stenosis (MS) associated with moderate to severe mitral regurgitation (MR). We sought to compare the safety and efficacy of PBMV in patients with severe MS and with moderate MR with those with less than moderate or no MR. Materials and methodsSymptomatic patients of MS with mitral valve area ≤1.5cm2 were screened into two groups: Group I with moderate MR and Group II with less than moderate or no MR. Clinical and echocardiographic assessments were done at 24h, 1 month, and 6 months post-procedure. A treadmill testing was done prior to PBMV and at 6 months.Primary safety outcome was a composite of cardiovascular death and development of severe MR with or without requirement for mitral valve replacement at 30 days of procedure. Efficacy of the procedure was measured as improvement in functional class, treadmill time, and mitral valve area (MVA) at 6 months. ResultsSeventeen patients with moderate MR and 208 patients with less than moderate MR underwent PBMV. Primary outcome showed no significant difference [2 (11.7%) in Group I vs. 8 (3.85%) in Group II, p=0.36]; occurrence of severe MR was higher in Group I [RR=4.87, 95% C.I.=1.42–16.69]. In Group I patients, improvement in treadmill time was seen in 12 (70.59%), functional class in 13 (76.47%), and MVA in all patients. ConclusionIn patients having severe MS associated with moderate MR, PBMV may be a safe option and provides sustained symptomatic benefit.

Successful Surgical Management for Severe Mitral Regurgitation Unmasked After Pericardiectomy for Chronic Constrictive Pericarditis

A 78-year-old cachectic woman who previously had repair of atrial septal defect was admitted to the hospital for congestive heart failure. Cardiac workup revealed chronic constrictive pericarditis; no evidence of coronary or valvular disease was found. She underwent corrective surgery for pericardiectomy. Intraoperative transesophageal echocardiography after pericardiectomy demonstrated acute development of severe mitral regurgitation, which was not preoperatively observed. She eventually required mitral valve replacement and tricuspid valve repair after conservative management failed. She recovered from the operation and was discharged. We believe that this is the first report of successful surgical management of mitral regurgitation that developed acutely after pericardiectomy.

785 How to predict development of severe mitral regurgitation after percutaneous mitral commissurotomy?

785 How to predict development of severe mitral regurgitation after percutaneous mitral commissurotomy?

Echocardiographic Prediction of Severe Mitral Regurgitation after Percutaneous Mitral Valvuloplasty with the Inoue Balloon

Background and Objectives:This study was designed to predict the development of severe mitral regurgitation (MR) following percutaneous mitral valvuloplasty (PMV) in patients with a favorable morphology of the mitral valve (MV). Subjects and Methods:We prospectively examined 253 patients with severe mitral stenosis from 1997 to 2000. Echocardiographic evaluation of MV morphology was performed prior to PMV. We proposed commissural calcification, severe relative prolapse, and uneven thickening of MV as predictors of MR following PMV and defined the MR risk group as patients with any of these 3 features. The balloon size was expressed as the value of the effective balloon dilating area divided by the body surface area. The larger balloon group was defined as patients in whom balloon size>3.8 cm/m was selected for PMV. The development of severe MR was defined as the presence of MR≥3+ on echocardiography following PMV. Results:Severe MR developed in 14 (5.5%) patients. On multiple logistic regression analysis, the MR risk group (p 8 and MR risk group was 43%, 88% and 71%, 86% respectively. In the MR risk group, severe MR developed in 8 (53.3%) of 15 patients of the larger balloon group as compared with 2 (6.9%) of 29 patients of the smaller balloon group (p=0.001). Conclusion: Echocardiography can identify patients with a high risk of developing MR after PMV and the use of a smaller Inoue balloon may prevent severe MR in selected patients. (Korean Circulation J 2001;31(12):1311-1317)

Echocardiography can predict the development of severe mitral regurgitation after percutaneous mitral valvuloplasty by the inoue technique

Severe mitral regurgitation (MR) following mitral balloon valvuloplasty is a major complication of this procedure. We recently described a new echocardiographic score that can predict the development of severe MR following mitral valvuloplasty with the double balloon technique. The present study was designed to test the usefulness of this score for predicting severe MR in patients undergoing the procedure using the Inoue balloon technique. From 117 consecutive patients who underwent mitral valvuloplasty using the Inoue technique, 14 (11.9%) developed severe MR after the procedure. A good quality echocardiogram before mitral valvuloplasty was available in 11 patients. These 11 patients were matched by age, sex, mitral valve area, and degree of MR before valvuloplasty with 69 randomly selected patients who did not develop severe MR after Inoue valvuloplasty. The total MR-echocardiographic (MR-echo) score was significantly greater in the severe MR group (10.5 ± 1.4 vs 8.2 ± 1.1; p <0.001). In addition, the component grades for the anterior leaflet (2.9 ± 0.5 vs 2.2 ± 0.4; p <0.001), posterior leaflet (2.6 ± 0.7 vs 1.9 ± 0.8), commissures (2.4 ± 0.8 vs 2.0 ± 0.5; p <0.05) and subvalvular apparatus (2.6 ± 0.5 vs 1.9 ± 0.4; p <0.001) were also higher in the MR group. Using a total score of ≥10 as a cut-off point for predicting severe MR with the Inoue technique, a sensitivity of 82%, specificity of 91%, accuracy of 90%, and negative predictive value of 97% were obtained. Stepwise logistic regression analysis identified the MR-echo score as the only independent predictor for developing severe MR with the Inoue technique (p <0.0001). Thus, the MR-echo score can also predict the development of severe MR following mitral balloon valvuloplasty using the Inoue technique.

Echocardiography can predict which patients will develop severe mitral regurgitation after percutaneous mitral valvulotomy

Using two-dimensional echocardiography, we sought to identify features that are associated with severe mitral regurgitation after percutaneous mitral valvulotomy and combine them into a predictive score. Severe mitral regurgitation after percutaneous mitral valvulotomy is a major complication carrying an adverse prognosis that, to date, has not been predictable in advance. In a consecutive series of 566 patients who underwent percutaneous mitral valvulotomy, 37 (6.5%) developed severe mitral regurgitation (assessed by angiography) after the procedure, 31 of whom had an echocardiogram available before percutaneous mitral valvulotomy. These 31 patients were matched by age, gender, mitral valve area and degree of mitral regurgitation before valvulotomy with 31 randomly selected patients who did not develop severe mitral regurgitation after percutaneous mitral valvulotomy. An echocardiographic score was developed on the basis of the pathologic studies of valves of patients who developed severe regurgitation after percutaneous mitral valvulotomy (leaflet rupture of relatively thin portions of nonhomogeneously thickened leaflets in the presence of commissural and subvalvular calcification) and evaluated uneven distribution of thickness in the anterior and posterior mitral leaflets, degree of commissural disease and subvalvular disease involvement, with each component graded from 0 to 4 (total, 0 to 16). Intraobserver and interobserver variability for score assessment were 6% and 7%, respectively. The total mitral regurgitation echocardiographic score was significantly greater in the severe mitral regurgitation group (11.7 +/- 1.9 [mean +/- SD] vs. 8.0 +/- 1.2, p < 0.001). In addition, the component grades for the anterior leaflet (3.2 +/- 0.7 vs. 2.3 +/- 0.6, p < 0.001), commissures (2.6 +/- 0.7 vs. 1.6 +/- 0.6, p < 0.001) and subvalvular apparatus (3.2 +/- 0.6 vs. 2.3 +/- 0.7, p < 0.001) were also higher in the mitral regurgitation group. With a total score > or = 10 as a cutoff point for predicting severe mitral regurgitation after percutaneous mitral valvulotomy, a sensitivity of 90 +/- 5% and a specificity of 97 +/- 3% were obtained. Stepwise logistic regression analysis identified the mitral regurgitation echocardiographic score as the only independent predictor for developing severe mitral regurgitation after percutaneous mitral valvulotomy (p < 0.0001). This new mitral regurgitation echocardiographic score can predict the development of severe mitral regurgitation after percutaneous mitral valvulotomy and can be useful in the selection of patients for this technique.

Observations suggesting a high incidence of exercise-induced severe mitral regurgitation in patients with mild rheumatic mitral valve disease at rest

Objectives. The aim of this study was to determine the hemodynamic effects of upright bicycle ergometry in symptomatic patients with mild, mixed mitral stenosis and regurgitation.Background. Patients with seemingly mild rheumatic mitral valve disease often complain of exertional dyspnea or fatigue. These symptoms are usually ascribed to flow-dependent increases in the gradient across the stenotic mitral valve. Although catheterization studies in these patients may demonstrate an increase in mitral valve gradient proportional to an increase in cardiac output, this approach does not specifically address the underlying mechanism of any observed increases in mitral gradient or left atrial (i.e., pulmonary capillary wedge) pressure. Exercise echocardiography is uniquely suited to the dynamic assessment of exercise-induced hemodynamic changes.Methods. Fourteen symptomatic patients with exertional dyspnea and mild mitral stenosis and regurgitation at rest performed symptom-limited upright bicycle ergometry with quantitative two-dimensional, Doppler and color Doppler echocardiographic analysis.Results. Average pulmonary artery systolic pressure in the 13 patients with adequate spectral signals of tricuspid regurgitation increased from 36 ± 5 mm Hg (mean ± SD) at rest to 63 ± 14 mm Hg at peak exercise (p < 0.001). The mean transmitral pressure gradient in all patients increased from 4.5 ± 1.4 mm Hg at rest to 12.7 ± 2.7 mm Hg at peak exercise (p < 0.001). Five patients developed severe mitral regurgitation during exercise.Conclusions. Patients with exertional dyspnea and mild mitral stenosis and regurgitation at rest demonstrate a marked increase in pulmonary artery systolic pressure and mean transmitral pressure gradient during dynamic exercise. In a subset of these patients, marked worsening of mitral regurgitation appears to be the underlying mechanism of this hemodynamic deterioration. Because of the small sample size, this novel observation must be considered preliminary with respect to the true prevalence of exercise-related development of severe mitral regurgitation. If additional studies confirm the importance of this phenomenon, it has important implications for the management of patients with rheumatic mitral valve disease.

Influence of intraballoon pressure on development of severe mitral regurgitation after percutaneous transvenous mitral commissurotomy.

To evaluate the influence of intra-balloon pressure on the development of severe mitral regurgitation (> or = grade 3+), we measured intraballoon pressure during percutaneous transvenous mitral commissurotomy (PTMC) in 62 patients using the Inoue balloon catheter. The peak intraballoon pressure was 2.29 +/- 0.55 kg/cm2. Severe mitral regurgitation as a result of leaflet tear occurred in 7 patients (11%). Patients were divided into two groups those with (n = 7) and those without (n = 55) severe mitral regurgitation. Intraballoon pressure had been significantly higher in those with vs. those without severe mitral regurgitation (2.76 +/- 0.31 kg/cm2 vs. 2.23 +/- 0.55 kg/cm2, P < 0.01). Multiple logistic regression analysis revealed that the occurrence of severe mitral regurgitation was related to only the peak intraballoon pressure. These data suggest that a high intraballoon pressure is a risk factor for severe mitral regurgitation as a result of leaflet tear.

Rapid appearance of severe mitral regurgitation under high-dosage corticosteroid therapy in a patient with systemic lupus erythematosus

Survival of patients with systemic lupus erythematosus has increased with corticosteroid therapy. However, adverse effects of corticosteroid therapy on cardiovascular structures, such as scarring and shrinking of affected valves, are not well known. We report the case of a 19-year-old patient who developed severe mitral insufficiency within a few weeks after high-dosage corticosteroid therapy had been instituted for an acute relapse of systemic lupus erythematosus. The rapid development of severe mitral regurgitation was documented by sequential colour Doppler echocardiography.