Mechanism of Recurrent Ischemic Mitral Regurgitation After Annuloplasty: Continued LV Remodeling as a Moving Target
TL;DR: Recurrent MR late after ring annuloplasty is associated with continued LV remodeling, emphasizing its dynamic relation to the LV.
Abstract: Background— Patients who undergo ring annuloplasty for ischemic mitral regurgitation (MR) often have persistent or recurrent MR. This may relate to persistent leaflet tethering from left ventricle (LV) dilatation that is not relieved by ring annuloplasty. Therefore, the purpose of this study was to test the hypothesis that recurrent MR in patients after ring annuloplasty relates to continued LV remodeling. Methods and Results— Serial echoes were reviewed in 30 patients (aged 72±11 years) who showed recurrent MR late (47±27 months) versus early (3.8±5.8 months) after ring annuloplasty for ischemic MR during coronary artery bypass grafting without interval infarction. Patients with intrinsic mitral valve disease were excluded. Echocardiographic measures of MR (vena contracta and jet area/left atrial area) and LV remodeling (LV dimensions, volumes, and sphericity) were assessed at each stage. The degree of MR increased from mild to moderate, on average, from early to late postoperative stages, without significant change in LV ejection fraction. Changes in MR paralleled increases in LV volumes and sphericity index at end-systole and end-diastole. The only independent predictor of late postoperative MR was LV sphericity index at end-systole. Conclusions— Recurrent MR late after ring annuloplasty is associated with continued LV remodeling, emphasizing its dynamic relation to the LV.
Citations
More filters
Duke University1, Icahn School of Medicine at Mount Sinai2, University of Virginia3, Emory University4, University of Pennsylvania5, Harvard University6, Université de Montréal7, Cleveland Clinic8, Columbia University9, University of Toronto10, Mount Sinai Hospital11, National Institutes of Health12, University of Maryland, Baltimore13, Laval University14
TL;DR: Mitral-valve repair provided a more durable correction of mitral regurgitation but did not significantly improve survival or reduce overall adverse events or readmissions and was associated with an early hazard of increased neurologic events and supraventricular arrhythmias.
Abstract: BackgroundIn a trial comparing coronary-artery bypass grafting (CABG) alone with CABG plus mitral-valve repair in patients with moderate ischemic mitral regurgitation, we found no significant difference in the left ventricular end-systolic volume index (LVESVI) or survival after 1 year. Concomitant mitral-valve repair was associated with a reduced prevalence of moderate or severe mitral regurgitation, but patients had more adverse events. We now report 2-year outcomes. MethodsWe randomly assigned 301 patients to undergo either CABG alone or the combined procedure. Patients were followed for 2 years for clinical and echocardiographic outcomes. ResultsAt 2 years, the mean (±SD) LVESVI was 41.2±20.0 ml per square meter of body-surface area in the CABG-alone group and 43.2±20.6 ml per square meter in the combined-procedure group (mean improvement over baseline, −14.1 ml per square meter and −14.6 ml per square meter, respectively). The rate of death was 10.6% in the CABG-alone group and 10.0% in the combined-...
772 citations
University of Pennsylvania1, Icahn School of Medicine at Mount Sinai2, Université de Montréal3, Laval University4, Duke University5, Harvard University6, Cleveland Clinic7, Emory University8, Columbia University9, University of Maryland, Baltimore10, Baylor University Medical Center11, East Carolina University12, National Institutes of Health13, Yeshiva University14, University of Virginia15, Christiana Care Health System16
TL;DR: Replacement provided a more durable correction of mitral regurgitation, but there was no significant between-group difference in clinical outcomes.
Abstract: Background Ischemic mitral regurgitation is associated with a substantial risk of death. Practice guidelines recommend surgery for patients with a severe form of this condition but acknowledge that the supporting evidence for repair or replacement is limited. Methods We randomly assigned 251 patients with severe ischemic mitral regurgitation to undergo either mitral-valve repair or chordal-sparing replacement in order to evaluate efficacy and safety. The primary end point was the left ventricular end-systolic volume index (LVESVI) at 12 months, as assessed with the use of a Wilcoxon rank-sum test in which deaths were categorized below the lowest LVESVI rank. Results At 12 months, the mean LVESVI among surviving patients was 54.6±25.0 ml per square meter of body-surface area in the repair group and 60.7±31.5 ml per square meter in the replacement group (mean change from baseline, −6.6 and −6.8 ml per square meter, respectively). The rate of death was 14.3% in the repair group and 17.6% in the replacement g...
741 citations
TL;DR: Ischemic MR is convenient shorthand for MR caused by changes in ventricular structure and function related ultimately to ischemia; it is predominantly postinfarction MR.
Abstract: “ More than once in history the discovery of paradox has been the occasion for major reconstruction at the foundations of thought .” — W.V. Quine, The Ways
One thing is certain: Ischemic mitral regurgitation (MR) conveys adverse prognosis, doubling mortality after myocardial infarction (MI), in chronic heart failure, and after surgical or catheter revascularization.1–9 It is common and increases mortality even when mild,3–5 with a graded relationship between severity and reduced survival (Figure 1A).5
Figure 1. A, Decreased survival after MI with increasing MR. Effective regurgitant orifice (ERO) area of 20 mm2 demarcates mild from moderate. Reprinted with permission from Grigioni et al.5 Copyright 2001, American Heart Association, Inc. B, Decreased survival after cardiogenic shock with increasing MR for comparable LV ejection fraction (LVEF). Reprinted with permission from Picard et al.8 Copyright 2003, American Heart Association, Inc.
In many other respects, however, ischemic MR has been a study in controversy and paradox. Its diagnosis is notoriously elusive, both by auscultation and intraoperatively. It may paradoxically decrease as driving pressure increases. Still commonly referred to as “papillary muscle dysfunction,” it cannot generally be produced by direct papillary muscle damage and may actually decrease with papillary muscle ischemia. Although leaflet motion is typically restricted, it may also be excessive, or both. Treatment benefit is hotly debated and will be difficult to resolve so long as existing therapies are incompletely effective in permanently abolishing MR. New therapeutic opportunities are perplexing in their diversity. By exploring such areas of confusion, we aim to clarify fundamental principles and achieve more effective solutions.
Ischemic MR is convenient shorthand for MR caused by changes in ventricular structure and function related ultimately to ischemia; it is predominantly postinfarction MR. Active ischemia can contribute, for example, creating intermittent “flash” pulmonary edema, …
438 citations
TL;DR: This independent, contemporary registry shows that TMVR is associated with high immediate success, low complication rates, and sustained 1-year reduction of the severity of mitral regurgitation and improvement of clinical symptoms.
371 citations
TL;DR: The pathophysiology, evaluation, and prognosis of secondary MR in patients with heart failure are discussed, and the evidence for the various therapeutic approaches for secondary MR is evaluated, including guideline-directed medication for left ventricular dysfunction, cardiac resynchronization therapy and revascularization when appropriate, and mitral valve surgery and transcatheter interventions.
362 citations
References
More filters
TL;DR: It is the opinion that current technology justifies the clinical use of the quantitative two-dimensional methods described in this article and the routine reporting of left ventricular ejection fraction, diastolic volume, mass, and wall motion score.
Abstract: We have presented recommendations for the optimum acquisition of quantitative two-dimensional data in the current echocardiographic environment. It is likely that advances in imaging may enhance or supplement these approaches. For example, three-dimensional reconstruction methods may greatly augment the accuracy of volume determination if they become more efficient. The development of three-dimensional methods will depend in turn on vastly improved transthoracic resolution similar to that now obtainable by transesophageal echocardiography. Better resolution will also make the use of more direct methods of measuring myocardial mass practical. For example, if the epicardium were well resolved in the long-axis apical views, the myocardial shell volume could be measured directly by the biplane method of discs rather than extrapolating myocardial thickness from a single short-axis view. At present, it is our opinion that current technology justifies the clinical use of the quantitative two-dimensional methods described in this article. When technically feasible, and if resources permit, we recommend the routine reporting of left ventricular ejection fraction, diastolic volume, mass, and wall motion score.
8,255 citations
TL;DR: A report from the American Society of Echocardiography’s Nomenclature and Standards Committee and The Task Force on Valvular Regurgitation developed in conjunction with the American College of Cardiology EchOCardiography Committee.
3,769 citations
2,056 citations
TL;DR: Color Doppler is a useful noninvasive technique that is not only highly sensitive and specific in the identification of mitral regurgitation but also provides accurate estimation of its severity.
Abstract: We evaluated 147 patients with adequate color Doppler and angiographic studies for mitral regurgitation. Sixty-five patients had no mitral regurgitation by both color Doppler and angiography and 82 patients had mitral regurgitation by both techniques. Thus the sensitivity and specificity of color Doppler for the detection of mitral regurgitation was 100%. Three two-dimensional echocardiographic planes (parasternal long and short axis, apical four-chamber view) were used to analyze variables of the mitral regurgitant jet signals in the left atrium. The best correlation with angiography was obtained when the regurgitant jet area (RJA) (maximum or average from three planes) expressed as a percentage of the left atrial area (LAA) obtained in the same plane as the maximum regurgitant area was considered. The maximum RJA/LAA was under 20% in 34 of 36 patients with angiographic grade I mitral regurgitation, between 20% and 40% in 17 of 18 patients with grade II mitral regurgitation, and over 40% in 26 of 28 patients with severe mitral regurgitation. Maximum RJA/LAA also correlated with angiographic regurgitant fractions (r = .78) obtained in 21 of 40 patients in normal sinus rhythm and with no evidence of associated aortic regurgitation. Other variables of the regurgitant jet such as maximal linear and transverse dimensions, maximal area, or maximal area expressed as a percentage of the LAA in one or two planes correlated less well with angiography. Color Doppler is a useful noninvasive technique that is not only highly sensitive and specific in the identification of mitral regurgitation but also provides accurate estimation of its severity.
1,223 citations
TL;DR: These structure-function correlations confirm the hypothesis that transition to HF occurs by fibrosis and myocyte degeneration partially compensated by hypertrophy involving DNA synthesis and transcription.
Abstract: Background— The progression of compensated hypertrophy to heart failure (HF) is still debated. We investigated patients with isolated valvular aortic stenosis and differing degrees of left ventricular (LV) systolic dysfunction to test the hypothesis that structural remodeling, as well as cell death, contributes to the transition to HF. Methods and Results— Structural alterations were studied in LV myectomies from 3 groups of patients (group 1: ejection fraction [EF] >50%, n=12; group 2: EF 30% to 50%, n=12; group 3: EF 1 were upregulated correlating with fibrosis, which increased 2.3-, 2.2-, and 3.2-fold over control in the 3 groups. Myocyte degeneration increased 10, 22, and 32 times over control. A significant correlation exists between EF and myocyte degeneration or fibrosis. Ubiquitin-related autophagic cell death was 0.5‰ in control and group 1, 1.05 in group 2, and 6.05‰ in group 3. Death by oncosis was 0‰ in control, 3‰ in group 1, and increased to 5‰ (groups 2 and 3). Apoptosis was not detectable in control and group 3, but it was present at 0.02‰ in group 1 and 0.01‰ in group 2. Cardiomyocyte mitosis was never observed. Conclusions— These structure-function correlations confirm the hypothesis that transition to HF occurs by fibrosis and myocyte degeneration partially compensated by hypertrophy involving DNA synthesis and transcription. Cell loss, mainly by autophagy and oncosis, contributes significantly to the progression of LV systolic dysfunction.
1,022 citations