Reverse remodelling and myocardial recovery in heart failure

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Abstract

Advances in medical and device therapies have demonstrated the capacity of the heart to reverse the failing phenotype. The development of normative changes to ventricular size and function led to the concept of reverse remodelling. Among heart failure therapies, durable mechanical circulatory support is most consistently associated with the largest degree of reverse remodelling. Accordingly, research to analyse human tissue after a period of mechanical circulatory support continues to yield a wealth of information. In this Review, we summarize the latest findings on reverse remodelling and myocardial recovery. Accumulating evidence shows that the molecular changes associated with heart failure, in particular in the transcriptome, metabalome, and extracellular matrix, persist in the reverse-remodelled myocardium despite apparent normalization of macrolevel properties. Therefore, reverse remodelling should be distinguished from true myocardial recovery, in which a failing heart regains both normal function and molecular makeup. These findings have implications for future research to develop therapies to repair fully the failing myocardium. Meanwhile, recognition by society guidelines of this new clinical phenotype, which is coming to be known as a state of heart failure remission, underscores the need to accurately define and identify reverse modelled myocardium for the establishment of appropriate therapies.

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Two-Year Outcomes of Surgical Treatment of Severe Ischemic Mitral Regurgitation.

Daniel Goldstein, Alan Moskowitz, Annetine Gelijns … (2016)

In a randomized trial comparing mitral-valve repair with mitral-valve replacement in patients with severe ischemic mitral regurgitation, we found no significant difference in the left ventricular end-systolic volume index (LVESVI), survival, or adverse events at 1 year after surgery. However, patients in the repair group had significantly more recurrences of moderate or severe mitral regurgitation. We now report the 2-year outcomes of this trial.

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Mitral regurgitation.

Maurice Enriquez-Sarano, Cary W Akins, Alec Vahanian (2009)

Mitral regurgitation affects more than 2 million people in the USA. The main causes are classified as degenerative (with valve prolapse) and ischaemic (ie, due to consequences of coronary disease) in developed countries, or rheumatic (in developing countries). This disorder generally progresses insidiously, because the heart compensates for increasing regurgitant volume by left-atrial enlargement, causes left-ventricular overload and dysfunction, and yields poor outcome when it becomes severe. Doppler-echocardiographic methods can be used to quantify the severity of mitral regurgitation. Yearly mortality rates with medical treatment in patients aged 50 years or older are about 3% for moderate organic regurgitation and about 6% for severe organic regurgitation. Surgery is the only treatment proven to improve symptoms and prevent heart failure. Valve repair improves outcome compared with valve replacement and reduces mortality of patient with severe organic mitral regurgitation by about 70%. The best short-term and long-term results are obtained in asymptomatic patients operated on in advanced repair centres with low operative mortality ( /=80-90%). These results emphasise the importance of early detection and assessment of mitral regurgitation.

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Mitral-Valve Repair versus Replacement for Severe Ischemic Mitral Regurgitation

Michael A Acker, Michael K Parides, Louis P Perrault … (2014)

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. 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. 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 group (hazard ratio with repair, 0.79; 95% confidence interval, 0.42 to 1.47; P=0.45 by the log-rank test). There was no significant between-group difference in LVESVI after adjustment for death (z score, 1.33; P=0.18). The rate of moderate or severe recurrence of mitral regurgitation at 12 months was higher in the repair group than in the replacement group (32.6% vs. 2.3%, P<0.001). There were no significant between-group differences in the rate of a composite of major adverse cardiac or cerebrovascular events, in functional status, or in quality of life at 12 months. We observed no significant difference in left ventricular reverse remodeling or survival at 12 months between patients who underwent mitral-valve repair and those who underwent mitral-valve replacement. Replacement provided a more durable correction of mitral regurgitation, but there was no significant between-group difference in clinical outcomes. (Funded by the National Institutes of Health and the Canadian Institutes of Health; ClinicalTrials.gov number, NCT00807040.).