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Long-term prognostic impact of left ventricular remodeling after a first myocardial infarction in modern clinical practice.

ABSTRACT: The association of left ventricular remodeling (LVR) after myocardial infarction (MI) with the subsequent risk of heart failure (HF) and death has not been studied in patients receiving optimal secondary prevention.We performed a long-term clinical follow-up of patients included in 2 prospective multicentric studies on LVR after first anterior MI. At 1-year echocardiography, LVR (?20% increase in end-diastolic volume from baseline to 1 year) occurred in 67/215 (31%) patients in cohort 1 and in 87/226 (38%) patients in cohort 2. The prescription rate of secondary prevention medications was very high (ß-blockers at 1 year: 90% and 95% for cohorts 1 and 2, respectively; angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers (ACE-I/ARB) at 1 year: 93% and 97% for cohorts 1 and 2, respectively). Median clinical follow-up after LVR assessment was 11.0 years in cohort 1 and 7.8 years in cohort 2. In both cohorts, LVR patients had a progressive increase in the risk of cardiovascular death or hospitalization for HF (p = 0.0007 in cohort 1 and 0.009 in cohort 2) with unadjusted hazard ratios of 2.52 [1.45-4.36] and 2.52 [1.23-5.17], respectively. Similar results were obtained when cardiovascular death was considered as an isolated endpoint. After adjustement on baseline characteristics including ejection fraction, the association with the composite endpoint was unchanged.In a context of a modern therapeutic management with a large prescription of evidence-based medications, LVR remains independently associated with HF and cardiovascular death at long-term follow-up after MI.

SUBMITTER: Bauters C

PROVIDER: S-EPMC5703528 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Long-term prognostic impact of left ventricular remodeling after a first myocardial infarction in modern clinical practice.

Bauters Christophe C Dubois Emilie E Porouchani Sina S Saloux Eric E Fertin Marie M de Groote Pascal P Lamblin Nicolas N Pinet Florence F

PloS one 20171127 11

<h4>Background</h4>The association of left ventricular remodeling (LVR) after myocardial infarction (MI) with the subsequent risk of heart failure (HF) and death has not been studied in patients receiving optimal secondary prevention.<h4>Methods and results</h4>We performed a long-term clinical follow-up of patients included in 2 prospective multicentric studies on LVR after first anterior MI. At 1-year echocardiography, LVR (≥20% increase in end-diastolic volume from baseline to 1 year) occurre ...[more]

PMID: 29176897

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Project description:PurposeNitric oxide (NO) is constitutively produced and released from the endothelium and several blood cell types by the isoform 3 of the NO synthase (NOS3). We have shown that NO protects against myocardial ischemia/reperfusion (I/R) injury and that depletion of circulating NOS3 increases within 24 h of ischemia/reperfusion the size of myocardial infarction (MI) in chimeric mice devoid of circulating NOS3. In the current study we hypothesized that circulating NOS3 also affects remodeling of the left ventricle following reperfused MI.MethodsTo analyze the role of circulating NOS3 we transplanted bone marrow of NOS3-/- and wild type (WT) mice into WT mice, producing chimerae expressing NOS3 only in vascular endothelium (BC-/EC+) or in both, blood cells and vascular endothelium (BC+/EC+). Both groups underwent 60 min of coronary occlusion in a closed-chest model of reperfused MI. During the 3 weeks post MI, structural and functional LV remodeling was serially assessed (24 h, 4 d, 1 w, 2 w and 3 w) by echocardiography. At 72 hours post MI, gene expression of several extracellular matrix (ECM) modifying molecules was determined by quantitative RT-PCR analysis. At 3 weeks post MI, hemodynamics were obtained by pressure catheter, scar size and collagen content were quantified post mortem by Gomori's One-step trichrome staining.ResultsThree weeks post MI, LV end-systolic (53.2±5.9 μl; ***p≤0.001; n = 5) and end-diastolic volumes (82.7±5.6 μl; *p<0.05; n = 5) were significantly increased in BC-/EC+, along with decreased LV developed pressure (67.5±1.8 mm Hg; n = 18; ***p≤0.001) and increased scar size/left ventricle (19.5±1.5%; n = 13; **p≤0.01) compared to BC+/EC+ (ESV: 35.6±2.2 μl; EDV: 69.1±2.6 μl n = 8; LVDP: 83.2±3.2 mm Hg; n = 24; scar size/LV13.8±0.7%; n = 16). Myocardial scar of BC-/EC+ was characterized by increased total collagen content (20.2±0.8%; n = 13; ***p≤0.001) compared to BC+/EC+ (15.9±0.5; n = 16), and increased collagen type I and III subtypes.ConclusionCirculating NOS3 ameliorates maladaptive left ventricular remodeling following reperfused myocardial infarction.

Project description:Myocardial infarction (MI), the globally leading cause of heart failure, morbidity and mortality, involves post-MI ventricular remodeling, a complex process including acute injury healing, scar formation and global changes in the surviving myocardium. The molecular mechanisms involved in adverse post-infarct left ventricular remodeling still remain poorly defined. Recently, microRNAs have been implicated in the development and progression of various cardiac diseases as crucial regulators of gene expression. We previously demonstrated that in a murine model of pressure overload, a model of heart failure secondary to aortic stenosis or chronic high blood pressure, elevated myocardial expression of miR-199b-5p is sufficient to activate calcineurin/NFAT signaling, leading to exaggerated cardiac pathological remodeling and dysfunction. Given the differences in left ventricular remodeling secondary to post-infarct healing and pressure overload, we evaluated miR-199b function in post-MI remodeling. We confirmed that the expression of miR-199b is elevated in the post-infarcted heart. Transgenic animals with cardiomyocyte-restricted overexpression of miR-199b-5p displayed exaggerated pathological remodeling after MI, reflected by severe systolic and diastolic dysfunction and fibrosis deposition. Conversely, therapeutic silencing of miR-199b-5p in MI-induced cardiac remodeling by using an antagomir to specifically inhibit endogenous miR-199b-5p in vivo, resulted in efficient suppression of cardiac miR-199b-5p expression and attenuated cardiac dysfunction and dilation following MI. Mechanistically, miR-199b-5p influenced the expression of three predicted target genes in post-infarcted hearts, dual specificity tyrosine-phosphorylation-regulated kinase 1A (Dyrk1a), the notch1 receptor and its ligand jagged1. In conclusion, here we provide evidence supporting that stress-induced miR-199b-5p participates in post-infarct remodeling by simultaneous regulation of distinct target genes.

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Long-term prognostic impact of left ventricular remodeling after a first myocardial infarction in modern clinical practice.

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Long-term prognostic impact of left ventricular remodeling after a first myocardial infarction in modern clinical practice.

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