Prognostic significance of left ventricular mass change during treatment of hypertension

University of Helsinki, Helsinki, Uusimaa, Finland
JAMA The Journal of the American Medical Association (Impact Factor: 35.29). 12/2004; 292(19):2350-6. DOI: 10.1001/jama.292.19.2350
Source: PubMed


Increased baseline left ventricular (LV) mass predicts cardiovascular (CV) complications of hypertension, but the relation between lower LV mass and outcome during treatment for hypertension is uncertain.
To determine whether reduction of LV mass during antihypertensive treatment modifies risk of major CV events independent of blood pressure change.
Prospective cohort substudy of the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) randomized clinical trial, conducted from 1995 to 2001. A total of 941 prospectively identified patients aged 55 to 80 years with essential hypertension and electrocardiographic LV hypertrophy had LV mass measured by echocardiography at enrollment in the LIFE trial and thereafter were followed up annually for a mean (SD) of 4.8 (1.0) years for CV events.
Composite end point of CV death, fatal or nonfatal myocardial infarction, and fatal or nonfatal stroke.
The composite end point occurred in 104 patients (11%). The multivariable Cox regression model showed a strong association between lower in-treatment LV mass index and reduced rate of the composite CV end point (hazard ratio [HR], 0.78 per 1-SD (25.3) decrease in LV mass index; 95% confidence interval [CI], 0.65-0.94; P = .009) over and above that predicted by reduction in blood pressure. There were parallel associations between lower in-treatment LV mass index and lower CV mortality (HR, 0.62; 95% CI, 0.47-0.82; P = .001), stroke (HR, 0.76; 95% CI, 0.60-0.96; P = .02), myocardial infarction (HR, 0.85; 95% CI, 0.62-1.17, P = .33), and all-cause mortality (HR, 0.72; 95% CI, 0.59-0.88, P = .002), independent of systolic blood pressure and assigned treatment. Results were confirmed in analyses adjusting for additional CV risk factors, electrocardiographic changes, or when only considering events after the first year of study treatment.
In patients with essential hypertension and baseline electrocardiographic LV hypertrophy, lower LV mass during antihypertensive treatment is associated with lower rates of clinical end points, additional to effects of blood pressure lowering and treatment modality.

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    • "Left ventricular hypertrophy (LVH) is an adaptive response by the human heart to pressure and volume overload associated with hypertension, obesity and diabetes. It is one of the most potent risk factors for cardiovascular disease (CVD), including ischemic heart disease, chronic heart failure and CVD morbidity [1], [2]. Reversal of LVH has been shown to reduce the rate of cardiac events and stroke, independent of blood pressure levels [3]. "
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    ABSTRACT: Cardiac hypertrophy is an independent risk factor for cardiovascular disease and heart failure. There is increasing evidence that microRNAs (miRNAs) play an important role in the regulation of messenger RNA (mRNA) and the pathogenesis of various cardiovascular diseases. However, the ability to comprehensively study cardiac hypertrophy on a gene regulatory level is impacted by the limited availability of human cardiomyocytes. Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) offer the opportunity for disease modeling. Here we utilize a previously established in vitro model of cardiac hypertrophy to interrogate the regulatory mechanism associated with the cardiac disease process. We perform miRNA sequencing and mRNA expression analysis on endothelin 1 (ET-1) stimulated hiPSC-CMs to describe associated RNA expression profiles. MicroRNA sequencing revealed over 250 known and 34 predicted novel miRNAs to be differentially expressed between ET-1 stimulated and unstimulated control hiPSC-CMs. Messenger RNA expression analysis identified 731 probe sets with significant differential expression. Computational target prediction on significant differentially expressed miRNAs and mRNAs identified nearly 2000 target pairs. A principal component analysis approach comparing the in vitro data with human myocardial biopsies detected overlapping expression changes between the in vitro samples and myocardial biopsies with Left Ventricular Hypertrophy. These results provide further insights into the complex RNA regulatory mechanism associated with cardiac hypertrophy.
    PLoS ONE 09/2014; 9(9):e108051. DOI:10.1371/journal.pone.0108051 · 3.23 Impact Factor
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    • "LV mass was calculated by using the end-diastolic LV dimensions with an anatomically validated formula [17], [18]. LV hypertrophy was determined by calculating the LV mass index for men (≥116 g/m2) and women (≥104 g/m2) by dividing LV mass by body surface area [19]. Aortic valve area index (AVAI) was calculated by determining the valve area using the continuity equation with the time velocity/time integral ratio [20] and then indexed for body surface area. "
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    ABSTRACT: Background Fibulin-1, a circulating extracellular matrix glycoprotein, has been associated with arterial disease and elevated N-terminal prohormone B-type natriuretic peptide (NT-proBNP) in diabetes. Soluble urokinase plasminogen activator receptor (suPAR), a marker of inflammation, has been associated with subclinical atherosclerosis. Therefore, we aimed to explore the interplay between these biomarkers and mild to moderate aortic valve stenosis (AS). Methods In 374 patients with mild to moderate AS, we investigated the relationship of fibulin-1 with NT-proBNP, levels of suPAR and the degree of AS at baseline and after one and four years of treatment with Simvastatin 40 mg and Ezetimibe 10 mg or placebo. Results During treatment, fibulin-1 became more closely associated with NT-proBNP (βyear0 = 0.10, p = 0.08, βyear1 = 0.16, p = 0.005, βyear4 = 0.22, p<0.001) and suPAR (βyear0 = 0.05, p = 0.34, βyear1 = 0.16, p = 0.006, βyear4 = 0.13, p = 0.03) at the expense of the association to aortic valve area index (AVAI) (βyear0 = −0.14, p = 0.005, βyear1 = −0.08, p = 0.11, βyear4 = −0.06, p = 0.22) independently of age, gender, creatinine, and serum aspartate aminotransferase (Adj.Ryear02 = 0.19, Adj.Ryear12 = 0.22, Adj.Ryear42 = 0.27). Fibulin-1 was unrelated to aortic regurgitation, left ventricular mass, and ejection fraction. In patients with baseline AVAI<0.58 cm2/m2 (median value), fibulin-1 was more closely associated to NT-proBNP (βyear0 = 0.25, βyear1 = 0.21, βyear4 = 0.22, all p<0.01), and suPAR (βyear0 = 0.09, p = 0.26, βyear1 = 0.23, βyear4 = 0.21, both p<0.01) independently of age, gender, AST and treatment allocation. Conclusions Increased levels of fibulin-1 were independently associated with higher levels of suPAR and NT-proBNP especially in patients with lower AVAI, suggesting that fibulin-1 may be an early marker of AS as well as cardiac fibrosis secondarily to elevated left ventricular hemodynamic load.
    PLoS ONE 07/2014; 9(7):e101522. DOI:10.1371/journal.pone.0101522 · 3.23 Impact Factor
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    • "Left ventricular (LV) hypertrophy is a recognized risk factor for cardiac morbidity and mortality [1] [2]. Prognostic studies have given rise to the hypothesis that regression of LV hypertrophy is the underlying determinant of longevity after aortic valve replacement (AVR) for aortic stenosis (AS) [3] [4] [5] [6]. "
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    ABSTRACT: Left ventricular (LV) hypertrophy in aortic stenosis (AS) is considered a compensatory response helping maintain systolic function, but constitutes a risk factor for cardiac morbidity and mortality. The aim of this study was to assess the degree of LV mass regression after sutureless implantation of the Perceval S aortic valve bioprosthesis (Sorin Group, Saluggia, Italy). Between March 2010 and July 2012, 78 patients with symptomatic AS underwent isolated aortic valve replacement (AVR) with the Perceval bioprosthesis. Mean age was 77.1 ± 5.3 years, 46 patients were female (59%) and mean logistic EuroSCORE was 11 ± 7.5%. Echocardiography was performed preoperatively, at discharge, and at follow-up (mean 13.5 ± 7.3 months). LV mass was calculated using the Devereux formula and indexed to body surface area. There was 1 in-hospital non-cardiac death and 3 late deaths. LV mass index decreased from 148.4 ± 46 g/m(2) at baseline to 119.7 ± 38.5 g/m(2) at follow-up (P = 0.002). No significant changes were observed in LV hypertrophy and/or relative wall thickness >0.42 as well as in LV ejection fraction. Mean aortic gradient decreased from 49.5 ± 15.8 mmHg at baseline to 11.6 ± 5.1 mmHg at discharge and 8.3 ± 4.4 mmHg at follow-up (P < 0.001), resulting in significant clinical improvement. No moderate or severe paravalvular leakage was observed at discharge and at follow-up. In AS patients, isolated AVR with the Perceval sutureless bioprosthesis is associated with significant LV mass regression at 1-year follow-up. However, longer-term follow-up is necessary to confirm these findings.
    Interactive Cardiovascular and Thoracic Surgery 10/2013; 18(1). DOI:10.1093/icvts/ivt362 · 1.16 Impact Factor
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