Effect of angiotensin II type 1 receptor antagonist valsartan on cardiac remodeling and left ventricular function in patients with acute ST-elevation myocardial infarction.

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Abstract

Background: Left ventricular (LV) remodeling after acute ST-elevation myocardial infarction (STEMI) is an important predictor of mid and long-term prognosis. Pathological cardiac remodeling is associated with the development of LV systolic dysfunction and of congestive heart failure. The role of angiotensin converting enzyme (ACE) inhibitors in preventing cardiac remodeling and LV function improvement is well-known. The aim of our study was to assess the impact of an angiotensin II type 1 receptor antagonist administration instead of ACE inhibitor, in the standardized therapy of STEMI, on LV remodeling and function.

Methods: We have studied 34 consecutive patients with STEMI (91% men, mean age 58.5±10.2 years, 41% with anterior location of MI, mean GISSI class 4.7±1.2) within 6 hours of symptom onset, who received standard fibrinolytic therapy with 1.5 million IU of streptokinase, followed by unfractionated heparin for at least 48 hours. These patients also received: aspirin (100%), valsartan (100%), statins (94%), beta-blockers (85%) and other drugs according to the physician's choice. Neither of them received ACE inhibitors. An echocardiography was performed at baseline and 6 months after STEMI. Left ventricular end-diastolic diameter (LVEDD) and left ventricular mass corrected to body surface (LVm_BS) were used to assess the remodeling process. Left ventricular ejection fraction (LVEF) and a wall motion index (WMI) based on the analysis of regional contractility of 17 segments were taken into account for the LV systolic function. Changes in these values from baseline to the end of the study were compared using the Wilcoxon statistical test for paired samples.

Results: After six months follow-up, there were no significant statistical differences from baseline in LVEDD (from 52.1±6.1 to 52.7±5.6 mm, Z=0.61, p=0.53) and in LVm_BS (from 104.8±27.5 to 105.2±27.8 g/m2, Z=-0.54, p=0.54). There was a significant improvement of WMI (from 1.57±0.29 to 1.43±0.34, Z=-3.05, p=0.002) and a significant increase of LVEF (from 41.0±7.1 to 45.2±10.0%, Z=2.96, p=0.003).

Conclusions: The results of this study suggested that administration of valsartan instead of ACE inhibitor, in consecutive patients with medium-risk STEMI, attenuates pathological LV remodeling and improves LV systolic function. However, as obtained within the first six months after the infarction, these results can not be generalized to the later period after STEMI.

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Most cited references 28

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Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings.

Richard Devereux, Daniel R. Alonso, Elizabeth M. Lutas … (1986)

To determine the accuracy of echocardiographic left ventricular (LV) dimension and mass measurements for detection and quantification of LV hypertrophy, results of blindly read antemortem echocardiograms were compared with LV mass measurements made at necropsy in 55 patients. LV mass was calculated using M-mode LV measurements by Penn and American Society of Echocardiography (ASE) conventions and cube function and volume correction formulas in 52 patients. Penn-cube LV mass correlated closely with necropsy LV mass (r = 0.92, p less than 0.001) and overestimated it by only 6%; sensitivity in 18 patients with LV hypertrophy (necropsy LV mass more than 215 g) was 100% (18 of 18 patients) and specificity was 86% (29 of 34 patients). ASE-cube LV mass correlated similarly to necropsy LV mass (r = 0.90, p less than 0.001), but systematically overestimated it (by a mean of 25%); the overestimation could be corrected by the equation: LV mass = 0.80 (ASE-cube LV mass) + 0.6 g. Use of ASE measurements in the volume correction formula systematically underestimated necropsy LV mass (by a mean of 30%). In a subset of 9 patients, 3 of whom had technically inadequate M-mode echocardiograms, 2-dimensional echocardiographic (echo) LV mass by 2 methods was also significantly related to necropsy LV mass (r = 0.68, p less than 0.05 and r = 0.82, p less than 0.01). Among other indexes of LV anatomy, only measurement of myocardial cross-sectional area was acceptably accurate for quantitation of LV mass (r = 0.80, p less than 0.001) or diagnosis of LV hypertrophy (sensitivity = 72%, specificity = 94%).(ABSTRACT TRUNCATED AT 250 WORDS)

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Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction: the CHARM-Preserved Trial.

Salim Yusuf, Jan Östergren, B. Olofsson … (2003)

Half of patients with chronic heart failure (CHF) have preserved left-ventricular ejection fraction (LVEF), but few treatments have specifically been assessed in such patients. In previous studies of patients with CHF and low LVEF or vascular disease and preserved LVEF, inhibition of the renin-angiotensin system is beneficial. We investigated the effect of addition of an angiotensin-receptor blocker to current treatments. Between March, 1999, and July, 2000, we randomly assigned 3023 patients candesartan (n=1514, target dose 32 mg once daily) or matching placebo (n=1509). Patients had New York Heart Association functional class II-IV CHF and LVEF higher than 40%. The primary outcome was cardiovascular death or admission to hospital for CHF. Analysis was done by intention to treat. Median follow-up was 36.6 months. 333 (22%) patients in the candesartan and 366 (24%) in the placebo group experienced the primary outcome (unadjusted hazard ratio 0.89 [95% CI 0.77-1.03], p=0.118; covariate adjusted 0.86 [0.74-1.0], p=0.051). Cardiovascular death did not differ between groups (170 vs 170), but fewer patients in the candesartan group than in the placebo group were admitted to hospital for CHF once (230 vs 279, p=0.017) or multiple times. Composite outcomes that included non-fatal myocardial infarction and non-fatal stroke showed similar results to the primary composite (388 vs 429; unadjusted 0.88 [0.77-1.01], p=0.078; covariate adjusted 0.86 [0.75-0.99], p=0.037). Candesartan has a moderate impact in preventing admissions for CHF among patients who have heart failure and LVEF higher than 40%.

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Effects of candesartan in patients with chronic heart failure and reduced left-ventricular systolic function taking angiotensin-converting-enzyme inhibitors: the CHARM-Added trial.

John J V McMurray, Jan Östergren, Karl Swedberg … (2003)

Angiotensin II type 1 receptor blockers have favourable effects on haemodynamic measurements, neurohumoral activity, and left-ventricular remodelling when added to angiotensin-converting-enzyme (ACE) inhibitors in patients with chronic heart failure (CHF). We aimed to find out whether these drugs improve clinical outcome. Between March, 1999, and November, 1999, we enrolled 2548 patients with New York Heart Association functional class II-IV CHF and left-ventricular ejection fraction 40% or lower, and who were being treated with ACE inhibitors. We randomly assigned patients candesartan (n=1276, target dose 32 mg once daily) or placebo (n=1272). At baseline, 55% of patients were also treated with beta blockers and 17% with spironolactone. The primary outcome of the study was the composite of cardiovascular death or hospital admission for CHF. Analysis was done by intention to treat. The median follow-up was 41 months. 483 (38%) patients in the candesartan group and 538 (42%) in the placebo group experienced the primary outcome (unadjusted hazard ratio 0.85 [95% CI 0.75-0.96], p=0.011; covariate adjusted p=0.010). Candesartan reduced each of the components of the primary outcome significantly, as well as the total number of hospital admissions for CHF. The benefits of candesartan were similar in all predefined subgroups, including patients receiving baseline beta blocker treatment. The addition of candesartan to ACE inhibitor and other treatment leads to a further clinically important reduction in relevant cardiovascular events in patients with CHF and reduced left-ventricular ejection fraction.

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Author and article information

Journal

Journal ID (nlm-ta): J Med Life

Journal ID (iso-abbrev): J Med Life

Journal ID (publisher-id): JMedLife

Title: Journal of Medicine and Life

Publisher: Carol Davila University Press (Romania )

ISSN (Print): 1844-122X

ISSN (Electronic): 1844-3117

Publication date (Print): 15 August 2008

Volume: 1

Issue: 3

Pages: 323-333

Affiliations

[* ]Bagdasar-Arseni Clinical Emergency Hospital

Author notes

Correspondence to: Crina Sinescu Department of Cardiology, Bagdasar-Arseni Clinical Emergency Hospital, 10-12 Berceni str. Bucharest IV, Romania, Phone/Fax: +(4021)-334.30.52

Article

Publisher ID: JMedLife-1-323

PMC ID: 5654306

PubMed ID: 20108509

SO-VID: 102717c3-6c85-4af2-b835-9f042906111d

License:

This article is distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/3.0/), which permits unrestricted use and redistribution provided that the original author and source are credited.