Key result
Atorvastatin increases LVEF by ~4 percentage points versus placebo in nonischemic heart failure.
Why the study?
Despite advances in therapy, morbidity and mortality from heart failure remain high, and the effect of atorvastatin on LV systolic function and inflammation in nonischemic HF was unclear.
Does atorvastatin 20 mg/day improve left ventricular systolic function and reduce markers of inflammation in patients with nonischemic heart failure?
RCT (n=108)
Double-blind
randomized
Does atorvastatin 20 mg/day improve left ventricular systolic function and reduce markers of inflammation in patients with nonischemic heart failure?
p-value: p=0.01
Atorvastatin 20 mg/day improves echocardiographic parameters of left ventricular function and reduces systemic inflammatory markers in patients with nonischemic heart failure.
Objectives This study examined the effect of statin therapy on vascular markers of inflammation and echocardiographic findings in patients with nonischemic forms of cardiomyopathy. Background Despite advances in therapy, morbidity and mortality from heart failure (HF) remain high. We wished to determine whether treatment with atorvastatin affects left ventricular (LV) systolic function and markers of inflammation in patients with nonischemic HF. Methods A total of 108 patients with nonischemic HF and a left ventricular ejection fraction (LVEF) < or =35% were randomized to either atorvastatin 20 mg/day or placebo in a double-blinded fashion for a 12-month period. The LVEF and LV end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) were determined by echocardiography. Serum markers of inflammation and oxidation were also measured. Results The LVEF increased from 0.33 +/- 0.05 to 0.37 +/- 0.04 (p = 0.01) in the atorvastatin group over the 12-month follow-up period, whereas those patients in the placebo group experienced a decline in ejection fraction during the same time period. In addition, LVEDD was reduced from 57.1 +/- 5.9 mm to 53.4 +/- 5.1 mm (p = 0.007) and LVESD was reduced from 42.4 +/- 3.8 mm to 39.1 +/- 3.8 mm (p = 0.02) in the cohort of patients treated with atorvastatin; these dimensions increased in the placebo group. There was an increase in erythrocyte superoxide dismutase (E-SOD) activity, and there were significant reductions in serum levels of high sensitivity C-reactive protein, interleukin-6 (IL-6), and tumor necrosis factor-alpha receptor II (TNF-alpha RII) in the atorvastatin group. Conclusions The use of atorvastatin in patients with nonischemic HF improves LVEF and attenuates adverse LV remodeling. The effects on soluble levels of several inflammatory markers with atorvastatin suggest, in part, mechanisms by which statins might exert their beneficial effects in nonischemic HF.
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Sola et al. (2005) conducted an RCT in Nonischemic heart failure (n=108). Atorvastatin vs. Placebo was evaluated on Left ventricular ejection fraction (LVEF) (p=0.01). Atorvastatin significantly increased left ventricular ejection fraction from 0.33 to 0.37 (P=0.01) and attenuated adverse remodeling compared to placebo in patients with nonischemic heart failure.
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