Key result
Simvastatin significantly improves NYHA functional class and LVEF versus placebo in idiopathic dilated cardiomyopathy.
Why the study?
Chronic heart failure is associated with inflammation and neurohormonal imbalance, and the potential benefits of short-term statin therapy in nonischemic heart failure were unclear.
Does short-term simvastatin therapy improve cardiac function and symptoms in patients with symptomatic, nonischemic, dilated cardiomyopathy?
RCT (n=63)
Does short-term simvastatin therapy improve cardiac function and symptoms in patients with symptomatic, nonischemic, dilated cardiomyopathy?
Absolute Event Rate: 2.04% vs 2.32%
p-value: p=<0.01
Short-term simvastatin therapy improves left ventricular ejection fraction, NYHA functional class, and inflammatory biomarkers in patients with nonischemic dilated cardiomyopathy.
Supports short-term simvastatin in nonischemic DCM; extends pleiotropic statin evidence in heart failure.
BACKGROUND: Chronic heart failure is associated with inflammation and neurohormonal imbalance. The 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors, or statins, exert anti-inflammatory and vascular protective effects. We hypothesized that short-term statin therapy may have beneficial effects in patients with nonischemic heart failure. METHODS AND RESULTS: Sixty-three patients with symptomatic, nonischemic, dilated cardiomyopathy were randomly divided into 2 groups. One group received simvastatin (n=24), and the other group received placebo (n=27). The initial dose of simvastatin was 5 mg/d, which was increased to 10 mg/d after 4 weeks. After 14 weeks, patients receiving simvastatin exhibited a modest reduction in serum cholesterol level compared with patients receiving placebo (130+/-13 versus 148+/-18, P<0.05). Patients treated with simvastatin had a lower New York Heart Association functional class compared with patients receiving placebo (2.04+/-0.06 versus 2.32+/-0.05, P<0.01). This corresponded to improved left ventricular ejection fraction in the simvastatin group (34+/-3 to 41+/-4%, P<0.05) but not in the placebo group. Furthermore, plasma concentrations of tumor necrosis factor-alpha, interleukin-6, and brain natriuretic peptide were significantly lower in the simvastatin group compared with the placebo group. CONCLUSIONS: Short-term statin therapy improves cardiac function, neurohormonal imbalance, and symptoms associated with idiopathic dilated cardiomyopathy. These findings suggest that statins may have therapeutic benefits in patients with heart failure irrespective of serum cholesterol levels or atherosclerotic heart disease.
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Node et al. (2003) conducted an RCT in Idiopathic dilated cardiomyopathy (n=63). Simvastatin vs. Placebo was evaluated on New York Heart Association functional class (p=<0.01). Simvastatin therapy for 14 weeks significantly improved NYHA functional class (2.04 vs 2.32, P<0.01) and left ventricular ejection fraction in patients with idiopathic dilated cardiomyopathy.
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