Why the study?
Does atorvastatin 40 mg/day improve inflammatory markers, endothelial function, and ventricular performance in patients with chronic symptomatic heart failure due to idiopathic dilated cardiomyopathy?
Does atorvastatin 40 mg/day improve inflammatory markers, endothelial function, and ventricular performance in patients with chronic symptomatic heart failure due to idiopathic dilated cardiomyopathy?
Short-term atorvastatin therapy improves functional capacity, endothelial function, and inflammatory markers in patients with idiopathic dilated cardiomyopathy, despite no significant change in LVEF.
Supports symptom and endothelial gains with atorvastatin in idiopathic DCM; hypothesis-generating and requires randomized confirmation.
Statins may provide additional benefits in patients with cardiac failure due to their pleiotropic effects besides their cholesterol-lowering actions. In this study, we aimed to evaluate the impact of 12-week 40 mg atorvastatin therapy on the inflammatory markers, endothelium dependent vasodilatation and the ventricular performance markers in patients with heart failure (HF). Thirty chronic symptomatic heart failure patients, all with idiopathic dilated cardiomyopathy (DCM) were included to this open label and prospective study. Thirty patients were subdivided into two groups: group I – 15 patients who were given 40 mg of atorvastatin and group II – 15 patients who were given a placebo. After a 12-week treatment with atorvastatin 40 mg/day; clinical functional capacity, echocardiographic indices of cardiac performance and inflammatory markers were evaluated. After the treatment, even though the left ventricular ejection fraction (LV EF) did not improve significantly in the group receiving statins (29.2 ± 6.18 to 29.73 ± 6.27 in the statin group and 28.13 ± 5.81 to 27.93 ± 5.56 in the control group), both the 6 min walk test and Minnesota living with heart failure questionnaire improved significantly (p = 0.000 and 0.022, respectively). The flow mediated dilatation in the brachial arteries also showed improvement in the statin receiving group (8.9–13.8 in the statin group p = 0.0001, and 9.5–10.2 in the control group p = 0.055). In addition, the statin receiving group showed significantly lower levels of highly sensitive C-reactive protein (hs-CRP) levels at follow up (4.6–1.93 in statin group p = 0.005, and 7.2–4.97 in the control group p = 0.176). Short term atorvastatin treatment improved functional capacity and the clinical symptoms in HF patients with idiopathic dilated cardiomyopathy. This positive effect of atorvastatin might be secondary to inflammatory modulation and improvement of endothelial function. Statins in HF deserve special attention by means of further large-scale trials.
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Awwad et al. (2011) studied this question.
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