Effect of statins on N-terminal pro-brain natriuretic peptide (NT-proBNP) in patients with heart failure has not been well elucidated. Purpose. To assess changes of NT-proBNP during short term use of simvastatin in patients with coronary heart disease (CHD) and chronic systolic heart failure. Patients and methods. Statin naive patients (n=70) with coronary heart disease (CHD), NYHA class II-IV hart failure and LV ejection fraction (EF) 35% or less after correction of treatment and 1 month of stabilization on standard therapy were randomized to open simvastatin 40 mg/day (n=36) or no statin (n=34). In 65.1% of pts (65.6 and 64.5% in statin and control groups, respectively) beta-blockers were either initiated or their dose was corrected during <> phase of the study. Blood plasma lipids, NT-proBNP were measured and echocardiography carried out at randomization and in 4 months. Seven patients were not restudied and analysis included data from 32 (statin) and 31 (control) patients. Results. Baseline characteristics of groups were similar. Addition of statin to standard therapy was associated with lowering of low density lipoprotein cholesterol (-42%) and triglycerides (-14%). Changes of other parameters were similar in both groups including equal increases of NT-proBNP (from 540.9 to 1082.2 fmol/ml, p<0.0001, and from 639.6 to 1119.72 fmol/ml, p<0.0001, in control and simvastatin group, respectively). Baseline NT-proBNP correlated negatively with ejection fraction and positively with left ventricular dimensions, heart failure class and blood serum creatinine. The patients were followed for 1 year. Baseline NT-proBNP level was related to hospitalizations because of heart failure exacerbation during this year. Conclusion. In a group of patients with systolic heart failure due to CHD and trivial relationships between baseline NT-proBNP level and characteristics of heart failure severity short term simvastatin use caused expected LDLCH lowering but was associated with NT-proBNP increase equal to that observed in control group. Rise of NT-proBNP in both groups was probably related to activation of beta-blocker therapy.

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