Beneficial Effects of Pitavastatin, a 3-Hydroxy-3-Methylglutaryl Coenzyme a Reductase Inhibitor, on Cardiac Function in Ischemic and Nonischemic Heart Failure

Teruhiko Aoyagi; Fúmitaka Nakamura; Takanobu Tomaru; Teruhiko Toyo‐oka

doi:10.1536/ihj.49.49

January 1, 2008International Heart JournalOpen Access

Beneficial Effects of Pitavastatin, a 3-Hydroxy-3-Methylglutaryl Coenzyme a Reductase Inhibitor, on Cardiac Function in Ischemic and Nonischemic Heart Failure

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Why the study?

Does pitavastatin improve cardiac function and reduce BNP levels in patients with heart failure?

Structured PICO

Does pitavastatin improve cardiac function and reduce BNP levels in patients with heart failure?

P

Population

23 patients with ischemic and nonischemic heart failure

I

Intervention

Pitavastatin 1-2 mg/day added to standard therapy

O

Outcome

Cardiac function evaluated by echocardiographic findings (LVEF, LVDd, LVDs) and plasma brain natriuretic peptide (BNP) levelssurrogate

Pitavastatin added to standard therapy may improve left ventricular ejection fraction and reduce BNP levels in patients with ischemic and nonischemic heart failure.

Implication

May support adjunctive pitavastatin in HF but should not change practice; leaves open confirmation in randomized trials.

Abstract

HMG-CoA reductase inhibitors (statins) have recently been reported to improve cardiac function, and decrease the incidence of heart failure (HF) in hyperlipidemic patients. However, evidence for statin treatment in patients with HF remains a subject of debate. Thus, a study was initiated to examine the effects of pitavastatin on cardiac function evaluated by echocardiographic findings and plasma brain natriuretic peptide (BNP) levels in patients with HF. Twenty-three patients with HF were treated with pitavastatin 1-2 mg/day in addition to standard therapy for 7.5 +/- 3.8 months. Left ventricular end-diastolic dimension (LVDd) and left ventricular end-systolic dimension (LVDs) were determined by echocardiography. Left ventricular ejection fraction (LVEF) was calculated using Teichholz's formula. Serum lipid and plasma BNP levels were also measured. During the follow-up period, LVEF was increased from 42 +/- 11 to 48 +/- 13% (P = 0.002). LVDs was reduced from 43 +/- 10 to 40 +/- 10 mm (P < 0.001), while there was no change in LVDd. E/A (n = 10) and deceleration time (n = 7), obtained in some patients, did not change significantly (0.89 +/- 0.33 to 0.77 +/- 0.17%, and 215 +/- 46 to 227 +/- 72 msec, respectively). In addition, the plasma BNP level was moderately, but significantly decreased from 94 +/- 78 to 70 +/- 56 pg/mL (P = 0.005). In subgroup analysis, LVEF was improved in both patients with ischemic and nonischemic HF. There was no significant correlation between the percent change in serum total cholesterol and the percent change in LVEF by pitavastatin treatment. Serum total cholesterol, LDL-cholesterol, and triglycerides decreased by 21%, 30%, and 15%, respectively, and HDL-cholesterol increased by 12%. Pitavastatin improved cardiac function in patients with HF, which generally worsens with time. The results suggest that pitavastatin may be beneficial for treatment of HF.