Vienna, Austria - Increasingly, the clinical benefits of statin therapy in patients with heart failure don't seem to be much about cholesterol. The results of a randomized pilot trial support what some observational studies and retrospective data from large trials have hinted, that the drugs protect against sudden cardiac death (SCD) in the setting of chronic heart failure [1].

In the single-center 110-patient study reported here at the European Society of Cardiology Congress 2007, atorvastatin at the unconventionally low dosage of 10 mg/day was associated with a significant drop in all-cause mortality over one year, a benefit mostly attributable to a reduction in the SCD rate that was independent of lipid levels, LVEF, and HF etiology. In multivariate analysis, predictors of sudden death included randomization to the control group and, consistent with prior research, a high degree of QT-interval variability.

Dr Bojan Vrtovec

In presenting the study, Dr Bojan Vrtovec (Ljubljana University Medical Center, Slovenia) cautioned that it was underpowered for making any real claims about SCD prevention with statins but also speculated that QT variability—which statin therapy can reduce, according to other data—might make an effective target for statin therapy in patients with heart failure.

The study's entry criteria included NYHA class 3 heart failure and an LVEF <30%, and patients were excluded if they were on statins or amiodarone or had an implantable cardioverter-defibrillator. Vrtovec conceded that those requirements made for an atypical HF population. Most patients with heart failure at his institution were already on statins, he said; the mean total cholesterol level for enrolled patients was in the normal range.

Almost all patients were on loop diuretics and ACE inhibitors; about 80% were on beta blockers. Heart failure was ischemic in about 60% of the population.

The rate of death from any cause over 12 months was 16% for the 55 patients in the atorvastatin group and 36% for the 55 who had been randomized to placebo (p=0.017), Vrtovec reported. The rates of SCD were 5% and 22%, respectively (p=0.012), while the difference in mortality from pump failure was less pronounced: 9% in the atorvastatin group and 15% among controls (p=0.38). The rate of SCD-free survival was 2.3 times higher in the statin group than in the control group (p=0.01).

Whereas age, HF etiology, and natriuretic peptide levels were not significant predictors of SCD in multivariate analysis, randomization to the control group and a QT-variability index in the 75th percentile were independent predictors, with hazard ratios of 1.45 (p=0.02) and 1.07 (p=0.04), respectively.

Speaking to heartwire, Vrtovec predicted that, in the future, the selection of statin drugs for patients with heart failure will depend more on non-lipid-related effects, especially their anti-inflammatory properties and promotion of electrical stability, while there will be less emphasis on how far down they can push cholesterol numbers.

Vrtovec said he has no industry relationships relevant to the current study.