Key result
Pitavastatin significantly inhibited the progression from left ventricular hypertrophy to heart failure in mice, preserving fractional shortening at 40.3% compared to 27.6% in the control group.
Why the study?
Does pitavastatin prevent the progression from left ventricular hypertrophy to heart failure in mice with pressure overload?
Does pitavastatin prevent the progression from left ventricular hypertrophy to heart failure in mice with pressure overload?
Absolute Event Rate: 40.3% vs 27.6%
p-value: p=<0.05
In a mouse model of pressure overload, pitavastatin prevented the progression of established left ventricular hypertrophy to heart failure, potentially through pro-angiogenic and anti-fibrotic mechanisms.
Should not change practice in LVH; leaves open whether pitavastatin prevents HF progression in humans.
BACKGROUND: 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), which are widely used to lower plasma cholesterol levels, have been reported to have various pleiotropic effects such as protective effect of endothelial cells, angiogenic effect, antioxidant effect and anti-inflammatory effect. It is unclear, however, whether statins have any effects on the progression from left ventricular (LV) hypertrophy to heart failure in the established hypertrophied heart. METHODS AND RESULTS: C57BL/6 mice were treated with pitavastatin (pitava) or vehicle (control) from 2 weeks (established hypertrophy stage) after transverse aortic constriction (TAC) and the treatment was continued for 4 weeks. Pitavastatin significantly inhibited the progression from LV hypertrophy to heart failure as assessed on echocardiography. The cardiomyocyte cross-sectional area was significantly increased in the control group compared to the sham-operated mice (sham group), but it was not significantly different between the control group and the pitava group at 6 weeks after TAC. Moreover, pitavastatin induced myocardial angiogenesis (ratio of number of endothelial cells to cardiomyocytes) and decreased the myocardial fibrosis and oxidative stress. The expression of angiopoietin-1 in the heart was significantly increased by pitavastatin at 6 weeks after TAC. CONCLUSIONS: Pitavastatin has preventive effects on the progression of heart failure even in the hypertrophied heart.
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Kameda et al. (2012) studied Pressure overload-induced heart failure. Pitavastatin vs. Vehicle was evaluated on Left ventricular fractional shortening (FS) at 6 weeks after TAC (p=<0.05). Pitavastatin significantly inhibited the progression from left ventricular hypertrophy to heart failure in mice, preserving fractional shortening at 40.3% compared to 27.6% in the control group.
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