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The prothrombotic state in atrial fibrillation: Pathophysiological and management implications

Balouiri, M., Sadiki, M

This deficit in mitochondrial energy reserve is well-documented in clinical literature [1]

Male-related factors account for about 30% of these cases

We have previously shown increased MPT in liver mitochondria from hypercholesterolemic mice treated for short term (2 weeks) with the lipophilic lovastatin (Velho et al., 2006) and a mild skeletal muscle mitochondrial oxidative stress after chronic treatment (3 months) with the hydrophilic pravastatin ( Considering the relevance of understanding the hepatic side effects of specific statin classes, the aim of the present work was to investigate the liver mitochondrial function and redox state in an appropriated biological context (hypercholesterolemia) under chronic treatment with moderate dose of a less toxic hydrophilic statin (pravastatin)