0315: Cardiovascular protection of statins could be mediated by an increase of total bile acids concentration in sera? A pilot study

Abstract

in animal models of atheroma (ApoE-/- and LDL -/- mice), bile acids (BAs) exerts an anti-atherosclerotic effect through the anti-inflammatory action of their receptors, TGR5 and FXR, decreasing dramatically the surface of the atheroma plaque. BAs are cholesterol derivatives synthetized by the liver. In a previous study, we found that a decrease in BAs (lithocholic acid) is an independent risk factor of coronary disease in human. Statins are known to reduce cardiovascular events in atherosclerotic patients. Given the experimental protective effect of BAs against atherosclerosis, the aim of this preliminary study was to dertermine the total BAs concentration in sera after statins administration. Between January 2015 and April 2015, patients hospitalized for a coronary angiogram and starting a statins treatment for coronary atheroma were included. Exclusion criteria were post cardiac arrest, non-fasting status, hepatic disease, antibiotics and corticosteroids. The total BAs concentration was measured before and 1 month after the initiation of statin therapy by liquid chromarography mass spectrometry. Wilcoxon test was used for statistical analysis. On a cohort of 360 patients, 37 were eligible and 17, aged of 54±9.6 years old have been retrospectively included. 95% were prescribed with atorvastatin (68% with atorvastatin 40mg). The mean concentration of the total BAs before statin was 0.68µmol/L (SEM 0.08µmol/L) and 1.37µmol/L after (SEM 0.21µmol/L) (p=0.013, figure 1). statins administration is associated with a doubling of circulating BAs after one month of treatment. This raises a question about statins increasing BAs synthesis by the liver: the deflection of the cholesterol synthesis by the liver into BAs instead, could participate to the efficacy of statins. This could theoretically be beneficial by slowing down the atheroma development through anti-inflammatory effects of BAs on the macrophage of the plaque. Abstract 0315 – Figure