Association Between Statin Use and Sex Hormone in the Multi-Ethnic Study of Atherosclerosis Cohort.

PURPOSE: Based on the 2018 American College of Cardiology/American Heart Association cholesterol guidelines, the number of individuals eligible for statin therapy to reduce atherosclerotic cardiovascular disease risk has greatly expanded. Statins inhibit cholesterol biosynthesis, which can impair gonadal steroidogenesis. We evaluated the effect of statins on endogenous sex hormones in a large epidemiological study. METHODS: A total of 6814 Multi-Ethnic Study of Atherosclerosis (MESA) participants underwent the baseline examination. Of these, 6171 had measurements of serum sex hormones available: dehydroepiandrosterone (DHEA), SHBG, estradiol, and total and bioavailable testosterone. Multivariable linear regression models were used to assess the relationship of statin use with each sex hormone. RESULTS: A total of 345 women (17.4%) and 464 men (14.7%) were statin users (mean age, 67 years; 41% white, 29% black, 11% Chinese, and 19% Hispanic). Among the users vs nonusers of statins, the mean SHBG was 3.54 nmol/L (P < 0.01) lower in women and 3.37 nmol/L (P < 0.001) lower in men; the mean DHEA was 1.06 nmol/L (P < 0.05) lower in women and 0.70 nmol/L (P < 0.01) lower in men, after adjustment for potential confounders. With further propensity score adjustment, the mean DHEA and SHBG levels were 0.67 nmol/L (P < 0.05) and 3.49 nmol/L (P < 0.001) lower, respectively, for statin users vs nonusers. No statistically significant association was noted between estradiol, total testosterone, and bioavailable testosterone and statin use. CONCLUSION: Statin users have lower levels of SHBG and DHEA. This is especially relevant owing to the increasing use of statin therapy.

Troponin T, B-type natriuretic peptide, C-reactive protein, and cause-specific mortality.

PURPOSE: We sought to evaluate the associations of high-sensitivity troponin T (Hs-TnT), N-terminal pro-brain natriuretic peptide (NT-proBNP), and high sensitivity C-reactive protein (Hs-CRP) with mortality from any cause, cardiovascular disease (CVD), coronary heart disease (CHD), stroke, cancer, and respiratory disease in the Atherosclerosis Risk in Communities cohort. METHODS: We included 11,193 participants aged 54 to 74 years, initially free of the conditions being studied, and who had biomarkers measured. Participants were followed for a mean of 9.9 years. RESULTS: Hazard ratios (HR), adjusted for multiple risk factors, for mortality in participants in the highest Hs-TnT category compared with those with undetectable levels were: Total 3.42 (95% confidence interval [CI], 2.75-4.26); CVD, 7.34 (95% CI, 4.64-11.6); CHD, 6.06 (95% CI, 2.91-12.6); stroke, 3.31 (95% CI, 1.26-8.66); cancer, 1.60 (95% CI, 1.08-2.38); and respiratory, 3.85 (95% CI, 1.39-10.7). Comparing the highest NT-proBNP quintile with those in the lowest quintile, the adjusted HRs for mortality were: Total, 3.05 (95% CI, 2.46-3.77); CVD, 7.48 (95% CI, 4.67-12.0); CHD, 4.07 (95% CI, 2.07-7.98); and stroke, 10.4 (95% CI, 2.26-47.7). Comparing extreme Hs-CRP quintiles, the adjusted HRs for mortality were: Total, 1.61 (95% CI, 1.32-1.97); CVD, 1.76 (95% CI, 1.19-2.62); and respiratory, 3.36 (95% CI, 1.34-8.45). Having multiple markers elevated simultaneously greatly increased cause-specific mortality risks. CONCLUSIONS: Greater levels of Hs-TnT, NT-proBNP and Hs-CRP are associated with increased risk of death, not just from CVD, but also from some noncardiovascular causes.