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Background: In heart failure (HF), lower total cholesterol (TC) levels associate with poor outcomes. Whether TC variations portend prognostic implication is unknown. We aimed to evaluate the impact of TC variation in HF.
Methods: We retrospectively analyzed adult outpatients with chronic HF with systolic dysfunction evaluated between January/2012 and December/2020. Patients with no TC measurement at baseline or at the 1-year follow-up visit were excluded. Variation of TC during the first year = [(baseline TC - TC at the 1-year visit)/baseline TC] × 100. Patients were followed-up until five years after the first-year visit. Endpoint: all-cause mortality. A Cox-regression analysis was performed to assess the association of TC variation (cutoff ≥10% decrease) with mortality. A multivariate model was built.
Results: We studied 362 patients, 67.4% male, mean age 69 years, 42.8% presented severe systolic dysfunction; 69.6% were on statin therapy. TC level decreased during the first year: 173 (47) vs. 166 (45) mg/dL respectively (P=0.002). In 127 (35.1%) patients there was a ≥10% decrease in TC. During a median follow-up of 57 (31-60) months, 130 (35.9%) patients died: 41.7% in those with a ≥10% TC decrease versus 32.8% in the remaining (P=0.09). Patients with at least 10% decrease in TC had higher mortality risk, after a multivariate adjustment the HR of all-cause death was 1.71 (1.15-2.55, P=0.008).
Conclusions: Patients with ≥10% decrease in TC had an independent 71% increase in the risk of death. Our results reinforce the cholesterol paradox and further question the use of statins in HF.
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http://dx.doi.org/10.23736/S2724-5683.24.06738-3 | DOI Listing |
ACS Chem Biol
August 2021
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, United States.
Bile acids play crucial roles in host physiology by acting both as detergents that aid in digestion and as signaling molecules that bind to host receptors. Gut bacterial bile salt hydrolase (BSH) enzymes perform the gateway reaction leading to the conversion of host-produced primary bile acids into bacterially modified secondary bile acids. Small molecule probes that target BSHs will help elucidate the causal roles of these metabolites in host physiology.
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