Abstract 061: Long-chain monounsaturated fatty acids and congestive heart failure incidence: the Atherosclerosis Risk in Communities Study

Abstract

Background: Animal experiments in 1970s demonstrated direct cardiotoxicity of long-chain monounsaturated fatty acid (LCMUFA, 22:1 and 24:1 fatty acids) consumption. We recently found plasma phospholipid 22:1 and 24:1 to be associated with 34% and 75% higher risk (quintiles 5 vs. 1), respectively, of congestive heart failure (CHF) among older adults in the Cardiovascular Health Study. We wished to validate these results in a second independent cohort of middle-aged adults. Methods: We evaluated 3,577 adults free of CHF at baseline (age=54.1±5.8) in the Minnesota subcohort of the Atherosclerosis Risk in Communities Study (ARIC) in whom plasma phospholipid LCMUFA were measured. Incident CHF was ascertained from 1988 to 2008 by annual phone contacts, hospitalization discharge codes, and death certificates. Using multivariate Cox models, we evaluated prospective association of each LCMUFA with incident CHF, and potential mediation via CHF risk factors, including ECG left ventricular hypertrophy, and incident coronary heart disease (CHD). As a negative control, we also evaluated incident stroke, given its many shared risk factors for CHF but no link to potentially direct cardiotoxicity. Results: Mean±SD plasma phospholipid levels (% of total fatty acids) of 22:1 and 24:1 were 0.01±0.03 and 0.58±0.17. Over the 64,438 person-years of follow-up, 330 CHF events occurred. After multivariable adjustment, higher levels of 22:1 and 24:1 were associated with higher risk of CHF (Figure). Hazard ratios (95%CI) for quintiles 5 vs. 1 of 22:1 and 24:1 levels were 1.57 (1.11–2.23) and 1.92 (1.22–3.03) (p trend=0.03 and 0.002), respectively. These associations were only partly attenuated by potential mediators, including incident CHD. Neither LCMUFA was associated with incident stroke (not shown). Conclusions: Higher 22:1 and 24:1 LCMUFA levels were associated with CHF risk in middle-aged adults, consistent with our prior findings in older adults. These findings support the possibility of clinical cardiotoxicity of LCMUFA in humans.