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Free fatty acids (FFAs) are non-esterified fatty acids that cir- culate in the bloodstream predominantly bound to albumin. FFAs are released from adipocyte triglyceride stores by lipo- lysis and from phospholipids by the action of phospholipases. Release of FFAs, as well as uptake of circulating FFAs by tissues such as skeletal muscle and liver, is regulated by the action of insulin and modulated by adrenergic activity. FFAs represent a significant energy source, being oxidized by myocardium, skeletal muscle, liver, and kidney. Specific FFAs may also directly regulate cellular function, either by exchange with membrane phospholipid fatty acids or in their role as natural ligands of cytoplasmic nuclear recep- tors, such as peroxisome proliferator-activated receptors. Utilizing data from a prospective cohort study of 3315 German patients with suspected acute coronary syn- drome undergoing coronary angiography in 1997-2000, Pilz et al.1 evaluated associations between total fasting FFA, measured using stored blood from the time of angio- graphy, and risk of mortality over 6.9 years. Results had previously been reported for total mortality and cardiovas- cular mortality at 5.4 years;2 this report evaluates sudden cardiac death (SCD) and includes additional follow-up time. After adjustment for traditional risk factors, medication use, left ventricular function, and levels of C-reactive protein, homocysteine, creatinine, B-type natriuretic protein (BNP), and noradrenaline, higher FFA levels were independently associated with SCD (P trend ¼ 0.01), with 76% higher risk comparing extreme quartiles (relative risk (RR) ¼ 1.76, 95% confidence interval (CI) ¼ 1.03-3.00). Notably, results were very similar for other cardiovascular deaths (RR ¼ 1.78, 95% CI ¼ 1.14-2.78), indicating lack of specificity for SCD in contrast to a prior report from the Paris Prospective Study among men free of known coronary disease, in whom FFA levels were associated with higher risk of SCD but not other fatal myocardial infarctions3.

Free fatty acids, cardiovascular mortality, and cardiometabolic stress