Targeting triglycerides in secondary prevention: should we bother?

Abstract

The link between high plasma triglyceride (TG) levels and clinical manifestations of atherosclerosis has been a topic of continuing debate. Univariate analyses in community-based studies show plasma TG levels to be prospectively associated with increased incidence of cardiovascular disease (CVD) (1-5). However, this relationship did not always remain significant after adjustment for other covariates, mainly high-density lipoprotein cholesterol (HDL-C) levels which are consistently inversely correlated with TG levels (6-8). Of note, an updated meta-analysis of 29 prospective studies in general Western populations involving a total of 10,158 incident coronary heart disease (CHD) cases from 262,525 participants showed an odds ratio for CHD (after adjustment for baseline values of several established risk factors) of 1.72 (95% CI: 1.56-1.90) in a comparison of individuals in the top third (> 2 mmol/l) with those in the bottom third (< 1.33 mmol/l) of usual TG values (9). This study also suggested that TGs have similar intra-individual variance (r = 0.64) to total cholesterol (r = 0.60) or systolic blood pressure (r=0.61) but more than that for HDL-C (r=0.71). In addition, evidence from a large Chinese long-term epidemiology prospective trial supports the association of TG levels with CHD, even in the setting of low total cholesterol and low-density lipoprotein cholesterol (LDL-C) (5). Moreover, in the PROspective CArdiovascular Munster epidemiological survey, Caucasian men with low HDL-C (< 45 mg/dl; 1.16 mmol/l) had a greater risk of myocardial infarction (MI) within each LDL-C subgroup according to increasing TG level (10).