Targeting triglycerides in secondary prevention: should we bother?

Targeting triglycerides in secondary prevention: should we bother?Overall, the evidence discussed above suggests that TG levels play a role in the pathogenesis of atherothrombosis although they are usually described as a marker of other changes in lipoprotein size, composition and particle number which be may be pathogenic (11).Nevertheless, a compelling way to prove that a CVD risk factor is appreciably independent is to show that altering the levels of this factor results in a related reduction in events.Until recently there was no evidence from an end-point trial suggesting that lowering elevated TG levels is associated with a reduction in CVD events.Such evidence is partially provided by two recent post hoc analyses of older trials: the PRavastatin Or atorVastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction (PROVE-IT) TIMI 22 trial (12) in patients with acute coronary syndromes (ACS) and the GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) (11) in patients with stable CHD.In PROVE-IT (13), 4162 men and women hospitalised for ACS were randomly assigned to intensive (atorvastatin 80 mg daily) or standard (pravastatin 40 mg daily) therapy for a mean follow-up period of 2 years (13).A Cox proportional hazards model was used to evaluate LDL-C, non-HDL-C, TG, HDL-C, and C-reactive protein (CRP) as continuous variables.In univariate analysis there was a relative reduction of 4.0% and 4.8%, respectively (p < 0.01, for both) in the incidence of the composite endpoint (death, MI, and recurrent ACS) associated with each 10 mg ⁄ dl (0.26 mmol ⁄ l) reduction in LDL-C or non-HDL-C, and a reduction of 1.8% with each 10 mg ⁄ dl of TG (p < 0.001).On the other hand, only TG, but not HDL-C, levels remained significantly associated with the composite end-point after covariate adjustment that included LDL-C (p < 0.001) or non-HDL-C (p = 0.01) (12).A Cox proportional model was also used to assess the effect of TG lowering on the composite end-point in statin-naı ¨ve subjects (n = 2587) only.For each 10% lowering of TG achieved during the first month of therapy, there was a 2.7% (p = 0.003) reduced incidence in subsequent events in unadjusted analysis and a 2.3% (p = 0.035) lower incidence after adjustment for covariates including high LDL-C (> 70 mg ⁄ dl, 1.8 mmol ⁄ l) and low HDL-C [< 40 mg ⁄ dl (1 mmol ⁄ l) in men and