Recent epidemiology attests that
hypertriglyceridemia may be a causal risk factor for
cardiovascular disease (CVD). The specific atherogenicity of
hypertriglyceridemia relates to the accumulation in plasma of
triglyceride-rich
lipoprotein remnants.
Hypertriglyceridemia also drives a 'global' atherogenic dyslipidemic profile, which is frequent in high-risk cardiovascular patients, such as Type 2 diabetics. Elevated
triglyceride in fasting or nonfasting blood samples should be a trigger for assessing atherogenic components of the
lipid profile, particularly
HDL-cholesterol, non-
HDL-cholesterol and
apoB. Residual risk of CVD remains high in
statin-treated diabetic patients owing to persistent atherogenic
dyslipidemia, which is not fully corrected by these agents nor by the addition of
ezetimibe.
Hypertriglyceridemia may then be targeted with
niacin,
fibrates or
n-3 fatty acids, after correcting aggravating factors, especially
obesity and
hyperglycemia.
Fibrates consistently decrease coronary events in dyslipidemic patients in outcome studies. New evidence supports adding
fenofibrate to a
statin in Type 2 diabetics with residual
hypertriglyceridemia and low
HDL-cholesterol; extrapolating from a recent meta-analysis, a 15% reduction in
triglycerides could translate into a further 15% reduction in coronary events. Ongoing clinical trials may provide new evidence for adding
niacin to a
statin. The value of higher doses of
n-3 fatty acids in reducing CVD risk remains to be demonstrated. The high
triglyceride/low HDL
nexus is an under-recognized risk factor for CVD that merits more detailed clinical assessment and treatment, particularly in patients with
Type 2 diabetes already receiving a
statin.