Hypertriglyceridemia: A new paradigm

Abstract

Low-density lipoprotein cholesterol (LDL-C) has been proven time and again to be independently associated with the risk of cardiovascular diseases (CVD). However, triglycerides (TG) are now also emerging as an important as well as independent risk factor for CVD. International lipid guidelines recommend statins as first-line drugs. However, there always remains a residual risk with statins, especially in the high-risk diabetes subset of patients. The most important reason cited for increased residual CV risk with statins is the non-high density lipoprotein cholesterol component, of which high TGs are an integral part. Several large epidemiological, Mendelian randomisation, population-based and genetic studies are emerging which are pointing towards the fact that high TG leads to CV morbidity and mortality. Pathophysiological basis of hypertriglyceridemia associated with increased CV risk has been attributed to increase circulating chylomicron and TG-rich lipoprotein remnants, increased small dense LDL, heightened risk of endothelial dysfunction and plaque formation. Recent international guidelines recommend TG lowering therapy at TG> 200 mg/dl when not controlled by optimal statin therapy. TG levels more than 500 mg/dl, however, require non-statin lipid-lowering agents as primary agents to reduce the risk of acute pancreatitis. Fibrates, niacin and omega 3 fatty acids are recommended as TG-lowering drugs. However, they are not without their share of adverse events. Saroglitazar is a novel dual peroxisome proliferator-activated enzyme agent which has been found to be free of many such adverse events and also adequate in providing dual control over hypertriglyceridemia along with significant glycaemic control.

Keywords

• Cardiovascular disease
• hypertriglyceridemia
• low-density lipoprotein cholesterol