Challenges in the treatment of hypertriglyceridemia: glass half empty or half full?

Fasting and postprandial hypertriglyceridemia appear to be causally related to atherosclerotic cardiovascular disease, and plasma triglyceride (TG) concentrations above 10 mmol/l increase susceptibility to acute pancreatitis. Exclusion of secondary causes of hypertriglyceridemia and implementation of lifestyle measures are the initial treatment in all types of hypertriglyceridemia. Current evidence regarding the benefit of adding non-statin agents, i.e. fibrates and n-3 polyunsaturated fatty acids, to statins in patients with hypertriglyceridemia (plasma 2.3 < TG ≤ 5.7 mmol/l) is insufficient. Therefore, the clinical use of non-statin agents in this context requires a careful trade-off between anticipated benefits and potential adverse events within the context of a clinical consultation. It is reasonable to consider adding fenofibrate to a maximally tolerated dose of a statin with or without ezetimibe in higher risk patients with metabolic syndrome or established atherosclerotic cardiovascular disease with persistent, residual elevation in TG > 2 mmol/l. Patients with very high fasting plasma TG levels (>10 mmol/l) need immediate expert review to offset pancreatitis and, along with strict dietary control and triglyceride-lowering pharmacotherapy, may need lipoprotein apheresis or plasma exchange.