For the past two decades, age-adjusted mortality rates for coronary artery disease have been steadily declining in the United States.1 While this encouraging decline can be attributed to continued improvements in diagnostic capabilities, medical therapy, interventional cardiology and coronary artery bypass surgery, the precise cause of this encouraging decline is complex.
Multiple theories have been proposed to explain the initiation and progression of atherosclerosis, yet researchers have yet to identify a unifying hypothesis that explains all aspects of coronary artery disease. The initial lipid hypothesis proposed more than 100 years ago was based on the premise that dyslipidemia is central to the process of atherosclerosis. The corollary of this hypothesis is that optimization of the lipid profile will reduce the risk of a future coronary event. While initially controversial, an overwhelming body of evidence accumulated from large-scale genetic, epidemiologic, pathologic and clinical studies has confirmed the primary role of dyslipidemia in coronary and peripheral atherosclerosis. Even so, the utilization of total cholesterol as both a marker for risk and target for therapy has significant limitations in individual patients.
There is considerable overlap in patient cholesterol levels regardless of documented coronary artery disease (Figure 1), and many clinicians are using lipid subfractions to enhance their ability to predict a patient's risk of experiencing a future coronary event. Cholesterol is carried in lipoproteins, which are associated with a variable impact on coronary risk (Figure 2): low-density lipoprotein (LDL) and lipoprotein (a) are clearly atherogenic, whereas elevated levels of high-density lipoprotein (HDL) are associated with reduced cardiovascular risk. While chylomicrons are considered a neutral cardiovascular risk despite dramatically elevated cholesterol and triglycerides, hyperchylomicronemia is associated with a significant risk for necrotizing pancreatitis.
The role of elevated triglyceride levels as an independent risk factor for coronary heart disease has been controversial. An increasing body of research has confirmed that subjects with hypertriglyceridemia are at risk for coronary heart disease, and trials performed with pharmacologic agents that directly affect hypertriglyceridemia have demonstrated clinical benefit in some but not all studies.
This review will discuss the epidemiologic relationships between elevated triglycerides and coronary risk, potential atherogenic mechanisms and recent clinical trials.
How to Cite:
1. Farmer JA. The Role of Hypertriglyceridemia as a Coronary Risk Factor. Methodist DeBakey Cardiovascular Journal. 2006;2(2):15-18. DOI: http://doi.org/10.14797/mdcvj.84