Abstract
An estimated 16 million adults in the United States have coronary heart disease (CHD), which accounts for more deaths than any single cause or group of causes of death in the United States (1). Atherosclerosis is a complex, multifactorial disease. Over the course of the past five decades, numerous prospective observational cohort studies have established beyond any doubt that risk for atherosclerotic disease is driven by a number of risk factors, which include dyslipidemia, hypertension, insulin resistance and diabetes mellitus, obesity, cigarette smoking, and age (2–6). The greater the burden of risk factors, the higher the likelihood for developing such manifestations of atherosclerosis as coronary artery disease (CAD), carotid artery disease, and peripheral arterial disease. Atherosclerotic disease is unequivocally associated with increased risk for myocardial infarction, stroke, renal artery disease and renal insufficiency, claudication and lower extremity amputation, and death. Progressive accumulation of lipid in arterial walls is a cardinal structural manifestation of atherosclerotic disease. Arresting this process of lipid infiltration and retention is an important goal in modern cardiovascular medicine.
Key Points
• Dyslipidemia is a highly heterogeneous class of metabolic disorders. The etiologies of dyslipidemias depend upon specific metabolic backgrounds (e.g., insulin resistance, thyroid dysfunction) as well as abnormalities in the gastrointestinal absorption of cholesterol and lipids and mutations in cell surface receptors and enzymes in pathways regulating lipid metabolism.
• Dyslipidemia is a widely prevalent risk factor for CAD and all forms of atherosclerotic disease. It is associated with elevations in serum LDL-C, non-HDL-C, lipoprotein(a), and triglycerides, and low levels of HDL-C.
• When making the diagnosis of dyslipidemia, it is important to rule out and treat secondary causes of dyslipidemia, such as alcoholism, thyroid dysfunction, metabolic syndrome, diabetes mellitus, and nephrotic syndrome, among others.
• A complete 10–12-h fasting lipoprotein profile should be performed on patients undergoing screening for dyslipidemia.
• The diagnosis of dyslipidemia requires comprehensive, global cardiovascular risk evaluation with 10-year Framingham risk estimation. Target levels for LDL-C and non-HDL-C are risk stratified. An HDL-C <40 mg/dL is a categorical risk factor for CAD.
• Dyslipidemia is a modifiable risk factor.
• LDL-C reduction is the primary goal of lipid-modifying therapy.
• Lifestyle modification is the first-line therapy for all patients with dyslipidemia. However, based on specific individual circumstances, health care providers may deem it essential to initiate lifestyle modification simultaneous with pharmacologic intervention, as in patients with an acute coronary syndrome or patients with established coronary artery disease.
• In patients with low HDL-C, therapeutic interventions should be made to increase the level of this lipoprotein as much as possible.
• Dyslipidemia can be treated with statins, fibrates, niacin, thiazolidenediones, ezetimibe, bile acid-binding resins, omega-3 fish oils, and combinations thereof.
• The treatment of dyslipidemia in both the primary and secondary prevention settings should always be done in tandem with the aggressive identification and management of all risk factors patients present, including hypertension, diabetes mellitus, obesity, cigarette smoking, as well as nephropathy and chronic kidney disease.
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Toth, P.P. (2011). Management of Dyslipidemia. In: Toth, P., Cannon, C. (eds) Comprehensive Cardiovascular Medicine in the Primary Care Setting. Contemporary Cardiology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-60327-963-5_3
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