The term acute coronary syndrome (ACS) is in some cases used interchangeably with the term coronary artery disease (CAD). Strictly speaking, however, acute coronary syndrome is a subcategory of coronary artery disease. For example, CAD can be asymptomatic, but ACS almost always represents a symptom such as unstable angina or myocardial infarction.


Coronary artery disease (CAD) is characterized by atherosclerosis in the epicardial coronary arteries. Atherosclerotic plaques, the hallmark of atherosclerosis, progressively narrow the coronary artery lumen and impair antegrade myocardial blood flow. The reduction in coronary artery flow may be symptomatic or asymptomatic, occur with exertion or at rest, and culminate in a myocardial infarction, depending on obstruction severity and the rapidity of development.


According to the National Center for Health Statistics 2011 report, cardiovascular disease (CVD) remains the leading cause of mortality in the United States in men and women of every major ethnic group. It accounted for nearly 616,000 deaths in 2008 and was responsible for 1 in 4 deaths in the U.S. in the same year. CAD is the most common type of heart disease and, in 2008, 405,309 individuals died in the U.S. from this specific etiology. Every year, approximately 785,000 Americans suffer a first heart attack and another 470,000 will suffer an additional myocardial infarction (MI). In 2010, CAD alone was projected to cost the U.S. $108.9 billion, including the cost of healthcare services, medications, and lost productivity. CVD claims more lives each year than the next 4 leading causes of death combined—cancer, chronic lower respiratory diseases, accidents, and diabetes mellitus.


CAD is a chronic process that begins during adolescence and slowly progresses throughout life. Independent risk factors include a family history of premature CAD, cigarette smoking, diabetes mellitus, hypertension, hyperlipidemia, sedentary lifestyle, and obesity. These risk factors accelerate or modify a complex and chronic inflammatory vascular process that ultimately manifests as fibrous atherosclerotic plaque.

The most widely accepted theory of atherosclerosis states that the process represents the body’s attempt to heal in response to an endothelial injury. The first step in the atherosclerotic process is the development of fatty streaks, which contain atherogenic lipoproteins and macrophage foam cells. These streaks form between the endothelium and internal elastic lamina. Over time, an intermediate lesion—composed of an extracellular lipid core and layers of smooth muscle and connective tissue matrix—eventually forms a fibrous cap. The edge of the fibrous cap (the shoulder region) plays a critical role in the development of acute coronary syndromes. The shoulder region is the site where most plaques lose their integrity or rupture. Plaque rupture exposes the underlying thrombogenic core of lipid and necrotic material to circulating blood and its thrombogenic particulates. This exposure results in platelet adherence, aggregation, and progressive luminal narrowing, which can rapidly progress and─often in the absence of coronary artery collateral development─are associated with acute coronary syndromes.

Vascular inflammation has emerged as a critical and established component of atherosclerosis genesis, activity, and potential plaque instability. Patients with established CAD who possess a confluence of risk factors known as the metabolic syndrome remain at particularly high risk for a future vascular event, such as an acute MI or cerebrovascular accident. Biochemical markers such as elevated levels of high sensitivity or ultrasensitive C-reactive protein in the absence of systemic inflammation are thought to signal an increased likelihood of vascular inflammation and to portend a higher risk of vascular events. This marker also may signal more rapidly advancing CAD and the need for aggressive preventive measures.

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