Acute coronary syndrome (ACS) is not a single diagnosis but a spectrum of disease. It encompasses ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina (UA). It is a disease process that, if unrecognized, imparts upon the patient profound morbidity, if not mortality. In fact, acute myocardial infarction is the leading cause of death in the United States, if not the entire developed world.1 For these reasons, ACS should be respected and treated expeditiously and aggressively.
In the United States, coronary heart disease (CHD) affected approximately 16 million people in 2005, and in 2008 an estimated 770,000 Americans had a new coronary event while 430,000 had a recurrent one.2 CHD includes ACS as well as UA. While stable angina is an important condition, it is not a focus of this discussion because on its own, it is not directly responsible for mortality statistics (although a small number of deaths due to CHD are coded as being from angina pectoris). With respect to mortality, one in every five deaths in the United States in 2004 was due to CHD with an American suffering a coronary event once every 26 seconds and one American dying every minute as a result of a myocardial infarction.2 The 2008 estimated cost of caring for these patients was $156.4 billion.2 The prevalence of ACS is expected to continue to climb as increasing numbers of patients are being diagnosed with NSTEMI and UA. This is not solely due to the aging of the population but also due to utilization of more sensitive diagnostic tests, increased availability of early invasive therapies, and treatment of comorbid conditions early and aggressively that delay the progression of disease to STEMI.3–5
With a heightened level of concern and recognition of these clinical entities, fewer patients have gone unrecognized. Consequently, mortality related to ACS has declined dramatically, particularly for STEMI. Unfortunately, the rate of decline has not been as great for NSTEMI and UA. This is likely due to a delay in the implementation of treatment guidelines for patients with these conditions.6,7
Understanding acute myocardial infarction requires understanding the pathophysiology of coronary artery thrombosis. While ACS can be caused by an embolic obstruction, this is much less common than ACS caused by atherosclerotic disease. There are two general types of atherosclerotic plaque, stable and unstable, and each produces a different presentation of ACS. The stable plaque has a thick fibrous cap that slowly thickens and produces the symptoms of classic angina such as progressively worsening exertional chest tightness. In this situation, oxygen delivery to the myocardium is gradually diminished, producing decreased tolerance of myocardial stress. Unstable plaques, however, have a thin fibrous cap suffused with inflammatory cells that make the plaques vulnerable to rupture. ACS associated with acute plaque rupture produces a spectrum of findings based on the location and degree of associated thrombosis and consequent impairment ...