EpidemiologyMortality following acute myocardial infarction has declined by approximately 30% over the past 2 decades (1), although the burden of coronary heart disease (CHD) remains high. This year, it is estimated, on average, approximately 1 American will have an acute coronary event every 25 s, resulting in 1 death per minute (2). The prevalence of NSTE-ACS is increasing relative to ST-segment elevation myocardial infarction (STEMI) due to changes in the distribution of risk factors in the population (e.g., older age, predominance of females, higher rate of diabetes) (1), use of preventative medications (3), and increasingly sensitive troponin assays (4). Two risk factors heading in opposite directions are smoking and obesity. Smoke-free legislation appears to have reduced hospitalization for ACS (5), whereas the obesity-diabetes pandemic has resulted in a disproportionate increase in non-ST-segment elevation myocardial infarction (NSTEMI) among young patients (each 5 kg/m 2 increase of body mass index is associated with a 3-year decrease in age of first NSTEMI) (6).
PathophysiologyOur understanding of the pathophysiology of ACS continues to improve, particularly with advances in imaging techniques and biomarkers. Two invasive imaging techniques-optical coherence tomography and intravascular ultrasound-can identify vulnerable plaques with thin-capped fibroatheromas (TCFA) and positive remodeling in patients with ACS (7). These plaque morphologies have been associated with subsequent adverse cardiac events (8). Interestingly, different stressors may cause a plaque to rupture in different locations (e.g., exertion: thick shoulder [9], diabetes: thin midportion [10]). This raises the hope that information regarding plaque morphology could be helpful in prioritizing risk factors and setting treatment goals.In addition to the well-known risk factors leading to lipid-rich vulnerable plaques, a number of intriguing studies have linked nontraditional factors such as panic disorder (11), physical distress (12), and insufficient sleep (13) to incident CHD. Evaluation of both pharmacologic (e.g., with serotonin reuptake inhibitors [14]) and nonpharmacologic therapies (e.g., use of music [15] and patient information sheets [16]) directed at reducing anxiety, depression, and stress are needed.Although plaque rupture and intraluminal obstruction are the most common mechanisms underlying an ACS, in the CASPAR study (17), nearly 25% of patients with ACS prospectively undergoing coronary angiography did not have a culprit lesion. Furthermore, nearly one-half of these patients without culprit lesions exhibited ischemic ST changes after administration of intracoronary acetylcholine, suggesting that these patients may benefit from therapies (e.g., calciumblockers, nitrates) directed at preventing spasm. Although the notion of coronary artery spasm serving as one of the important mechanisms underlying ACS is not new (18), the findings of the CASPAR study remind us that coronary artery endothelial function, in addition to vessel m...