CHAPTER SUMMARY AND CENTRAL ILLUSTRATION
PACMAN-AMI: Effects of the PCSK9 Antibody Alirocumab on Coronary Atherosclerosis in Patients with Acute Myocardial Infarction
The PACMAN-AMI trial sought to evaluate effects of PCSK9 inhibition on atherosclerotic plaque progression via serial intracoronary imaging of non-culprit plaques in patients presenting with acute myocardial infarction (MI) on high-intensity statin therapy. Read More
This chapter describes the epidemiology, mechanisms of disease, and management of ST-segment elevation myocardial infarction (STEMI; see Fuster and Hurst’s Central Illustration). The incidence of STEMI is decreasing in the United States and Europe. However, while advances in treatment and secondary prevention strategies have led to a reduction of short-term and long-term mortality in patients with STEMI, mortality remains substantial. STEMI results from acute occlusion of an epicardial coronary artery. Depending on the size of the territory distal to the occlusion site, the global left ventricular function can be significantly impaired, resulting in postinfarction chronic heart failure. Electrical and mechanical complications may also complicate STEMI and are discussed. The final extent of necrosis (myocardial infarct size) is one of the major determinants of prognosis after STEMI and is mainly the result of two processes: ischemia and subsequent reperfusion. Timely reperfusion (by primary percutaneous coronary intervention [PCI] or a pharmaco-invasive strategy, i.e. fibrinolysis combined with early PCI) is the cornerstone of STEMI treatment. Antithrombotic therapy comprising both anticoagulants and platelet inhibitors is also central to the management of patients with STEMI, as is timing of revascularization of nonculprit multivessel disease. Since thrombotic potential diminishes over time after myocardial infarction, and ongoing exposure to dual antiplatelet therapy increases the risk of bleeding, the risk-benefit calculus favoring potent antithrombotic therapy gradually declines beyond the acute phase of STEMI. The benefits of lipid-lowering therapies, ß-blockers, renin-angiotensin-aldosterone system inhibitors, and other pharmacological and nonpharmacological interventions are additionally discussed.
eFig 18-01 Chapter 18: ST-Elevation Myocardial Infarction
EPIDEMIOLOGY OF STEMI: CHANGE IN TEMPORAL TRENDS IN PROGNOSIS
ST-elevation myocardial infarction (STEMI, Fig. 18–1), resulting from an abrupt coronary artery occlusion, is the most severe presentation of ischemic heart disease, the leading cause of death worldwide. Opposed to non-STEMI (NSTEMI), the relative incidence of STEMI is decreasing.1,2 The adjusted incidence of STEMI in the United States has decreased from 133 per 100,000 in 1999 to 50 per 100,000 in 2008.3 While there are regional differences, incidence rates of STEMI in Europe are similar, as shown by a Swedish registry in 2015, which was 58 per 100,000 per year.4 STEMI is relatively more common in younger than older people and in men than in women; however, the incidence in women increases after the menopause.4,5 Average age at first myocardial infarction (MI) is 65.6 years for males and 72.0 years for females.6
Twelve-lead ECG tracing ...