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CHAPTER SUMMARY AND CENTRAL ILLUSTRATION

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BIOVASC: Immediate Versus Staged Complete Revascularization in ACS and Multivessel Disease

The BIOVASC trial was a prospective, open-label, non-inferiority, randomized, multinational clinical trial designed to assess whether immediate versus staged (within 6 weeks after the index procedure) complete revascularization improves outcomes in patients with acute coronary syndromes (ACS) and multivessel coronary disease. Read More

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BRIGHT-4: a randomized trial of bivalirudin in patients with ST-segment elevation myocardial infarction

BRIGHT-4 was an open-label, randomized trial comparing bivalirudin utilizing a post-percutaneous coronary intervention (PCI) high-dose infusion protocol to heparin alone in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary PCI. Read More

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SECURE Trial

The SECURE trial is an open-label, multinational trial that randomized 2,499 patients aged ≥65 years with a prior type 1 myocardial infarction (MI) within the 6 months preceding enrollment to a polypill-based strategy with a single pill containing aspirin (100 mg), ramipril (2.5, 5 or 10 mg) and atorvastatin (20 or 40 mg), or to usual care. Read More

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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

Chapter Summary

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

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