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Chapter 1

The Thrombotic AMI Lesion: Lessons from Pathology more...

Chapter 2

Electrocardiographic Identification of the Culprit Lesion in ST-Segment Elevation Myocardial more...

Chapter 3

The Role of Thrombolysis in the Era of STEMI Interventions more...

Chapter 4

STEMI Interventions: A Review of Relevant Clinical Trials more...

Chapter 5

Updated Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction more...

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Chapter 6
Adjunctive Pharmacologic Therapy in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Coronary Intervention
Gary M. Idelchik, MD and James J. Ferguson, MD, FACC, FAHA

ST-elevation Myocardial Infarction and the Pro-Thrombotic State
Plaque rupture frequently initiates the pathophysiologic processes that culminate in occlusion of a coronary artery and clinical manifestations of ST-segment elevation myocardial infarction (STEMI). Thrombus formation at the site of plaque rupture results in obstruction of coronary blood flow, leading to subsequent myocardial necrosis. More than 90% of patients presenting with STEMI have evidence of coronary thrombus formation at the site of plaque disruption. In order to prevent myocardial cell death and subsequent ventricular remodeling, reperfusion therapy (by either catheter-based or pharmacological approaches) is undertaken in patients presenting with STEMI to rapidly and completely reestablish coronary blood flow. Ancillary therapy with anti-thrombin and anti-platelet agents to inhibit coagulation is also important to both facilitate reperfusion and maintain infarct-related artery patency. The formation of de novo clot during percutaneous coronary intervention (PCI) or thrombolysis has been independently associated with both lower rates of reperfusion and increased incidence of abrupt vessel closure.

This chapter will summarize our current clinical understanding of contemporary anti-platelet and anti-thrombotic agents used as adjunctive therapy in the treatment of patients presenting with STEMI who undergo coronary intervention. A brief description of platelet activation and the coagulation cascade, as well as the pharmacologic mechanisms of action of each of the current anti-platelet and anti-thrombotic agents, will provide a conceptual framework on which to position the potential pharmacologic adjuncts. The indications for specific anticoagulation therapies in STEMI patients undergoing coronary intervention,treated with both primary PCI and non-primary PCI (rescue or delayed) strategies will also be discussed. A brief presentation of future options is included to highlight forthcoming developments as the standard of care continues to evolve.

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