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March 18, 2019
Additional Antithrombotic Therapy for the Secondary Prevention of Acute Coronary Syndrome: Vorapaxar and low-dose rivaroxaban have been approved for the prevention of atherothrombotic events in patients with a history of stable coronary artery disease. This strategy represents a different approach for long-term prevention than prolonged dual antiplatelet therapy or aspirin monotherapy. While both new therapies reduce ischemic events in high-risk patient populations, major and/or fatal bleeding complications are also increased, though the net clinical benefit continues to favor enhanced antithrombotic therapy. Societal guidelines providing recommendations for the place of these novel therapies in practice have not been developed at this time and providers should carefully weigh risks and benefits prior to use.
Upon completion of the chapter, the reader will be able to:
Define the role of atherosclerotic plaque, platelets, and the coagulation system in an acute coronary syndrome (ACS).
List key electrocardiographic (ECG), biomarker, and clinical features identifying a patient with non–ST-segment elevation (NSTE)–ACS and ST-segment elevation myocardial infarction (STEMI).
Devise an initial, early pharmacotherapy treatment and monitoring plan for a patient presenting with either NSTE-ACS or STEMI given patient-specific data.
Devise an antithrombotic pharmacotherapy treatment and monitoring plan for a patient with NSTE-ACS or STEMI undergoing percutaneous coronary intervention (PCI) given patient-specific data.
Devise an antithrombotic pharmacotherapy treatment and monitoring plan for a patient with NSTE-ACS or STEMI not undergoing PCI given patient-specific data.
Develop a pharmacotherapy and risk factor modification treatment plan for secondary prevention of coronary heart disease (CHD) events in a patient following NSTE-ACS or STEMI.
Cardiovascular disease (CVD) is the leading cause of death in the United States and one of the major causes of death worldwide. Acute coronary syndromes (ACSs), including unstable angina (UA) and myocardial infarction (MI), are a form of CHD that comprises the most common cause of CVD death.1 ACS is primarily caused by rupture of an atherosclerotic plaque with subsequent platelet adherence, activation, aggregation, and the activation of the clotting cascade. Ultimately, a thrombus composed of fibrin and platelets may develop, resulting in incomplete or complete occlusion of a coronary artery.2 ACS is a spectrum of disease encompassing ST-segment elevation MI (STEMI) or non-ST segment elevation (NSTE)-ACS, which are classified according to ECG changes and underlying pathophysiology.3,4 The American Heart Association (AHA), American College of Cardiology (ACC), and American College of Cardiology Foundation (ACCF) recommend strategies or guidelines for ACS patient care for STEMI and NSTE-ACS which includes both UA and non–ST-elevation MI (NSTEMI). In collaboration with the Society for Cardiovascular Angiography and Interventions (SCAI), the ACCF and AHA issue joint guidelines for percutaneous coronary intervention (PCI), including PCI in the setting of ACS. These practice guidelines are based ...