Antiplatelet and Anticoagulant Treatments for Unstable Angina/Non-ST Elevation Myocardial Infarction: Comparative Effectiveness Review Number 129

ISBN-13: 9781494489328 / Angielski / Miękka / 2013 / 820 str.

U. S. Department of Healt Human Services; Agency for Healthcare Resea And Quality

Opis

Acute coronary syndrome (ACS) encompasses three similar yet distinct disorders: (1) ST-elevation myocardial infarction (STEMI), (2) non-ST elevation myocardial infarction (NSTEMI), and (3) unstable angina (UA). These disorders are often collapsed into just two categories-STEMI and UA/NSTEMI-because UA and NSTEMI have a similar pathophysiology, mortality rate, and management strategy when compared with STEMI. In the United States, approximately 1.4 million people are diagnosed with ACS each year, and 70 percent of them have UA/NSTEMI. UA/NSTEMI is defined by the presence of ischemic chest pain (or an equivalent), the notable absence of ST segment elevation on electrocardiography, and the presence of either ST segment depression or T-wave inversion on electrocardiography and/or abnormal cardiac biomarkers. The pathophysiology of UA/NSTEMI involves six possible etiologies: (1) thrombus arising from a disrupted or eroded plaque, (2) thromboembolism from an erosive plaque, (3) dynamic obstruction (such as coronary spasm), (4) progressive mechanical obstruction, (5) inflammation, or (6) coronary artery dissection. Most patients with UA/NSTEMI have thrombus formation or progressive arterial narrowing that leads to subtotal occlusion of an epicardial coronary artery. The difference between UA and NSTEMI is based on the presence of myocardial necrosis or infarction as suggested by serum tests such as creatine kinase-myocardial band, troponin I, or troponin T in NSTEMI. The standard treatment goals for patients with UA/NSTEMI involve the elimination of ischemic pain and the prevention of adverse events-death, recurrent ischemia, or myocardial infarction (MI). The cornerstone of short- and long-term treatment in all cases is medical therapy with antiplatelet and anticoagulant medications. Antiplatelet medications work by decreasing platelet aggregation and inhibiting thrombus formation. The timing of initiation of antiplatelet therapy in patients presenting with UA/NSTEMI is broadly classified as upstream if the therapy is initiated after admission but prior to cardiac catheterization or periprocedural if the agent is initiated at the time of or during the procedure. Antiplatelet therapy initiated during a hospitalization for UA/NSTEMI and continued for long-term management has been shown to reduce future cardiovascular events. Anticoagulant medications work by inhibiting blood clotting, either by antagonizing the effects of vitamin K or by blocking/inhibiting thrombin. The use of a parenteral anticoagulant, traditionally heparin, is standard treatment for patients hospitalized with ACS, and newer anticoagulants have been developed that improve outcomes, with similar or reduced bleeding risk compared with heparin. By virtue of its ability to inhibit factors associated with thrombosis and to reduce ischemic outcomes, each antiplatelet or anticoagulant agent has the potential to increase the risk of bleeding. The tradeoff between reduced ischemic risk and increased bleeding risk has been highlighted in a number of recent large clinical trials that evaluated antiplatelet and anticoagulant therapies, as discussed below. Despite these recent data, a number of questions remain about the use of antiplatelet and anticoagulant agents, including the optimal dosing of certain agents and the timing of their use, and whether certain agents might be preferred for specific subgroups of patients. There are a number of challenges in determining optimal medical management in patients with UA/NSTEMI.