Medical Treatment

An overview of the medical treatment of ACS is shown in Fig. 9. As discussed, aspirin has been shown in numerous studies to be beneficial across the entire spectrum of myocardial ischemia, from primary prevention of MI (103,104) to prevention of death or MI in all ACS (71-74,94,105). Aspirin is also a very effective agent for secondary prevention of events (106,107).

Heparin has also been shown to be beneficial in reducing death or MI in non-STE ACS (73,75-77). Low-molecular-weight heparin also significantly reduces death or MI com-

Fig. 8. The paradigm of antithrombotic therapy for non-STE ACS: antithrombotic therapy plays a major role in the treatment and prevention of ACS. If present at the time of plaque rupture (or administered acutely at the time of a clinical event), antithrombotic therapy can limit the development of thrombosis or the degree of thrombosis and subsequent lesion stenosis, which causes clinical ischemia (e.g., UA). Antithrombotic therapy could also prevent the local thrombosis from progressing to a complete occlusion (i.e., an MI). Over a period of days to weeks, antithrombotic therapy acts to passivate the lesion and allow endogenous fibrinolysis to dissolve the acute thrombosis and restore the acute lesion to a stable plaque. Adapted with permission from ref. 135.

Fig. 8. The paradigm of antithrombotic therapy for non-STE ACS: antithrombotic therapy plays a major role in the treatment and prevention of ACS. If present at the time of plaque rupture (or administered acutely at the time of a clinical event), antithrombotic therapy can limit the development of thrombosis or the degree of thrombosis and subsequent lesion stenosis, which causes clinical ischemia (e.g., UA). Antithrombotic therapy could also prevent the local thrombosis from progressing to a complete occlusion (i.e., an MI). Over a period of days to weeks, antithrombotic therapy acts to passivate the lesion and allow endogenous fibrinolysis to dissolve the acute thrombosis and restore the acute lesion to a stable plaque. Adapted with permission from ref. 135.

Key Event Myocardial Ischemia

Fig. 9. Medical treatments across the spectrum of myocardial ischemia. Aspirin, heparin, beta-blockers, and nitrates are all uniformly beneficial across the spectrum; fibrinolytic therapy and the acute use of angiotensin converting enzyme inhibitors is only beneficial in patients presenting with acute MI with STE (or new left bundle branch block). Glycoprotein IIb/IIIa inhibitors are more beneficial in patients with non-STEMI (i.e., positive troponin) and in those undergoing primary percutaneous coronary intervention (PCI), and of some benefit in conjunction with reduced-dose fibrinolytic therapy. Clopidogrel has been shown to be beneficial in patients with UA/non-STEMI, and in those undergoing PCI, but trials are still ongoing in patients with fibrinolytic therapy.

Fig. 9. Medical treatments across the spectrum of myocardial ischemia. Aspirin, heparin, beta-blockers, and nitrates are all uniformly beneficial across the spectrum; fibrinolytic therapy and the acute use of angiotensin converting enzyme inhibitors is only beneficial in patients presenting with acute MI with STE (or new left bundle branch block). Glycoprotein IIb/IIIa inhibitors are more beneficial in patients with non-STEMI (i.e., positive troponin) and in those undergoing primary percutaneous coronary intervention (PCI), and of some benefit in conjunction with reduced-dose fibrinolytic therapy. Clopidogrel has been shown to be beneficial in patients with UA/non-STEMI, and in those undergoing PCI, but trials are still ongoing in patients with fibrinolytic therapy.

pared with aspirin alone (78), and one agent, enoxaparin, has been shown to be superior to heparin in patients with non-STE ACS (79,80) In STEMI, heparin improves infarct-related artery patency following tissue plasminogen activator (108-110). The low-molecular-weight heparin enoxaparin has also recently been shown to reduce the incidence of death, MI, or recurrent ischemia following thrombolytic therapy (111-113).

Beta-blockers, nitrates, and calcium antagonists are useful in the majority of patients with ACS (10,114). Angiotensin converting enzyme (ACE) inhibitors have been shown to be beneficial in patients post-MI (115,116) and, more recently, in acute STEMI in the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-3, International Study of Infarct Survival (ISIS)-4, and Chinese trials (117-119).

Most recently, inhibition of the platelet glycoprotein IIb/IIIa receptor has been shown to be beneficial in patients with non-STE ACS (82,83), especially those who have a positive troponin (120,121). In STEMI, promising results with IIb/IIIa inhibitors have been observed with primary angioplasty (122-124), and reduction in recurrent ischemic events (but not mortality) has been seen when used in conjunction with reduced-dose firbinotlytic therapy (113,125,126).

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