摘要

Acute ST-segment elevation myocardial infarction (STEMI) is caused by coronary plaque disruption with exposure of substances that promote platelet activation, adhesion, and aggregation; thrombin generation; and thrombus formation leading to an occluded infarct-related artery (IRA) (1). Thus, patients presenting with STEMI receive reperfusion therapy either fibrinolysis or primary percutaneous coronary intervention (PCI)-to restore coronary flow, limit myocardial necrosis, and improve clinical outcomes (2-4). Even if adequate restoration of flow with reperfusion therapy is established in the epicardial IRA, perfusion of the infarct zone might still be compromised. Microvascular damage occurs in part as a consequence of downstream embolization of platelet microemboli and thrombi followed by release of substances from activated platelets that promote occlusion or spasm. Adjunctive antithrombotics are therefore critical to maintain IRA patency (decreasing thrombus accretion and preventing reocclusion) and potentially minimize microvascular damage (2).

  • 出版日期2010-2

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