摘要
Patients with myocardial infarction resulting from acute coronary syndrome are classified by electrocardiographic presentation: 1-acute ST-segment elevation myocardial infarction (STEMI) or 2-non-ST-segment elevation myocardial infarction (NSTEMI). Prompt reperfusion of an infarct-related artery by percutaneous coronary interventions provides some relief of symptoms;long-term prognosis appears to be worse in STEMI compared to NSTEMI patients but clinical findings remain controversial. Reduced myocardial perfusion to the infarct area, caused in part by microvascular obstruction, is a privileged target for diverse pharmacologic or non-pharmacologic interventions (or combinations thereof) to improve clinical outcomes. To date, benefits of both pharmacologic and non-pharmacologic strategies to either limit microvascular obstruction and myocardial injury or improve myocardial perfusion are inconsistent. This review focuses on the physiopathological aspects of myocardial infarction in relation to development of STEMI/NSTEMI and on potential cardioprotective strategies.
Patients with myocardial infarction resulting from acute coronary syndrome are classified by electrocardiographic presentation: 1-acute ST-segment elevation myocardial infarction (STEMI) or 2-non-ST-segment elevation myocardial infarction (NSTEMI). Prompt reperfusion of an infarct-related artery by percutaneous coronary interventions provides some relief of symptoms;long-term prognosis appears to be worse in STEMI compared to NSTEMI patients but clinical findings remain controversial. Reduced myocardial perfusion to the infarct area, caused in part by microvascular obstruction, is a privileged target for diverse pharmacologic or non-pharmacologic interventions (or combinations thereof) to improve clinical outcomes. To date, benefits of both pharmacologic and non-pharmacologic strategies to either limit microvascular obstruction and myocardial injury or improve myocardial perfusion are inconsistent. This review focuses on the physiopathological aspects of myocardial infarction in relation to development of STEMI/NSTEMI and on potential cardioprotective strategies.
