ABSTRACT
Acute ST-elevation myocardial infarction (AMI) is usually caused by the rupture of an atherosclerotic plaque with subsequent thrombosis of the coronary artery.1 It is associated with a high risk of morbidity and mortality, which has improved considerably in the past few decades with the development of better monitoring and immediate defibrillation in cardiac intensive care units along with improved antiischaemic, cardioprotective and reperfusion therapies. Reperfusion of the occluded coronary artery with thrombolytic therapy has been shown to reduce infarct size and preserve left ventricular (LV) function but most importantly has an even larger effect on improving overall survival.2,3 AMI, however, remains the leading cause of morbidity and mortality in the United States with 600 000 deaths annually. Patients surviving an AMI remain at a higher risk for reinfarction and sudden death.
