Cardiac MRI is a valuable imaging modality for the in vivo characterization of acute myocardial infarction pathophysiology, including the assessment of necrosis, edema, and microvascular damage.
Although acute myocardial infarction (AMI) is still one of the main causes of high morbidity in Western countries, the rate of mortality has decreased significantly. The main cause of this drop appears to be the decline of the incidence of ST-segment elevation myocardial infarction (STEMI) along with an absolute reduction in case fatality rate once STEMI has occurred. Myocardial ischaemia progresses with the duration of coronary occlusion and the delay in time to reperfusion determines the extent of irreversibile necrosis from subendocarial layers towards the epicardium in accordance with the so-called 'wave-front phenomenon'. Coronary artery recanalization, either by thrombolitic therapy or primary percutaneous intervention, may prevent myocardial cell necrosis increasing salvage of damaged, but still viable, myocardium within the area at risk. Magnetic resonance imaging (MRI) can provide a wide range of clinically useful information in AMI by detecting not only location of transmural necrosis, infarct size and myocardial oedema, but also showing in vivo important microvascular pathophysiological processes associated with AMI in the reperfusion era, such as intramyocardial haemorrhage and no-reflow. The focus of this review will be on the impact of cardiac MRI in the characterization of AMI pathophysiology in vivo in the current reperfusion era, concentrating also on clinical applications and future perspectives for specific therapeutic strategies.
Marra et al. (Thu,) studied this question.
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