Microvascular obstruction: underlying pathophysiology and clinical diagnosis

Successful restoration of epicardial coronary artery patency after prolonged occlusion might result in microvascular obstruction (MVO) and is observed both experimentally as well as clinically. In reperfused myocardium, myocytes appear edematous and swollen from osmotic overload. Endothelial cell changes usually accompany the alterations seen in myocytes but lag behind myocardial cell injury. Endothelial cells become voluminous, with large intraluminal endothelial protrusions into the vascular lumen, and together with swollen surrounding myocytes occlude capillaries. The infiltration and activation of neutrophils and platelets and the deposition of fibrin also play an important role in reperfusion-induced microvascular damage and obstruction. In addition to these ischemia-reperfusion-related events, coronary microembolization of atherosclerotic debris after percutaneous coronary intervention is responsible for a substantial part of clinically observed MVO. Microvascular flow after reperfusion is spatially and temporally complex. Regions of hyperemia, impaired vasodilatory flow reserve and very low flow coexist and these perfusion patterns vary over time as a result of reperfusion injury. The MVO first appears centrally in the infarct core extending toward the epicardium over time. Accurate detection of MVO is crucial, because it is independently associated with adverse ventricular remodeling and patient prognosis. Several techniques (coronary angiography, myocardial contrast echocardiography, cardiovascular magnetic resonance imaging, electrocardiography) measuring slightly different biological and functional parameters are used clinically and experimentally. Currently there is no consensus as to how and when MVO should be evaluated after acute myocardial infarction.