Microvascular Injury and Intramyocardial Hemorrhage in Cardiac Ischemia/Reperfusion. Analysis of Clinical and Experimental Data

Acute myocardial infarction (AMI) is one of the main reasons of death and disability worldwide. The pathophysiological changes such as microvascular obstruction (MVO), cardiac microvascular injury (CMI), and intramyocardial haemorrhage (IMH) play an essential role in its development. IMH is associated with larger infarct size and contractile dysfunction. IMH precedes the occurrence of adverse remodeling. IMH is accompanied by inflammation. Experimental studies demonstrate that the appearance of IMH occurs after recanalization of the infarct-related artery and its size depends on the duration of ischemia. IMH is accompanied by contractile dysfunction and adverse remodeling of the heart. The most likely cause of IMH is CMI. CMI is accompanied by an increase in the myocardial and plasma proinflammatory cytokine levels and also the downregulation of tight junction proteins in cardiac vascular endothelial cells. However, there is no convincing evidence that proinflammatory cytokines trigger CMI. An increase in the proinflammatory cytokine and CMI can be two independent processes. In this review, we analyse clinical and experimental data on intramyocardial haemorrhage and cardiac microvascular injury during cardiac ischaemia/reperfusion.