Intra-myocardial hemorrhage and cardiac microvascular injury in ischemia/reperfusion. A Systematic Review of Current Evidences
Abstract
The in-hospital mortality rate in acute myocardial infarction (AMI) remains high despite the undoubted achievements in treatment of this disease achieved in the last 40 years. The dangerous complications of AMI remain cardiac microvascular injury (CMI) and intramyocardial hemorrhage (IMH). IMH is a widespread pathology that occurs in 42 - 57% of patients with ST-segment elevation myocardial infarction and percutaneous coronary intervention. IMH is associated with larger infarct size and contractile dysfunction. IMH is accompanied by inflammation. The appearance of IMH is depending on the duration of ischemia and requires reperfusion of the heart. IMH is accompanied by contractile dysfunction and adverse remodeling of the heart. The most likely cause of IMH is CMI. Pretreatment with ATL-146e, melatonin, tanshinone IIA, relaxin, empagliflozin, dapagliflozin, and astragaloside IV can mitigate I/R-induced 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 levels and CMI could be two independent processes.
How strong is the evidence?
Evidence Hub reads this as a systematic review. Its evidence level is 1 of 5 (Highest · pooled evidence). Pooled evidence from several studies sits at the top of the evidence pyramid.
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