Bursts of reperfusion arrhythmias occur independently of area at risk size and are the first marker of reperfusion injury

Weg, Kirian van der; Kuijt, Wichert J.; Bekkers, Sebastiaan C.A.M.; Tijssen, Jan G.P.; Green, Cynthia L.; Smulders, Martijn W.; Lemmert, Miguel E.; Krucoff, Mitchell W.; Gorgels, Anton P.M.

doi:10.1016/j.ijcard.2018.05.083

Cited by 3 publications

(1 citation statement)

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“…Final infarct size following reperfusion depends on the presence, extend and reversibility of IRI [6]. Several mechanisms have been proposed to operate during IRI [1,3,[7][8][9][10] while endogenous protective mechanisms have been also described (Fig. 1).…”

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confidence: 99%

Cellular mechanisms and pathways in myocardial reperfusion injury

Valikeserlis¹,

Athanasiou

Stakos

2021

Coronary Artery Disease

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Despite the progress of cardiovascular medicine, ischemia-reperfusion injury can contribute to increased mortality and prolonged hospitalization after myocardial infarction. Ischemia-reperfusion injury pathophysiology encompasses many cells including cardiomyocytes, fibroblasts, mesenchymal stromal cells, vascular endothelial and smooth muscle cells, platelets, polymorphonuclear cells, macrophages, and T lymphocytes. However, specific mechanisms for all contributing cells and molecular pathways are still under investigation. What is definitely known is that endothelial dysfunction, immunity activation and inflammatory response are crucial events during ischemia-reperfusion injury while toll-like receptors, inflammasomes, reactive oxygen species, intracellular calcium overload and mitochondrial permeability transition pore opening consist of key molecular mediators. Indicatively, cardiac fibroblasts through inflammasome activation mediate the initial inflammatory response. Cardiac mesenchymal stromal cells can respond to myocardial injury by pro-inflammatory activation. Endothelial cell activation contributes to the impaired vasomotion, inflammation and thrombotic events and together with platelet activation leads to microcirculation dysfunction and polymorphonuclear cells recruitment promoting inflammation. Polymorphonuclear cells and monocytes/macrophages subsets are critically involved in the inflammation process by producing toxic proteolytic enzymes and reactive oxygen species. T cells subsets are also involved in several stages of ischemia-reperfusion injury. In this review, we summarize the specific contribution of each of the above cells and the related molecular pathways in the pathophysiology of ischemia-reperfusion injury.

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