Ventricular arrhythmia burst is an independent indicator of larger infarct size even in optimal reperfusion in STEMI

Weg, Kirian van der; Majidi, Mohamed; Haeck, Joost D.E.; Tijssen, Jan G.P.; Green, Cynthia L.; Koch, Karel T.; Kuijt, Wichert J.; Krucoff, Mitchell W.; Gorgels, Anton P.M.; Winter, Robbert J. de

doi:10.1016/j.jelectrocard.2016.03.013

Cited by 9 publications

(8 citation statements)

References 20 publications

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“…The same pathophysiology that exists in IR injury, e.g., apoptosis and mitochondrial dysfunction, drives many forms of arrhythmias, including the main type, accelerated idioventricular rhythms [47]. Thus, the two conditions complement each other and, together, contribute to larger infarct size, meaning more myocyte death and decreased ventricular functioning [47][48][49][50][51][52][53]. Notably, studies support that reperfusion without arrhythmia has a smaller infarct size regardless of the same initial areas at risk [47][48][49][50][51][52].…”

Section: Role Of Cardiac Mir-1 In Ir Injurymentioning

confidence: 99%

Role of miRNA-1 and miRNA-21 in Acute Myocardial Ischemia-Reperfusion Injury and Their Potential as Therapeutic Strategy

Jayawardena

Medzikovic

Ruffenach

et al. 2022

IJMS

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Coronary artery disease remains the leading cause of death. Acute myocardial infarction (MI) is characterized by decreased blood flow to the coronary arteries, resulting in cardiomyocytes death. The most effective strategy for treating an MI is early and rapid myocardial reperfusion, but restoring blood flow to the ischemic myocardium can induce further damage, known as ischemia-reperfusion (IR) injury. Novel therapeutic strategies are critical to limit myocardial IR injury and improve patient outcomes following reperfusion intervention. miRNAs are small non-coding RNA molecules that have been implicated in attenuating IR injury pathology in pre-clinical rodent models. In this review, we discuss the role of miR-1 and miR-21 in regulating myocardial apoptosis in ischemia-reperfusion injury in the whole heart as well as in different cardiac cell types with special emphasis on cardiomyocytes, fibroblasts, and immune cells. We also examine therapeutic potential of miR-1 and miR-21 in preclinical studies. More research is necessary to understand the cell-specific molecular principles of miRNAs in cardioprotection and application to acute myocardial IR injury.

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Section: Role Of Cardiac Mir-1 In Ir Injurymentioning

confidence: 99%

Role of miRNA-1 and miRNA-21 in Acute Myocardial Ischemia-Reperfusion Injury and Their Potential as Therapeutic Strategy

Jayawardena

Medzikovic

Ruffenach

et al. 2022

IJMS

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“…31 This increase in arrhythmias include higher risk for ventricular arrhythmias with larger infarct size. 32 However, there is no conclusive evidence that the rate of arrhythmias are higher in patients with STEMI versus patients with non-STEMI.…”

Section: Discussionmentioning

confidence: 99%

High-Density Lipoprotein Cholesterol (HDL-C) Levels Independently Correlates With Cardiac Arrhythmias and Atrial Fibrillation

Boudi

Kalayeh

Movahed³

2018

J Intensive Care Med

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“…This connection is supported by previous findings by our group. [3][4][5][6][7][8][9] We found, in several independent cohorts, the presence of a 'burst' of ventricular reperfusion arrhythmias (VA burst) to be related to clinically significant larger infarct size. This increase remained while correcting for other known factors of increased infarct size.…”

Section: Correlation Between Fatal Reperfusion Injury and Reperfusionmentioning

confidence: 96%

“…reopening of the infarct vessel, more recent studies have shown that reperfusion without arrhythmias resulted in smaller infarcts in spite of equal initial areas at risk. [3][4][5][6][7][8]…”

Section: Reperfusion Arrhythmiasmentioning

confidence: 99%

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Editor’s Choice- Reperfusion cardiac arrhythmias and their relation to reperfusion-induced cell death

Weg

Prinzen

Gorgels

2018

European Heart Journal: Acute Cardiovascular Care

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Reperfusion does not only salvage ischaemic myocardium but can also cause additional cell death which is called lethal reperfusion injury. The time of reperfusion is often accompanied by ventricular arrhythmias, i.e. reperfusion arrhythmias. While both conditions are seen as separate processes, recent research has shown that reperfusion arrhythmias are related to larger infarct size. The pathophysiology of fatal reperfusion injury revolves around intracellular calcium overload and reactive oxidative species inducing apoptosis by opening of the mitochondrial protein transition pore. The pathophysiological basis for reperfusion arrhythmias is the same intracellular calcium overload as that causing fatal reperfusion injury. Therefore both conditions should not be seen as separate entities but as one and the same process resulting in two different visible effects. Reperfusion arrhythmias could therefore be seen as a potential marker for fatal reperfusion injury.

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Ventricular arrhythmia burst is an independent indicator of larger infarct size even in optimal reperfusion in STEMI

Abstract: In the event of MBG 3, VA bursts were associated with significantly larger infarct size even if optimal epicardial and microvascular reperfusion was present.

Cited by 9 publications

References 20 publications

Role of miRNA-1 and miRNA-21 in Acute Myocardial Ischemia-Reperfusion Injury and Their Potential as Therapeutic Strategy

Role of miRNA-1 and miRNA-21 in Acute Myocardial Ischemia-Reperfusion Injury and Their Potential as Therapeutic Strategy

High-Density Lipoprotein Cholesterol (HDL-C) Levels Independently Correlates With Cardiac Arrhythmias and Atrial Fibrillation

Editor’s Choice- Reperfusion cardiac arrhythmias and their relation to reperfusion-induced cell death

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