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

Weg, Kirian van der; Prinzen, Frits W.; Gorgels, Anton P.M.

doi:10.1177/2048872618812148

Cited by 29 publications

(23 citation statements)

References 98 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The incidence and severity of reperfusion-induced arrhythmias is more frequently occurred under experimental conditions in comparison with human beings (Jennings and Reimer, 1983;Manning and Hearse, 1984;Nakata et al, 1990;Kloner, 1993;Yellon and Hausenloy, 2007;Van Der Weg et al, 2019). Under clinical conditions, reperfusion-induced arrhythmias could mainly be observed during the process of thrombolysis following myocardial ischemia and infarction, after an insult of angina and percutaneous coronary intervention (Corr and Witkowski, 1983;Tzivoni et al, 1983;Tolg et al, 2006;Yu et al, 2017;Van Der Weg et al, 2019). Thrombolytic agents, including urokinase, ataplase, tissue plasminogen activator, are used to dissolve coronary thrombus during early hours of cardiac infarction.…”

Section: Reperfusion-induced Injury and Arrhythmias: Major Componentsmentioning

confidence: 99%

“…The role of NO was also intensively studied in ischemia/ reperfusion-induced injury in the myocardium during the past two and half decades (Pabla and Curtis, 1995;Liu et al, 1997;Csonka et al, 1999a;Masini et al, 1999;Varga et al, 1999;Fauconnier et al, 2011;Bienvenu et al, 2017;Van Der Weg et al, 2019). The substantial role and investigation of precise mechanisms of NO, both under physiological or pathological conditions, are not a question of debate in cell signaling and myocardial function.…”

Section: No Co H 2 S (Gaseous Molecules)mentioning

confidence: 99%

See 1 more Smart Citation

ArrhythmoGenoPharmacoTherapy

Tósaki

2020

Front. Pharmacol.

View full text Add to dashboard Cite

This review is focusing on the understanding of various factors and components governing and controlling the occurrence of ventricular arrhythmias including (i) the role of various ion channel-related changes in the action potential (AP), (ii) electrocardiograms (ECGs), (iii) some important arrhythmogenic mediators of reperfusion, and pharmacological approaches to their attenuation. The transmembrane potential in myocardial cells is depending on the cellular concentrations of several ions including sodium, calcium, and potassium on both sides of the cell membrane and active or inactive stages of ion channels. The movements of Na + , K + , and Ca 2+ via cell membranes produce various currents that provoke AP, determining the cardiac cycle and heart function. A specific channel has its own type of gate, and it is opening and closing under specific transmembrane voltage, ionic, or metabolic conditions. APs of sinoatrial (SA) node, atrioventricular (AV) node, and Purkinje cells determine the pacemaker activity (depolarization phase 4) of the heart, leading to the surface manifestation, registration, and evaluation of ECG waves in both animal models and humans. AP and ECG changes are key factors in arrhythmogenesis, and the analysis of these changes serve for the clarification of the mechanisms of antiarrhythmic drugs. The classification of antiarrhythmic drugs may be based on their electrophysiological properties emphasizing the connection between basic electrophysiological activities and antiarrhythmic properties. The review also summarizes some important mechanisms of ventricular arrhythmias in the ischemic/ reperfused myocardium and permits an assessment of antiarrhythmic potential of drugs used for pharmacotherapy under experimental and clinical conditions.

show abstract

Section: Reperfusion-induced Injury and Arrhythmias: Major Componentsmentioning

confidence: 99%

Section: No Co H 2 S (Gaseous Molecules)mentioning

confidence: 99%

ArrhythmoGenoPharmacoTherapy

Tósaki

2020

Front. Pharmacol.

View full text Add to dashboard Cite

show abstract

“…Thrombolytic therapy has a significantly higher rate of Accelerated Idioventricular Rhythm (AIVR) and atrial fibrillation in contrast to PPCI, while the prevalence of other arrhythmias did not differ significantly (25). The most common cause of reperfusion arrhythmia is Delayed afterdepolarization (DAD) (26). The calcium overload within the cardiac cell, because of calcium inflow or release by endoplasmic reticulum, is responsible for DAD in cardiac tissue.…”

Section: Discussionmentioning

confidence: 99%

“…These oscillations of cardiac cells membrane potentials appear after repolarization, which will further result in arrhythmias, especially AIVR. Furthermore, reduction in Adenosine triphosphate (ATP) which is a result of excessive intracellular calcium is also responsible for further arrhythmias because of closure of potassium ATP dependent channels and shortened action potentials (26). There are numerous cardio-protective approaches available to prevent reperfusion injury, which can be categorized into postconditioning and peri-conditioning.…”

Section: Discussionmentioning

confidence: 99%

Effect of remote ischemic Pre-conditioning on primary percutaneous coronary intervention outcomes: a randomized clinical trial

Dastani¹,

Ramezani²,

Gholoobi³

et al. 2019

Electron. physician

View full text Add to dashboard Cite

Background: Remote ischemic preconditioning (RIPC) is a simple non-invasive method by using cycles of ischemia and reperfusion on a remote organ. Objective: To determine the effect of RIPC outcomes in patients with ST-segment-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). Methods: This double blind randomized clinical trial was conducted in two teaching and reference hospitals in Mashhad, Iran. Sixty patients with acute STEMI were enrolled from October 2018 to January 2019. The patients were allocated into two groups, by using sealed envelope randomization i.e., a study group of patients who had undergone RIPC intervention and a control group of patients who had not undergone RIPC. Half an hour before PPCI, a sphygmomanometer cuff was placed around the left upper arm and inflated up to 200mmHg for five minutes; then the cuff was deflated for another five minutes, and this cycle was repeated 3 times before or during PPCI. Corrected Thrombolysis in Myocardial Infarction (TIMI) frame count, ST-segment resolution, reperfusion arrhythmias and contrast induced nephropathy (CIN) were evaluated in both groups after PPCI. Study data was analyzed by SPSS version 16. Results: A total number of 26 males and 14 females were studied in study groups (n=20 for each). Both groups were homogenous according to their baseline characteristics. Both TIMI grade and Corrected Thrombolysis in Myocardial Infarction Frame Count CTFC significantly improved after RIPC (p=0.001 and p<0.0001 respectively). Moreover, CIN and reperfusion arrhythmias were reduced in the intervention group (p=0.028 and p=0.016 respectively). Also, ST-segment resolution was significantly different among groups (p=0.002). After adjusting for baseline factors only a significant relationship was observed between performing intervention and final TIMI grade (OR=26.416, 95% CI for OR=1.063, 656.184, p=0.046). Conclusion: RIPC can effectively reduce CIN and reperfusion arrhythmias in patients undergoing PPCI. Also, RIPC improved ST segment resolution and TIMI flow grade, and corrected TIMI frame count. Based on our results, RIPC may have a protective effect of on PPCI outcomes. Trial registration: The trial was registered at the Iranian Clinical Trial Registry (IRCT) (http://www.irct.ir) with the IRCT identification number IRCT20150614022713N2.

show abstract

“…There is a growing line of advance that cardiac mitochondria are implicated in the pathogenesis of cardiac arrhythmias [77][78][79][80][81], beyond their role in the pathogenesis of HF and mitochondrial cardiomyopathies [82]. Moreover, skeletal muscle mitochondrial pathology is well recognized to play a fundamental role in the decline in functional capacity of HFpEF patient population and decreased peak oxygen consumption during exercise [83,84].…”

Section: Metabolic Remodeling In Hfmentioning

confidence: 99%

Mitochondrial Pathobiology and Metabolic Remodeling in Progression to Overt Systolic Heart Failure

Chaanine

LeJemtel

Delafontaine

2020

JCM

View full text Add to dashboard Cite

The mitochondria are mostly abundant in the heart, a beating organ of high- energy demands. Their function extends beyond being a power plant of the cell including redox balance, ion homeostasis and metabolism. They are dynamic organelles that are tethered to neighboring structures, especially the endoplasmic reticulum. Together, they constitute a functional unit implicated in complex physiological and pathophysiological processes. Their topology in the cell, the cardiac myocyte in particular, places them at the hub of signaling and calcium homeostasis, making them master regulators of cell survival or cell death. Perturbations in mitochondrial function play a central role in the pathophysiology of myocardial remodeling and progression of heart failure. In this minireview, we summarize important pathophysiological mechanisms, pertaining to mitochondrial morphology, dynamics and function, which take place in compensated hypertrophy and in progression to overt systolic heart failure. Published work in the last few years has expanded our understanding of these important mechanisms; a key prerequisite to identifying therapeutic strategies targeting mitochondrial dysfunction in heart failure.

show abstract

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

Cited by 29 publications

References 98 publications

ArrhythmoGenoPharmacoTherapy

ArrhythmoGenoPharmacoTherapy

Effect of remote ischemic Pre-conditioning on primary percutaneous coronary intervention outcomes: a randomized clinical trial

Mitochondrial Pathobiology and Metabolic Remodeling in Progression to Overt Systolic Heart Failure

Contact Info

Product

Resources

About