Ventricular arrhythmias in acute coronary syndromes—mechanisms and management

Thomas, Dierk; Jex, Nicholas; Thornley, Andrew

doi:10.1002/cce2.51

Cited by 22 publications

(14 citation statements)

References 48 publications

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“…After adjusting for several potentially confounding variables, we found that patients with hyperglycemia were at increased risk for developing early VT. Early VT may be triggered by increased sympathetic activity or the inflammatory response to acute ischemic injury, each of which have been shown to be associated with elevated serum glucose levels in patients with AMI [ 31 ]. Inflammatory responses to the acute ischemic insult predominately occur during the first few days after an AMI and are associated with increased resting membrane potential and prolonged action potential duration [ 25 , 29 ], which may contribute to the triggering of early onset VT [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia and risk of ventricular tachycardia among patients hospitalized with acute myocardial infarction

Tran

Gore

Darling

et al. 2018

Cardiovasc Diabetol

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BackgroundLittle is known about the association of hyperglycemia with the development of ventricular tachycardia (VT) in patients hospitalized with acute myocardial infarction (AMI) which we examined in the present study. The objectives of this community-wide observational study were to examine the relation between elevated serum glucose levels at the time of hospital admission for AMI and occurrence of VT, and time of occurrence of VT, during the patient’s acute hospitalization.MethodsWe used data from a population-based study of patients hospitalized with AMI at all central Massachusetts medical centers between 2001 and 2011. Hyperglycemia was defined as a serum glucose level ≥ 140 mg/dl at the time of hospital admission. The development of VT was identified from physicians notes and electrocardiographic findings by our trained team of data abstractors.ResultsThe average age of the study population was 70 years, 58.0% were men, and 92.7% were non-Hispanic whites. The mean and median serum glucose levels at the time of hospital admission were 171.4 mg/dl and 143.0, respectively. Hyperglycemia was present in 51.9% of patients at the time of hospital admission; VT occurred in 652 patients (15.8%), and two-thirds of these episodes occurred during the first 48 h after hospital admission (early VT). After multivariable adjustment, patients with hyperglycemia were at increased risk for developing VT (adjusted OR = 1.48, 95% CI = 1.23–1.78). The presence of hyperglycemia was significantly associated with early (multivariable adjusted OR = 1.39, 95% CI = 1.11–1.73) but not with late VT. Similar associations were observed in patients with and without diabetes and in patients with and without ST-segment elevation AMI.ConclusionsEfforts should be made to closely monitor and treat patients who develop hyperglycemia, especially early after hospital admission, to reduce their risk of VT.

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Section: Discussionmentioning

confidence: 99%

Hyperglycemia and risk of ventricular tachycardia among patients hospitalized with acute myocardial infarction

Tran

Gore

Darling

et al. 2018

Cardiovasc Diabetol

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“…Accelerated idioventricular rhythm is common in the clinical practice and may result from increasing autonomic stimulation of Purkinje fibers near the ischemic region, thus enhancing automaticity or triggered activity [ 23 ]. Several factors increase the susceptibility of ischemic myocardium to reperfusion arrhythmia, including acidosis, α-adrenergic stimulation, and angiotensin II release [ 24 ].…”

Section: Linical Manifestations Of Ischemia/reperfusion Imentioning

confidence: 99%

Clinical manifestations and basic mechanisms of myocardial ischemia/reperfusion injury

Yang

2018

Tzu Chi Med J

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Acute myocardial ischemia/reperfusion (I/R) injury is a significant, unsolved clinical puzzle. In the disease context of acute myocardial infarction, reperfusion remains the only effective strategy to salvage ischemic myocardium, but it also causes additional damage. Myocardial I/R injury is composed of four types of damage, and these events attenuate the benefits of reperfusion therapy. Thus, inventing new strategies to conquer I/R injury is an unmet clinical need. A variety of pathological processes and mediators, including changes in the pH, generation of reactive oxygen radicals, and intracellular calcium overload, are proposed to be crucial in I/R-related cell injury. Among the intracellular events that occur during I/R, we stress the importance of protein phosphorylation signaling and elaborate its regulation. A variety of protein kinase pathways could be activated in I/R, including reperfusion injury salvage kinase and survivor-activating factor enhancement pathways, which are critical to cardiomyocyte survival. In addition to serine/threonine phosphorylation signaling, protein tyrosine phosphorylation is also critical in multiple cell functions and survival. However, the roles of protein kinases and phosphatases in I/R have not been extensively studied yet. By better understanding the mechanisms of I/R injury, we may have a better chance to develop new strategies for I/R injury and apply them in the clinical patient care.

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“…Although the absolute rates of VT and VF have declined during the era of percutaneous coronary intervention, patients suffering from VT or VF prior to revascularization still have a significantly impaired outcome and are at a higher risk for stent thrombosis. These data may underestimate the true incidence, since prehospital SCD before fibrinolysis or any other interventions were not included in this analysis 35 . In the present study, we modeled a clinical scenario of myocardial ischemia by LAD ligation and demonstrated that intraperitoneal injection of NO 2 -OA 20 min before he ischemic episode sustainably reduced ventricular arrhythmic events specifically in the acute phase after AMI.…”

Section: Discussionmentioning

confidence: 99%

Nitro-fatty acids suppress ischemic ventricular arrhythmias by preserving calcium homeostasis

Mollenhauer

Mehrkens

Klinke

et al. 2020

Sci Rep

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Nitro-fatty acids are electrophilic anti-inflammatory mediators which are generated during myocardial ischemic injury. Whether these species exert anti-arrhythmic effects in the acute phase of myocardial ischemia has not been investigated so far. Herein, we demonstrate that pretreatment of mice with 9- and 10-nitro-octadec-9-enoic acid (nitro-oleic acid, NO2-OA) significantly reduced the susceptibility to develop acute ventricular tachycardia (VT). Accordingly, epicardial mapping revealed a markedly enhanced homogeneity in ventricular conduction. NO2-OA treatment of isolated cardiomyocytes lowered the number of spontaneous contractions upon adrenergic isoproterenol stimulation and nearly abolished ryanodine receptor type 2 (RyR2)-dependent sarcoplasmic Ca2+ leak. NO2-OA also significantly reduced RyR2-phosphorylation by inhibition of increased CaMKII activity. Thus, NO2-OA might be a novel pharmacological option for the prevention of VT development.

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Ventricular arrhythmias in acute coronary syndromes—mechanisms and management

Cited by 22 publications

References 48 publications

Hyperglycemia and risk of ventricular tachycardia among patients hospitalized with acute myocardial infarction

Hyperglycemia and risk of ventricular tachycardia among patients hospitalized with acute myocardial infarction

Clinical manifestations and basic mechanisms of myocardial ischemia/reperfusion injury

Nitro-fatty acids suppress ischemic ventricular arrhythmias by preserving calcium homeostasis

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