β-Adrenergic stimulation and rapid pacing mutually promote heterogeneous electrical failure and ventricular fibrillation in the globally ischemic heart

Garg, Vivek; Taylor, T. G.; Warren, Mark; Venable, Paul W.; Sciuto, Katie J.; Shibayama, Junko; Av, Zaĭtsev

doi:10.1152/ajpheart.00768.2014

Cited by 10 publications

(12 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It can be hypothesized that patients who are without limitation of physical activity (i.e., NYHA class I) are physically more active, thereby exposing themselves to a greater risk of exercisedinduced VTA. 19,20 Our findings are in line with a subanalysis of the DANISH Trial indicating that younger patients and patients with a lower NT-proBNP have an increased benefit of ICD implantation, 14 further supporting the hypothesis of a higher risk of exercised-induced VTA in younger and more active patients. An alternative Unadjustedvalues for time to ADT between NYHA-I and NYHA-II-III patients: HR 1.6, 95% CI 1.14 to 2.49, p = 0.009.…”

Section: Discussionsupporting

confidence: 83%

The Benefit of Prophylactic Implantable Cardioverter Defibrillator Implantation in Asymptomatic Heart Failure Patients With a Reduced Ejection Fraction

Lingen

Timmer

Allaart

et al. 2019

The American Journal of Cardiology

View full text Add to dashboard Cite

Recommendations for prophylactic implantable cardioverter defibrillator (ICD) implantation in asymptomatic heart failure patients with a reduced left ventricular ejection fraction (LVEF) differ between guidelines. Evidence on the risk of appropriate device therapy (ADT) and death in New York Heart Association (NYHA) class I patients is scarce. Aim of this study is to evaluate ADT and mortality in NYHA-I primary prevention ICD patients with a LVEF ≤35%. A retrospective cohort was studied, including 572 patients with LVEF ≤35% who received a prophylactic ICD with or without resynchronization therapy (CRT-D). To evaluate the incidence of ADT and mortality, NYHA-I was compared with NYHA-II-III using Cox regression analysis. During a follow-up of 4.1 § 2.4 years, 33% of the NYHA-I patients received ADT compared with 20% of the NYHA-II-III patients (hazard ratio 1.5, 95% confidence interval 1.04 to 2.31, p = 0.03). No differences in mortality were observed (hazard ratio 0.70, 95% confidence interval 0.49 to 1.07, p = 0.10). Additional analyses showed no difference in time to ADT excluding CRT patients (ICD-NYHA-I patients vs ICD-NYHA-II-III patients, p = 0.17) and comparing ischemic and nonischemic cardiomyopathy NYHA-I patients (p = 0.13). Multivariable Cox regression analyses showed that NYHA class was the strongest independent predictor of ADT. In conclusion, primary prevention NYHA-I ICD patients showed a higher incidence of ADT compared with NYHA-II-III ICD patients. These results strongly suggest that primary prevention NYHA-I patients with a LVEF ≤35% are likely to benefit from ICD therapy and should not be excluded from a potentially life-saving therapy.

show abstract

Section: Discussionsupporting

confidence: 83%

The Benefit of Prophylactic Implantable Cardioverter Defibrillator Implantation in Asymptomatic Heart Failure Patients With a Reduced Ejection Fraction

Lingen

Timmer

Allaart

et al. 2019

The American Journal of Cardiology

View full text Add to dashboard Cite

show abstract

“…It has been deduced that the detrimental action of isoproterenol is mainly due to β-adrenergic stimulation with rapid heart rhythm. Electrical depression and failure in the globally ischemic heart may contribute to adverse outcomes as asystole and ventricular fibrillation (7,41). The observed increased level of serum CK and troponin I in ISO-treated rats in this study was in consonance with an earlier report (1,34).…”

Section: Control Groupsupporting

confidence: 92%

Effect of cerebrolysin on oxidative stress-induced apoptosis in an experimental rat model of myocardial ischemia

Boshra¹,

Atwa²

2016

Physiology International

View full text Add to dashboard Cite

Apoptosis plays a role in the process of tissue damage after myocardial infarction (MI). This study was designed to investigate the possible effect of cerebrolysin against apoptosis triggered by oxidative cell stress in myocardial ischemia induced by isoproterenol in rat. Rats were pretreated with cerebrolysin 5 mL/kg intraperitoneally for 7 days and intoxicated with isoproterenol (ISO, 85 mg/kg, sc) on the last 2 days. Hearts were excised and stained to detect the infarction size. Serum levels of cardiotoxicity indices as creatine kinase isoenzyme (CK-MB) and troponin I (cTnI) as well as the cardiac oxidative stress parameters as thiobarbituric acid reactive substances and superoxide dismutase were estimated. The expression of prodeath gene p53 and antideath gene Bcl-2 was also assessed from the excised heart tissues. Leakage of cardiac enzymes, elevated oxidative stress markers, and apoptotic indices confirmed the MI occurring as a consequence of isoproterenol-induced ischemia. Cerebrolysin pretreatment caused significant attenuation of the oxidative stress-induced apoptosis in the ischemic myocardial tissue. These findings provided an evidence that cerebrolysin could protect rat myocardium against ischemic insult that was attributed to its antioxidant as well as its anti-apoptotic properties.

show abstract

“…Changes in the APD, i.e., prolongation and shortening, were documented under ischemic/hypoxic conditions and during reperfusion ( Garg et al, 2015 ; Barbic et al, 2017 ; Chen et al, 2017 ; Garrott et al, 2017 ). The activation of ATP-dependent K + channels due to a lack of ATP results in AP shortening ( Benndorf et al, 1992 ).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Action Potential Prolongation During Metabolic Inhibition in the Whole Rabbit Heart

et al. 2018

View full text Add to dashboard Cite

Myocardial ischemia is associated with significant changes in action potential (AP) duration, which has a biphasic response to metabolic inhibition. Here, we investigated the mechanism of initial AP prolongation in whole Langendorff-perfused rabbit heart. We used glass microelectrodes to record APs transmurally. Simultaneously, optical AP, calcium transient (CaT), intracellular pH, and magnesium concentration changes were recorded using fluorescent dyes. The fluorescence signals were recorded using an EMCCD camera equipped with emission filters; excitation was induced by LEDs. We demonstrated that metabolic inhibition by carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP) resulted in AP shortening preceded by an initial prolongation and that there were no important differences in the response throughout the wall of the heart and in the apical/basal direction. AP prolongation was reduced by blocking the ICaL and transient outward potassium current (Ito) with diltiazem (DTZ) and 4-aminopyridine (4-AP), respectively. FCCP, an uncoupler of oxidative phosphorylation, induced reductions in CaTs and intracellular pH and increased the intracellular Mg2+ concentration. In addition, resting potential depolarization was observed, clearly indicating a decrease in the inward rectifier K+ current (IK1) that can retard AP repolarization. Thus, we suggest that the main currents responsible for AP prolongation during metabolic inhibition are the ICaL, Ito, and IK1, the activities of which are modulated mainly by changes in intracellular ATP, calcium, magnesium, and pH.

show abstract

β-Adrenergic stimulation and rapid pacing mutually promote heterogeneous electrical failure and ventricular fibrillation in the globally ischemic heart

Cited by 10 publications

References 62 publications

The Benefit of Prophylactic Implantable Cardioverter Defibrillator Implantation in Asymptomatic Heart Failure Patients With a Reduced Ejection Fraction

The Benefit of Prophylactic Implantable Cardioverter Defibrillator Implantation in Asymptomatic Heart Failure Patients With a Reduced Ejection Fraction

Effect of cerebrolysin on oxidative stress-induced apoptosis in an experimental rat model of myocardial ischemia

Mechanism of Action Potential Prolongation During Metabolic Inhibition in the Whole Rabbit Heart

Contact Info

Product

Resources

About