β-Adrenergic blocking drugs as antifibrillatory agents

Reiter, Michael J.

doi:10.1007/s11886-002-0043-3

Cited by 10 publications

(6 citation statements)

References 60 publications

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“…Reduction in the incidence of sudden death is responsible (at least in part) for the survival benefit afforded by beta blockade in clinical trials (1). β-Blockers reduce arrhythmogenesis following infarction by attenuating both neural and humoral sympathetic actions (235,297,303). Several additional actions of β-blockers may contribute to their beneficial effects.…”

Section: β-Blockersmentioning

confidence: 99%

Pathophysiology of Myocardial Infarction

Frangogiannis

2015

Comprehensive Physiology

501

391

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Myocardial infarction is defined as sudden ischemic death of myocardial tissue. In the clinical context, myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function. Prolonged myocardial ischemia activates a "wavefront" of cardiomyocyte death that extends from the subendocardium to the subepicardium. Mitochondrial alterations are prominently involved in apoptosis and necrosis of cardiomyocytes in the infarcted heart. The adult mammalian heart has negligible regenerative capacity, thus the infarcted myocardium heals through formation of a scar. Infarct healing is dependent on an inflammatory cascade, triggered by alarmins released by dying cells. Clearance of dead cells and matrix debris by infiltrating phagocytes activates anti-inflammatory pathways leading to suppression of cytokine and chemokine signaling. Activation of the renin-angiotensin-aldosterone system and release of transforming growth factor-β induce conversion of fibroblasts into myofibroblasts, promoting deposition of extracellular matrix proteins. Infarct healing is intertwined with geometric remodeling of the chamber, characterized by dilation, hypertrophy of viable segments, and progressive dysfunction. This review manuscript describes the molecular signals and cellular effectors implicated in injury, repair, and remodeling of the infarcted heart, the mechanistic basis of the most common complications associated with myocardial infarction, and the pathophysiologic effects of established treatment strategies. Moreover, we discuss the implications of pathophysiological insights in design and implementation of new promising therapeutic approaches for patients with myocardial infarction.

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Section: β-Blockersmentioning

confidence: 99%

Pathophysiology of Myocardial Infarction

Frangogiannis

2015

Comprehensive Physiology

501

391

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“…In human and animal experiments, 23,24 β 1 ‐adrenoceptor antagonists have been shown to exert pronounced antifibrillatory effects in preventing the occurrence of ventricular tachycardia and ventricular fibrillation. Ogawa et al 25 .…”

Section: Discussionmentioning

confidence: 99%

Bisoprolol Inhibits Sodium Current in Ventricular Myocytes of Rats With Diastolic Heart Failure

Tang

Chun-yu

et al. 2007

Clin Exp Pharma Physio

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1. Changes in sodium currents (I(Na)) in heart failure contribute to cardiac electrophysiological alterations and, thereby, to ventricular arrhythmias. Bisoprolol has anti-arrhythmic effects, but its direct effect on I(Na) in cardiac cells remains unclear. Accordingly, in the present study we investigated the effects of bisoprolol on ventricular I(Na) in diastolic heart failure (DHF) and normal rats. 2. The DHF model was produced by abdominal aortic coarctation for 4 weeks and single ventricular myocytes were isolated by enzymatic dissociation. The electrophysiological actions of bisoprolol on I(Na) currents were investigated using a whole-cell patch-clamp technique. 3. The membrane capacitance of rats in the DHF group was significantly greater than that of the control group and the current-voltage curve was simultaneously shifted downward. Bisoprolol concentration-dependently decreased I(Na) in ventricular myocytes of both groups (at -45 mV), with IC(50) values of 19.53 +/- 0.06 and 40.78 +/- 0.03 micromol/L in the control and DHF groups, respectively. 4. In both groups, the current-voltage curves were shifted upwards, whereas activation potentials, peak currents and reversal potentials showed no significant changes. At -45 mV, the descent ratio of current densities in the DHF group was lower than that of the control group. In both groups, inactivation curves were shifted to more negative potentials, but activation curves and recovery curves were not altered. Changes in the half-inactivation voltage, V(0.5), and the slope of the inactivation curve, S, were similar for both groups. 5. In conclusion, bisoprolol concentration-dependently decreases I(Na) in ventricular myocytes of DHF and normal rats, which could be responsible, at least in part, for its anti-arrhythmic effects.

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“…[25][26][27][28] β-blockers in general, and carvedilol in particular, may decrease mortality by a variety of mechanisms, including direct and indirect antiarrhythmic effects. [29][30][31] An early study revealed that carvedilol decreases the incidence of ventricular premature beats and nonsustained ventricular tachycardia. 32 A more recent doubleblind placebo-controlled study showed that the antiarrhythmic efficacy of carvedilol in patients with ischemic or nonischemic cardiomyopathy was paralleled by an improvement in ejection fraction independent of the etiology of heart failure.…”

Section: Clinical Correlationmentioning

confidence: 99%

“…35 In recent years interest has grown in examining the role of β-blockers in rate control and conversion to sinus rhythm in patients with atrial fibrillation. 31,38,39 Carvedilol is known to reduce morbidity and mortality and to improve hemodynamic status in patients with heart failure across a broad spectrum of clinical severity. Recent data indicate that these benefits extend to patients with chronic heart failure complicated by atrial fibrillation.…”

Section: Clinical Correlationmentioning

confidence: 99%

Electrophysiologic Effects of Carvedilol: Is Carvedilol an Antiarrhythmic Agent?

El‐Sherif

Turitto

2005

Pacing Clinical Electrophis

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The cardiovascular drug carvedilol is characterized by multiple pharmacological actions, which translate into a wide-spectrum therapeutic potential. Its major molecular targets are membrane adrenoceptors, ion channels, and reactive oxygen species. Carvedilol's favorable hemodynamic effects are due to the fact that the drug competitively blocks beta(1)-, beta(2)-, and alpha(1)- adrenoceptors. Several additional properties have been documented and may be clinically important, including antioxidant, antiproliferative/antiatherogenic, anti-ischemic, and antihypertrophic effects. The antiarrhythmic action of carvedilol may be related to a combination of its beta-blocking effects with its modulating effects on a variety of ion channels and currents. Several studies suggest that the drug may be useful in reducing cardiac death in high-risk patients with prior myocardial infarction and/or heart failure, as well as for primary and secondary prevention of atrial fibrillation. This article will review experimental data available on the electrophysiologic properties of carvedilol, with a focus on their clinical relevance.

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β-Adrenergic blocking drugs as antifibrillatory agents

Cited by 10 publications

References 60 publications

Pathophysiology of Myocardial Infarction

Pathophysiology of Myocardial Infarction

Bisoprolol Inhibits Sodium Current in Ventricular Myocytes of Rats With Diastolic Heart Failure

Electrophysiologic Effects of Carvedilol: Is Carvedilol an Antiarrhythmic Agent?

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