Effects of Carvedilol on Ventricular Arrhythmias

Senior, Roxy; Müller-Beckmann, B.; Dasgupta, P; Does, R. van der; Lahiri, Avijit

doi:10.1097/00005344-199219001-00023

Cited by 29 publications

(18 citation statements)

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“…A significant QT prolongation has not been observed in patients treated with carvedilol (95). In patients with nonischemic dilated cardiomyopathy, treatment with carvedilol reduced QTc dispersion in their electrocardiograms (ECGs) (28).…”

Section: Electrophysiologic Effectsmentioning

confidence: 99%

Carvedilol: Molecular and Cellular Basis for Its Multifaceted Therapeutic Potential

Cheng

Kamiya

Kodama

2001

Cardiovascular Drug Reviews

115

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Carvedilol is a unique cardiovascular drug of multifaceted therapeutic potential. Its major molecular targets recognized to date are membrane adrenoceptors (â 1 , â 2 , and á 1 ), reactive oxygen species, and ion channels (K + and Ca 2+ ). Carvedilol provides prominent hemodynamic benefits mainly through a balanced adrenoceptor blockade, which causes a reduction in cardiac work in association with peripheral vasodilation. This drug assures remarkable cardiovascular protection through its antiproliferative/atherogenic, antiischemic, antihypertrophic, and antiarrhythmic actions. These actions are a consequence of its potent antioxidant effects, amelioration of glucose/lipid metabolism, modulation of neurohumoral factors, and modulation of cardiac electrophysiologic properties. The usefulness of carvedilol in the treatment of hypertension, ischemic heart disease, and congestive heart failure is based on a combination of hemodynamic benefits and cardiovascular protection.

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Section: Electrophysiologic Effectsmentioning

confidence: 99%

Carvedilol: Molecular and Cellular Basis for Its Multifaceted Therapeutic Potential

Cheng

Kamiya

Kodama

2001

Cardiovascular Drug Reviews

115

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“…12 The clinical antiarrhythmic efficacy of carvedilol was demonstrated by Holter monitoring in an uncontrolled open study of 65 patients who were treated for hypertension, HF, or angina. 13 After 4-8 weeks of carvedilol treatment, the number of premature ventricular contractions (PVCs) had decreased from 26 to 6/h, and 23% of patients with multifocal PVCs converted to a unifocal morphology. Nonsustained VT that had been present in four patients was absent at follow-up.…”

Section: Ventricular Arrhythmiasmentioning

confidence: 99%

“…8). 13 The effect of carvedilol on complex, nonsustained ventricular arrhythmias was more rigorously evaluated in a randomized, placebo-controlled clinical trial in patients with dilated cardiomyopathy. 46 In this study, carvedilol or placebo was added to conventional therapy that included digitalis, diuretics, and ACE inhibitors in 168 patients with ischemic or nonischemic cardiomyopathy and Lown class III-V ventricular arrhythmias (multifocal or repetitive PVCs, VT, or R-on-T).…”

Section: Ventricular Arrhythmiasmentioning

confidence: 99%

“…Carvedilol's other electrophysiologic effects are underappreciated and include direct membrane-stabilizing activity (Class IA); prolonging repolarization by blocking potassium channels (Class III); and inhibiting L-type calcium channels (Class IV). [9][10][11][12][13] These effects appear to be without any known ventricular proarrhythmic activity.…”

Section: Introductionmentioning

confidence: 99%

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Carvedilol's antiarrhythmic properties: Therapeutic implications in patients with left ventricular dysfunction

Naccarelli

Lukas

2005

Clinical Cardiology

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Summary:Carvedilol is a beta-and alpha-adrenergic-blocking drug with clinically important antiarrhythmic properties. It possesses anti-ischemic and antioxidant activity and inhibits a number of cationic channels in the cardiomyocyte, including the HERG-associated potassium channel, the L-type calcium channel, and the rapid-depolarizing sodium channel. The electrophysiologic properties of carvedilol include moderate prolongation of action potential duration and effective refractory period; slowing of atrioventricular conduction; and reducing the dispersion of refractoriness. Experimentally, carvedilol reduces complex and repetitive ventricular ectopy induced by ischemia and reperfusion.In patients, carvedilol is effective in controlling the ventricular rate response in atrial fibrillation (AF), with and without digitalis, and is useful in maintaining sinus rhythm after cardioversion, with and without amiodarone. In patients with AF and heart failure (HF), carvedilol reduces mortality risk and improves left ventricular (LV) function. Large-scale clinical trials have demonstrated that combined carvedilol and angiotensin-converting enzyme inhibitor therapy significantly reduces sudden cardiac death, mortality, and ventricular arrhythmia in patients with LV dysfunction (LVD) due to chronic HF or following myocardial infarction (MI).Despite intensive neurohormonal blockade, mortality rates remain relatively high in patients with post-MI and nonischemic LVD. Recent trials of implantable cardioverter-defibrillators added to pharmacologic therapy, especially beta blockers, have shown a further reduction in arrhythmic deaths in these patients.

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“…8,[10][11][12] Indeed, it has been demonstrated that carvedilol suppresses ventricular arrhythmias in patients with hypertension, angina pectoris, and congestive heart failure, and reduces the frequency of lethal ventricular arrhythmias in severe heart failure. 12,14) However, it is not clear whether the reduction in these arrhythmic events is due to a direct action of the drug or secondary effects caused by improved cardiac function.…”

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confidence: 99%

Electrophysiological Effects of Carvedilol on Rabbit Heart Pacemaker Cells

et al. 2007

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SUMMARYThe electrophysiological effects of carvedilol, a β-blocking agent with vasodilating actions, have been studied on rabbit pacemaker cells using the whole-cell patch clamp technique. Nystatin-perforated patch recordings from the sinoatrial (SA) and atrioventricular (AV) nodes demonstrated that 1-3 µM of carvedilol caused a decrease in the spontaneous firing frequency, depolarization of the maximal diastolic potential, and prolongation of the action potential duration in both species. Voltage clamp experiments were performed using SA and AV node myocytes to identify and define the carvedilolinduced changes in the Ca 2+ current, I Ca , delayed rectifier K + current, I K , and hyperpolarization-activated inward current, I f . In the SA node cells, 1 µM of carvedilol blocked I K , I Ca , and I f by 72%, 47%, and 22%, respectively. In the AV node cells, the corresponding reductions were 64% (I K ) and 46% (I Ca ), respectively. In both the SA and AV nodes the decrease in I K appeared to be mainly due to the rapidly activating component of the delayed rectifier, I Kr , since the high dose of carvedilol blocked I K in the SA and AV nodes to a submaximal degree. In conclusion, effective doses of carvedilol have classical class III antiarrhythmic actions and a negative chronotropic effect resulting from the inhibition of I K and I Ca . Both actions may be efficacious for treating supraventricular tachyarrhythmias. (Int Heart J 2007; 48: 347-358)

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Effects of Carvedilol on Ventricular Arrhythmias

Cited by 29 publications

References 0 publications

Carvedilol: Molecular and Cellular Basis for Its Multifaceted Therapeutic Potential

Carvedilol: Molecular and Cellular Basis for Its Multifaceted Therapeutic Potential

Carvedilol's antiarrhythmic properties: Therapeutic implications in patients with left ventricular dysfunction

Electrophysiological Effects of Carvedilol on Rabbit Heart Pacemaker Cells

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