Suppression of Repeatedly Occurring Ventricular Fibrillation with Nifedipine in Variant Form of Angina Pectoris

Kimura, Eiichi; Tanaka, Keiji; Mizuno, Kyoichi; Honda, Yukiharu; Hashimoto, Haruo

doi:10.1536/ihj.18.736

Cited by 18 publications

(3 citation statements)

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“…This accords with several studies, of which that by Wellens et al (1977) exemplifies the failure of verapamil to inhibit chronic recurrent ventricular tachycardia during electrophysiological testing; with isolated and unpredictable exceptions, verapamil does not appear to be of clinical value against serious ventricular arrhythmias (Heng et al, 1975). Of course when the ventricular arrhythmias arise directly from ischaemia and this is relieved, calcium antagonists have, as a secondary phenomenon, antiarrhythmic value (Kimura et al, 1979) and the decrease in-reperfusion-induced ventricular arrhythmias seen experimentally with verapamil may be shown to be clinically useful (Ribeiro et al, 1981): further studies will demonstrate or negate this. Occasionally, patients with idiopathic, and prognostically usually benign, ventricular tachycardia do respond well to verapamil, so this may be a positive indication for trying it (Delise et al, 1985).…”

Section: Ventricular Arrhythmiassupporting

confidence: 73%

Verapamil in arrhythmia.

Krikler¹

1986

Brit J Clinical Pharma

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The antiarrhythmic effects of verapamil were observed before it was appreciated that it was a calcium ion‐antagonist. Intravenous verapamil is highly effective in the termination of paroxysmal reciprocating atrioventricular tachycardia, whether associated with preexcitation or involving the atrioventricular node alone. It consistently slows and regularises the ventricular response in atrial fibrillation, and usually increases the degree of AV‐nodal block in atrial flutter though it occasionally induces a return to sinus rhythm. Given orally it is useful for the prophylaxis of atrioventricular reentry tachycardia, and also in modulating the atrioventricular nodal response in atrial fibrillation. Favourable response in ventricular tachycardia is exceptional and then seen in specific benign varieties. Verapamil is the agent of choice for the termination of paroxysmal supraventricular tachycardia.

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Section: Ventricular Arrhythmiassupporting

confidence: 73%

Verapamil in arrhythmia.

Krikler¹

1986

Brit J Clinical Pharma

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“…Verapamil [75], nifedipine [58,59] as well as diltiazem [76] have all been shown to be strikingly effective in controlling frequent attacks of Prinzmetal's angina. Re peated attacks of ventricular fibrillation com plicating attacks of variant angina have also been shown to respond to slow channel in hibitors [77], The antiarrhythmic mechanism here is likely to be secondary' to the ameliora tion of myocardial ischemia resulting from coronary vasospasm. Especially noteworthyare the observations of Yasue et al [78] who have shown that recurrent episodes of vari ant angina in patients subject to coronaryvasospasm w'ere aggravated by p-adrenergic blockade but were abolished by orally ad ministered diltiazem.…”

Section: Asospastic a Nginamentioning

confidence: 98%

An Overview of Slow Channel Blocking Drugs: Pharmacological Basis for Therapeutic Applications

Singh¹

1982

Cardiology

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The use of voltage clamps in cardiac muscle has permitted the separation of two inward depolarizing membrane currents. The first is the fast sodium current, with rapid kinetics of activation and inactivation, which is blocked by local anesthetics. The second is the slow current carried largely by calcium ions, having slow kinetics with a long time constant of inactivation. Agents which selectively block this current are called Ca antagonists. Such agents are heterogeneous structurally; they also block calcium currents in smooth muscle and therefore produce coronary as well as peripheral vasodilatation. The most significant agents are verapamil, gallopamil, nifedipine, diltiazem and tiapamil. They have a varying spectrum of pharmacological effects with respect to changes they produce on heart rate, afterload, preload, contractility, coronary flow and on the AV node. A similar spectrum of therapeutic effects is apparent in different clinical disorders, in particular vasospastic angina, stable and unstable angina, cardiac arrhythmias, hypertension, hypertrophic cardiomyopathy and possibly other disorders. Indeed, the full range of clinical disorders which may respond to calcium antagonists is still not fully delineated and may well be at least as extensive as that for β-adrenoceptor blocking drugs. The advent of calcium antagonists in the last decade represents one of the most significant advances in cardiovascular therapeutics.

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“…Oral verapamil and digitalis can, however, safely be combined.78 While hypotension may occur, this is usually mild and transient; indeed verapamil can be given without ill-effect in patients with myocardial infarction.79 (b) VENTRICULAR ARRHYTHMIAS Though electrophysiological studies80 suggest that some ventricular arrhythmias arise because ischaemic cells become depolarised by the slow as opposed to the fast inward channel, and that this is blocked by verapamil, this drug has not proved effective under experimental conditions.8' Indeed, verapamil given during electrophysiological testing failed to inhibit chronic recurrent ventricular tachycardia.82 Some ventricular extrasystoles, whether or not associated with acute myocardial infarction, are suppressed by intravenous verapamil,7483 but clinical value against more serious ventricular arrhythmias has not been demonstrated.84 There is one clear exception: where coronary spasm induces ventricular arrhythmias, reversal of the spasm by a calcium antagonist has Dargie, Rowland, Knikler secondary but significant antiarrhythmic value. 85 Though there is good evidence that verapamil protects against the ventricular fibrillation in dogs caused either by coronary artery occlusion8687 or by release of occlusion, its clinical value under these circumstances would be difficult to demonstrate, and such evidence is lacking.…”

Section: Arrhythmias (A) Supraventricularmentioning

confidence: 99%

Role of calcium antagonists in cardiovascular therapy.

Dargie¹,

Rowland²,

Krikler³

1981

Heart

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SUMMARYThe development of drugs which selectively block the "slow" channels by which calcium enters the cell (calcium antagonists) has provided valuable information about the role of transmembrane calcium exchange in man and has offered new therapeutic approaches. The principal effect on the cardiovascular system is relaxation of vascular smooth muscle but some of these drugs also have electrophysiological effects, especially slowing of conduction in the atrioventricular node; verapamil is the agent of choice in supraventricular tachycardia. Significant myocardial depression does not usually occur with doses used clinically. The calcium antagonists have specific value in variant angina. By causing peripheral vasodilatation they are also effective hypotensive agents and do not cause reflex tachycardia in chronic use. Their value in hypertrophic cardiomyopathy and in the protection of ischaemic myocardium remains to be proven.

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Suppression of Repeatedly Occurring Ventricular Fibrillation with Nifedipine in Variant Form of Angina Pectoris

Cited by 18 publications

References 1 publication

Verapamil in arrhythmia.

Verapamil in arrhythmia.

An Overview of Slow Channel Blocking Drugs: Pharmacological Basis for Therapeutic Applications

Role of calcium antagonists in cardiovascular therapy.

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