Clinical Evaluation of Verapamil in Angina Pectoris

Sandler, Gerald; Clayton, Gerald; Thornicroft, S. G.

doi:10.1136/bmj.3.5612.224

Cited by 143 publications

(19 citation statements)

References 27 publications

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“…Verapamil has received both animal and clinical trial as an antiarrhythmic agent and as a coronary vasodilator for patients with angina pectoris (33)(34)(35)(36)(37)(38)(39)(40). Although verapamil seems to be fairly well tolerated intravenously and orally, the slowchannel inhibitors do possess a negative inotropic effect which may produce detrimental …”

Section: Effects On Av Nodal Conduction Of a Single Infusion Into Thementioning

confidence: 99%

Effects of Agents which Inhibit the Slow Channel on Sinus Node Automaticity and Atrioventricular Conduction in the Dog

Zipes

Fischer

1974

Circulation Research

267

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A slow ionic current carried by calcium, sodium, or both constitutes transmembrane ionic flow through the slow channel; such a current may be involved in normal action potentials of sinus and atrioventricular (AV) nodal cells. In this study, we investigated the effects of the slow-channel inhibiting agents verapamil, D600, manganous chloride, and lanthanum chloride on sinus node automaticity and AV nodal conduction in open-chest dogs treated with atropine (0.5 mg/kg) and propranolol (1.0 mg/kg). The arteries to the sinus node and the AV node were cannulated and perfused with agents that inhibit the slow current. These agents slowed sinus node discharge rate, depressed AV nodal conduction, and lengthened the effective and the functional AV nodal refractory period. Effects were dose related and reversed with time. His-Purkinje conduction remained normal. Isoproterenol and epinephrine reversed the effects of slow-channel inhibiting agents, but calcium, sodium, glucagon, and phenylephrine did not. Concentrations of propranolol which produced beta-receptor blockade prevented isoproterenol-induced reversal of the effects of slow-channel inhibitors. We concluded that (l) agents which inhibit the slow channel directly depress sinus node discharge rate and AV nodal conduction, (2) effects of slow-channel inhibiting agents are not mediated through the activation of cholinergic discharge or inhibition of adrenergic discharge, and (3) beta-receptor stimulation reverses these effects.

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Section: Effects On Av Nodal Conduction Of a Single Infusion Into Thementioning

confidence: 99%

Effects of Agents which Inhibit the Slow Channel on Sinus Node Automaticity and Atrioventricular Conduction in the Dog

Zipes

Fischer

1974

Circulation Research

267

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“…Verapamil also relieves effort angina. 5 The mode of action of verapamil is not fully understood, but side effects even at high dosage are uncommon. Objective studies comparing the effects of f3 blockers with those of verapamil in the treatment of stable effort angina are few.…”

mentioning

confidence: 99%

A double-blind randomized trial of propranolol and verapamil in the treatment of effort angina.

Sadick¹,

Tan²,

Fletcher³

et al. 1982

Circulation

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“…[1][2][3][4] Hence, verapamil appears to be an effective therapeutic alternative to /-adrenergic blocking drugs; it is especially useful in patients refractory to or experiencing important side effects from /3-blocking drugs.4…”

Section: Discussionmentioning

confidence: 99%

Effects of verapamil and propranolol on left ventricular systolic function and diastolic filling in patients with coronary artery disease: radionuclide angiographic studies at rest and during exercise.

Bonow¹,

Leon²,

Rosing³

et al. 1982

Circulation

139

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To determine the effects of verapamil on left ventricular (LV) systolic function and diastolic filling in patients with coronary artery disease (CAD), we performed gated radionuclide angiography at rest and during exercise in 16 symptomatic patients before and during oral verapamil therapy (480 mg/day). Twelve patients were also studied during oral propranolol (160--320 mg/day). LV ejection fraction at rest was normal in 13 patients, but abnormal diastolic filling at rest, defined as peak filling rate (PFR) less than 2.5 end-diastolic volumes (EDV)/sec or time to PFR greater than 180 msec, was present in 15. During verapamil, resting ejection fraction decreased (control 50 +/- 10% [+/- SD), verapamil 45 +/- 12%, p less than 0.005), but resting diastolic filling improved: PFR increased (control 1.9 +/- 0.6 EDV/sec, verapamil 2.3 +/- 0.9 ECV/sec, p less than 0.005) and time to PFR decreased (control 185 +/- 38 msec, verapamil 161 +/- 27 msec, p less than 0.05). Exercise ejection fraction did not change during verapamil (control 42 +/- 13%, verapamil 43 +/- 12%, NS), but exercise PFR increased (control 3.1 +/- 0.9 EDV/sec, verapamil 3.6 +/- 1.1 EDV/sec, p less than 0.05) and exercise time to PFR decreased (control 108 +/- 30 msec, verapamil 91 +/- 17 msec, p less than 0.05). In contrast, propranolol did not alter ejection fraction, PFR, or time to PFR at rest or during exercise. Thus, LV ejection fraction is decreased by verapamil at rest but is unchanged during exercise. While LV systolic function is not improved by verapamil, LV diastolic filling is enhanced by verapamil, both at rest and during exercise. These mechanisms may account in part for the symptomatic improvement in many patients during verapamil therapy.

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Clinical Evaluation of Verapamil in Angina Pectoris

Cited by 143 publications

References 27 publications

Effects of Agents which Inhibit the Slow Channel on Sinus Node Automaticity and Atrioventricular Conduction in the Dog

Effects of Agents which Inhibit the Slow Channel on Sinus Node Automaticity and Atrioventricular Conduction in the Dog

A double-blind randomized trial of propranolol and verapamil in the treatment of effort angina.

Effects of verapamil and propranolol on left ventricular systolic function and diastolic filling in patients with coronary artery disease: radionuclide angiographic studies at rest and during exercise.

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