Effect on paroxysmal re-entrant supraventricular tachycardia of a drug affecting calcium transport (Ro 11-1781)

Self Cite

The effects of tiapamil were studied in 10 patients with antegrade preexcitation using programmed stimulation of the heart. Before administration of the drug, it was possible to initiate sustained orthodromic tachycardia in 7 patients, antidromic tachycardia in 2 and atrial echoes in 1 case by premature atrial and/or ventricular stimulation. An intravenous bolus of 2 mg/kg tiapamil terminated the tachycardia in 7 out of 8 cases by blocking the A-V node. The tachycardia continued at a reduced heart rate in 1 case with a nodoventricular bypass. Tiapamil lengthened the effective A-V nodal refractory period in 1 patient in whom it could be measured and the atrial effective refractory period in 1 case but did not prolong the antegrade or retrograde refractory periods of the accessory pathway. Only in 1 case was the antegrade effective refractory period of the accessory pathway shortened by tiapamil. The A-V nodal conduction time (A-H interval) was prolonged. Following tiapamil it was not possible to initiate the tachycardia in 4 cases and atrial echoes in 1 case; in 2 patients the tachycardia zone widened and in 3 it was not altered. In the latter, the cycle length of the tachycardia increased. Tiapamil appears to be of therapeutic value for the termination of tachycardia and also for its prevention in some cases. In others, it may facilitate the initiation of tachycardia. The delayed A-V nodal conduction during sinus rhythm augments the area of ventricular preexcitation which may facilitate the electrocardiographic localization of the accessory pathway.

Section: Introductionsupporting

confidence: 66%

“…Our methods of stimulation and record ing techniques have been described elsewhere [1,2]. In brief, three or four catheters were positioned in the high right atrium, below the tricuspid valve, and at the apex of the right ventricle.…”

Section: Methodsmentioning

confidence: 99%

Effect of Tiapamil in the Preexcitation Syndrome

Gmeiner¹,

Ng²,

Hochleitner³

1982

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“…scsses electrophysiological effects similar to those of verapamil, provided that the dose employed is high enough [3]. An intravenous dose of 2 mg/kg tiapamil terminated circus movement tachycardias which involved the A-V node as an essential part of the reentry circuit [1,4]. The present report reviews our experience with intravenous tiapamil in a special subset of reciprocating tachycardias.…”

Section: Discussionmentioning

confidence: 99%

“…White syndrome [1][2][3][4], The present paper reviews our experience with intravenous tia pamil in patients with concealed accessory pathways.…”

Section: Introductionmentioning

confidence: 99%

Electrophysiology of Tiapamil in Concealed Accessory Pathways

Gmeiner¹,

Ng²

1982

Self Cite

The effect of 2 mg/kg intravenous tiapamil was studied by programmed stimulation of the heart in 6 patients. Before tiapamil, sustained tachycardias were initiated in 5, and only atrial echoes in 1. In all patients, the reentrant circuit involved an accessory pathway conducting only in the ventriculoatrial direction. When administered during tachycardia, tiapamil promptly terminated the arrhythmia in 5 cases. Tiapamil lengthened the atrio-His (A-H) interval and the effective refractory period of the A-V node. As a result of these changes, it was not possible to initiate the tachycardia in 1 patient. In 1 case, tiapamil permitted the induction of sustained tachycardia, while only echoes had been initiated before the drug. In 2 cases, the tachycardia zone narrowed, in 2 others it widened following tiapamil. The ability to sustain the arrhythmia was lost in 1 patient. Tiapamil may be useful for the termination of reentrant supraventricular tachycardia involving concealed accessory pathways. Whether tiapamil prevents or favors the initiation of tachycardia in these patients depends on the interplay between the prolongation of the effective A-V nodal refractory period and the prolongation of the transnodal conduction time in individual patients.

“…This com ponent may contribute to the antiarrhythmic activity of tiapamil observed in both experi mental [Kievans and Kovacs, unpubl.) and clinical studies [28][29][30].…”

Section: Discussionmentioning

confidence: 99%

Overview on the Pharmacological and Toxicological Characterization of the Calcium Antagonist Tiapamil

Haeusler¹,

Eigenmann²,

Gerold³

et al. 1982

The results obtained in a variety of isolated organ preparations characterize tiapamil as a calcium antagonist or calcium entry blocker. Tiapamil inhibited in a concentration-dependent manner calcium-induced contractions in isolated, potassium-depolarized preparations of rat renal artery, dog coronary artery and rabbit main pulmonary artery and reduced ⁴⁵Ca influx into depolarized vascular smooth muscle cells. The inhibitory effects of tiapamil were surmountable by an elevation of the extracellular calcium concentration. Calcium-mediated, slowly rising potentials in partially depolarized guinea pig papillary muscle, evoked by electrical stimulation in the presence of isoprenaline, were also antagonized by tiapamil. As in vascular muscle, the tiapamil effects in cardiac muscle were reduced by elevation of external calcium.Tiapamil altered haemodynamic parameters in a characteristic sequence, with an increase in coronary flow appearing at the lowest effective doses, followed by decreases in blood pressure, total peripheral vascular resistance and, eventually, heart rate. A depression of myocardial contractility was not found at doses which are considered to be therapeutic. After cardiac autonomic denervation, tiapamil produced a dose-dependent bradycardia. However, cardiac denervation did not alter the extent of tiapamil-induced decreases in coronary vascular resistance and did not unmask a potential negative inotropic effect of the drug. A comparison of various vascular preparations suggested a certain degree of selectivity for coronary arteries in the calcium antagonistic action of tiapamil. The haemodynamic findings are in line with these in vitro results.A coronary segmental analysis revealed that tiapamil acts on small coronary arteries. It differs in this respect from nitroglycerin which dilates large coronary arteries. Tiapamil increased pO₂ in the subendocardial layers of the myocardium percentagewise more than in the subepicardial layers. Furthermore, it reduced experimentally-induced myocardial ischaemia as determined by a reduction of the S-T segment elevation of the epicardial ECG after ligation of a coronary artery.