Action of verapamil on sinus node, atrioventricular, and intraventricular conduction.

Husaini, M; Kvasnička, J; Ryèn, L; Holmberg, Stig

doi:10.1136/hrt.35.7.734

Cited by 111 publications

(13 citation statements)

References 9 publications

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“…As has previously been shown by Neuss and Schlepper (1971), Husaini et al (1973), and Roy et al (1974), verapamil lengthens the refractory period of the AV node and the transnodal conduction time. We found that both in patients with re-entrant AV nodal tachycardia and in patients with a concealed AV pathway, termination of Ag-H2 interval at the time of initiation of tachycardia before verapamil, as in Fig.…”

Section: Discussionsupporting

confidence: 70%

Effect of verapamil studied by programmed electrical stimulation of the heart in patients with paroxysmal re-entrant supraventricular tachycardia.

Wellens¹,

Tan²,

Bär³

et al. 1977

Heart

153

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Section: Discussionsupporting

confidence: 70%

Effect of verapamil studied by programmed electrical stimulation of the heart in patients with paroxysmal re-entrant supraventricular tachycardia.

Wellens¹,

Tan²,

Bär³

et al. 1977

Heart

153

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“…However, it has been suggested that verapamil can promote adverse cardiovascular effects, especially in coronary heart disease and in the failing heart, probably due to its pro-ischemic, negative inotropic and proarrhythmic effects [25,26]. Moreover, excessive concentrations of verapamil may cause sinoatrial (SA) nodal asystole and varying degrees of AV blocks [27]. In line with these side effects we could demonstrate arrhythmic beating of cardiac clusters within EBs in the presence of this drug, up to the complete excitation block.…”

Section: Discussionmentioning

confidence: 99%

Effect of Cardioactive Drugs on Action Potential Generation and Propagation in Embryonic Stem Cell-Derived Cardiomyocytes

Reppel

Igelmund

Egert

et al. 2007

Cell Physiol Biochem

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Extracellular recordings of spontaneous electrical activity in contracting cardiac clusters differentiated from murine embryonic stem cells enable to study electrophysiological features of this in-vitro cardiac-like tissue as well as effects of pharmacological compounds on its chronotropy and electrical conduction. To test if the microelectrode array (MEA) system could serve as a basis for development of a pharmacological screening tool for cardioactive drugs, we used spontaneously beating outgrowths of three-dimensional ES cell aggregates (“embryoid bodies”, EBs) plated onto substrate-integrated MEAs. The effects of the L-type Ca²⁺ channel antagonist verapamil and Na⁺ and K⁺ channel blockers (tetrodotoxin, 4-aminopyridine, and sparfloxacin) on the deduced interrelated cardiac network function were investigated. Application of 10^-6 M verapamil led to arrhythmic spiking with a burst-like pattern; at a higher concentration (10^-5 M) the drug caused a sustained negative chronotropy up to complete stop of beating. In the presence of tetrodotoxin a conduction block was observed. Since modulation of K⁺ channel activity can cause anti- or proarrhythmic effects, the influence of K⁺ channel blockers, namely 4-aminopyridine and sparfloxacin, was investigated. 4-aminopyridine (2x10^-3 M) significantly stabilized beating frequency, while the field potential duration (FPD) was concentration-dependently prolonged up to 2.7-fold. Sparfloxacin (3x10^-6 M) stabilized the beating frequency as well. At a higher concentration of sparfloxacin (3x10^-5 M), a significant prolongation of the spike duration was registered; application of the drug caused also early afterdepolarizations. The results demonstrate a suitability of the studied in-vitro cardiac cell model for pharmacological drug testing in cardiovascular research.

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“…We did not observe verapamil-induced changes of the spontaneous heart rate after intravenous application, which can be due to the fact that the blood pressure remained stable during our study in supine patients. An increased heart rate 5-10 min after intravenous injection is described by other investigators due to a drop in blood pressure [14]. The significant difference of the verapamil effects on the heart rate in hypercalcemia and normocalcemia could be explained by the observation that verapamil action can be abolished by high calcium levels.…”

Section: Discussionmentioning

confidence: 64%

“…The significant difference of the verapamil effects on the heart rate in hypercalcemia and normocalcemia could be explained by the observation that verapamil action can be abolished by high calcium levels. In particular, the AV node conduction time prolongation and the negative inotropic effects [14,16] can be reversed.…”

Section: Discussionmentioning

confidence: 99%

Effects of calcium channel blocking and atrial stimulation on QT time during hyper- and normocalcemia in man

Behrmann

Runge²,

Ringe

1992

Clin Investig

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We investigated how calcium channel blocking agents modify the known decrease of QT time with increasing heart rate and calcium level. Furthermore, we examined how the influence of calcium channel blocking agents is modulated by atrial stimulation. To answer these questions, we measured the QT time both at a spontaneous heart rate and during atrial stimulation with 90 and 110 beats/min before and after intravenous administration of 5 mg verapamil in 23 patients with primary hyperparathyroidism, pre- and postoperatively. Atrial stimulation increased the frequency-related standard values of QT time. The spontaneous heart rate (HR) was influenced by neither the calcium level nor verapamil. The statistically significant correlations QT vs. HR and QT vs. Ca were reduced by verapamil, which indicated its influence. However, this effect did not achieve statistical significance.

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Action of verapamil on sinus node, atrioventricular, and intraventricular conduction.

Cited by 111 publications

References 9 publications

Effect of verapamil studied by programmed electrical stimulation of the heart in patients with paroxysmal re-entrant supraventricular tachycardia.

Effect of verapamil studied by programmed electrical stimulation of the heart in patients with paroxysmal re-entrant supraventricular tachycardia.

Effect of Cardioactive Drugs on Action Potential Generation and Propagation in Embryonic Stem Cell-Derived Cardiomyocytes

Effects of calcium channel blocking and atrial stimulation on QT time during hyper- and normocalcemia in man

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