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

C Behrmann1, M Runge, J D Ringe

  • 1Medizinische Kernklinik und Poliklinik, Universitätsklinik Hamburg Eppendorf.

The Clinical Investigator
|October 1, 1992
PubMed

Insights

Calcium channel blockers like verapamil may influence heart rate and calcium level effects on QT time. This study explored verapamil

Area of Science:

  • Cardiology
  • Pharmacology
  • Electrophysiology

Background:

  • QT time typically decreases with increased heart rate and calcium levels.
  • Calcium channel blockers (CCBs) are known to affect cardiac electrophysiology.
  • Primary hyperparathyroidism can alter calcium metabolism and cardiac function.

Purpose of the Study:

  • To investigate how CCBs modify the QT interval's relationship with heart rate and calcium.
  • To examine the impact of atrial stimulation on CCB effects on QT time.
  • To assess verapamil's influence in patients with primary hyperparathyroidism.

Main Methods:

  • Measured QT time at spontaneous and stimulated heart rates (90-110 bpm) before and after verapamil.
  • Included 23 patients with primary hyperparathyroidism, assessed pre- and postoperatively.
  • Analyzed correlations between QT interval, heart rate (HR), and calcium (Ca) levels.

Main Results:

  • Atrial stimulation increased frequency-adjusted QT time values.
  • Verapamil reduced statistically significant correlations between QT vs. HR and QT vs. Ca.
  • Spontaneous heart rate was not affected by calcium levels or verapamil.

Conclusions:

  • Verapamil demonstrated an influence on the QT interval's relationship with heart rate and calcium.
  • The observed effect of verapamil did not reach statistical significance in this cohort.
  • Further research is needed to fully elucidate CCB modulation of QT interval dynamics in hyperparathyroidism.

Related Concept Videos

Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which indirectly block calcium...
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of the heart's...
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
Antiepileptic Drugs: Calcium Channel Blockers01:17

Antiepileptic Drugs: Calcium Channel Blockers

Calcium channel blockers, a class of antiepileptic drugs, regulate the flow of calcium ions within neurons.
Calcium channel blockers exert their antiepileptic effects by targeting T-type calcium channels, which are integral to transmitting nerve signals in the central nervous system. These channels allow the passage of calcium ions, which are vital for neuronal communication. By inhibiting T-type calcium channels, calcium channel blockers effectively reduce the release of neurotransmitters and...