Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
Targets for Drug Action: Overview01:26

Targets for Drug Action: Overview

Drugs target macromolecules to modify ongoing cellular processes. Primary drug targets include receptors, ion channels, transporters, and enzymes.
Receptors are either membrane-spanning or intracellular proteins, which upon binding a ligand, get activated and transmit the signal downstream to elicit a response. Drugs bind receptors, either mimicking the action of endogenous ligands or blocking the receptor activity to bring about a modified response. Nearly 35% of approved drugs target the G...
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...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

National genomic profiling of Plasmodium falciparum antimalarial resistance in Zambian children participating in the 2018 malaria indicator survey.

Scientific reports·2026
Same author

Cost and cost-effectiveness of attractive targeted sugar baits (ATSB) in the context of a phase III cluster randomized control trial in Western Province, Zambia.

Malaria journal·2025
Same author

Localized Re-Entry Involving the Coronary Sinus: The Latest Model of Manufactured Arrhythmias.

JACC. Clinical electrophysiology·2025
Same author

Plasmodium falciparum Genomic Surveillance Reveals a Diversity of Kelch 13 Mutations in Zambia.

The American journal of tropical medicine and hygiene·2025
Same author

Impact of proactive malaria community case management (proCCM) on parasite prevalence and incidence from 2021 to 2023: a randomised controlled trial in Chadiza District, Eastern Province, Zambia.

BMJ global health·2025
Same author

High-Density Lipoprotein Particles, Inflammation, and Coronary Heart Disease Risk.

Nutrients·2025

Related Experiment Video

Updated: Jul 11, 2026

Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation
28:13

Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation

Published on: February 26, 2013

Pharmacologic targets for atrial fibrillation.

Deepak Bhakta1, John M Miller

  • 1Indiana University School of Medicine, Krannert Institute of Cardiology, 1800 N. Capitol Avenue, Indianapolis, IN 46202, USA. dbhakta@iupui.edu

Expert Opinion on Therapeutic Targets
|September 12, 2007
PubMed
Summary

New antiarrhythmic drugs targeting atrial fibrillation (AF) focus on novel mechanisms beyond ion channels. These next-generation therapies aim for improved safety and efficacy in treating this common heart arrhythmia.

More Related Videos

The WATCHMAN Left Atrial Appendage Closure Device for Atrial Fibrillation
23:33

The WATCHMAN Left Atrial Appendage Closure Device for Atrial Fibrillation

Published on: February 28, 2012

Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats
05:12

Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats

Published on: February 14, 2022

Related Experiment Videos

Last Updated: Jul 11, 2026

Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation
28:13

Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation

Published on: February 26, 2013

The WATCHMAN Left Atrial Appendage Closure Device for Atrial Fibrillation
23:33

The WATCHMAN Left Atrial Appendage Closure Device for Atrial Fibrillation

Published on: February 28, 2012

Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats
05:12

Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats

Published on: February 14, 2022

Area of Science:

  • Cardiology
  • Pharmacology
  • Biomedical Science

Background:

  • Atrial fibrillation (AF) is the most prevalent human arrhythmia, persisting despite treatment advances.
  • Current antiarrhythmic drugs, primarily targeting cardiac ion channels, offer limited efficacy and carry risks like ventricular proarrhythmia.

Purpose of the Study:

  • To explore novel therapeutic strategies for atrial fibrillation (AF).
  • To investigate the potential of targeting non-ionic mechanisms and atrial-specific ion channels for improved AF treatment.

Main Methods:

  • Review of current antiarrhythmic drug therapies and their limitations.
  • Analysis of emerging drug development focusing on novel molecular targets in AF.

Main Results:

  • Conventional antiarrhythmic drugs show modest AF suppression and proarrhythmic risks.
  • New drug development is exploring atrial-specific ion channels and non-ionic targets.

Conclusions:

  • Targeting novel non-ionic mechanisms in AF may lead to drugs with greater potency.
  • Future antiarrhythmic agents acting on new targets hold promise for enhanced safety and efficacy in AF management.