Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

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 Blockers

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...

Pharmacokinetics: Drug–Drug Interactions

Pharmacokinetics: Drug–Drug Interactions

Drug interactions occur when the pharmacological effect of one drug is altered by another substance, either enhancing or diminishing its activity. The drug whose activity is altered is known as the object drug, and the substance causing the alteration is called the agent drug or the precipitant. The net effects of these interactions are mostly undesirable, leading to decreased effectiveness or increased adverse effects. In rare cases, interactions can be beneficial, such as the enhanced...

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

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 Blockers

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...

Pharmacokinetic–Pharmacodynamic Relationship: Influence of Elimination Half-Life on Effect Duration

Pharmacokinetic–Pharmacodynamic Relationship: Influence of Elimination Half-Life on Effect Duration

Drug elimination from the body primarily occurs through metabolic and excretion pathways. Hepatic metabolism transforms lipophilic drugs into hydrophilic forms for excretion, typically via enzymatic processes classified as phase I (modification) and phase II (conjugation). Renal excretion eliminates drugs and metabolites through filtration and secretion in the kidneys. Impairment in liver or kidney function can hinder these processes, delaying drug clearance and extending the drug’s half-life.

You might also read

Related Articles

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

Sort by

Same author

Predicted benefit of an implantable cardioverter-defibrillator: the MADIT-ICD benefit score.

European heart journal·2021

Same author

QRS fragmentations as predictors of arrhythmic events.

Kardiologia polska·2020

Same author

Remote Monitoring of Cardiac Implantable Electronic Devices in Patients Undergoing Hybrid Comprehensive Telerehabilitation in Comparison to the Usual Care. Subanalysis from Telerehabilitation in Heart Failure Patients (TELEREH-HF) Randomised Clinical Trial.

Journal of clinical medicine·2020

Same author

Reassessing the role of antitachycardia pacing in fast ventricular arrhythmias in primary prevention implantable cardioverter-defibrillator recipients: Results from MADIT-RIT.

Heart rhythm·2020

Same author

Effect of Hydroxychloroquine on Clinical Status at 14 Days in Hospitalized Patients With COVID-19: A Randomized Clinical Trial.

JAMA·2020

Same author

Mexiletine in Myotonic Dystrophy Type 1: A Randomized, Double-Blind, Placebo-Controlled Trial.

Neurology·2020

Search research articles

Related Experiment Video

Updated: Jul 3, 2026

Electrocardiogram Recordings in Anesthetized Mice using Lead II

Electrocardiogram Recordings in Anesthetized Mice using Lead II

Published on: June 20, 2020

Drug induced QT prolongation.

Wojciech Zareba

Cardiology Journal

|July 25, 2008

Summary

This summary is machine-generated.

Drug-induced QT prolongation, a risk factor for dangerous heart rhythms like torsades de pointes (TdP), is monitored using ECG. Understanding drug effects on ion channels aids in predicting and preventing TdP events.

More Related Videos

Zebra II as A Novel System to Record Electrophysiological Signals in Zebrafish

Zebra II as A Novel System to Record Electrophysiological Signals in Zebrafish

Published on: August 16, 2024

Related Experiment Videos

Last Updated: Jul 3, 2026

Electrocardiogram Recordings in Anesthetized Mice using Lead II

Electrocardiogram Recordings in Anesthetized Mice using Lead II

Published on: June 20, 2020

Zebra II as A Novel System to Record Electrophysiological Signals in Zebrafish

Zebra II as A Novel System to Record Electrophysiological Signals in Zebrafish

Published on: August 16, 2024

Area of Science:

Cardiology
Pharmacology
Electrophysiology

Background:

Drug-induced QT prolongation increases the risk of torsades de pointes (TdP) and sudden cardiac death.
QT prolongation serves as a surrogate marker for proarrhythmia risk due to the difficulty in directly linking specific drugs to TdP.
Most drugs prolong the QT interval by blocking the potassium IKr current or affecting channel protein trafficking.

Purpose of the Study:

To explore the mechanisms of drug-induced QT prolongation and TdP.
To highlight the importance of ECG in monitoring drug safety.
To discuss challenges in QT measurement and the need for advanced methods.

Main Methods:

Review of existing literature on drug-induced QT prolongation and TdP.
Discussion of the role of ion channel kinetics in cardiac repolarization.
Emphasis on ECG monitoring and emerging computerized methods for T wave analysis.

Main Results:

Understanding ion channel function is crucial for comprehending drug-induced QT prolongation.
Proarrhythmia often results from a combination of factors, including drug interactions and patient-specific conditions.
ECG monitoring, despite methodological challenges, is vital for drug safety.

Conclusions:

Novel computerized methods are being developed to quantify T wave alterations, aiding drug safety monitoring.
Individualized drug administration and monitoring systems, considering baseline QTc and drug effects, are necessary.
Further research into ion channel mechanisms and advanced ECG analysis can improve patient safety.