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Related Concept Videos

Decreased pulse rate01:14

Decreased pulse rate

Bradycardia is a medical condition in which the heart rate is slower than normal. It occurs when the heart's natural pacemaker, the sinus node, generates slower electrical impulses than the standard rhythm. In adults, bradycardia is diagnosed when the pulse rate falls below 60 beats per minute, indicating a deviation from the normal heart rate range.
There are specific risk factors that can elevate the likelihood of developing bradycardia. Advanced age is a significant factor, with bradycardia...
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...
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 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...
Adrenergic Antagonists: ɑ and β-Receptor Blockers01:31

Adrenergic Antagonists: ɑ and β-Receptor Blockers

Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is clinically...
Dysrhythmias IV: Characteristics of Bradyarrhythmias01:18

Dysrhythmias IV: Characteristics of Bradyarrhythmias

Bradyarrhythmias are cardiac rhythm disorders characterized by a slower-than-normal heart rate, typically defined as fewer than 60 beats per minute. Some of which are discussed here:Sinus BradycardiaSinus bradycardia presents a heart rate lower than 60 beats per minute, with a regular rhythm originating from the SA node. The ECG typically shows normal P waves preceding each QRS complex, a normal PR interval (0.12 to 0.20 seconds), and a normal QRS duration (0.06 to 0.10 seconds).First-Degree AV...

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Related Experiment Video

Updated: Jul 5, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
10:44

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

Thalidomide causes sinus bradycardia in ALS.

Thomas Meyer1, André Maier, Nadja Borisow

  • 1Dept. of Neurology, Charité University Hospital, Campus Virchow-Klinikum, Ambulanz für ALS und andere Motoneuronenerkrankungen, Augustenburger Platz 1, 13353 Berlin, Germany. thomas.meyer@charite.de

Journal of Neurology
|April 22, 2008
PubMed
Summary

Thalidomide treatment for Amyotrophic Lateral Sclerosis (ALS) caused significant bradycardia in 50% of patients, leading to study termination. This cardiac toxicity suggests Thalidomide is not suitable for ALS treatment.

Related Experiment Videos

Last Updated: Jul 5, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
10:44

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

Area of Science:

  • Neuroscience
  • Clinical Pharmacology
  • Cardiology

Background:

  • Neuroinflammation is implicated in motor neuron degeneration in Amyotrophic Lateral Sclerosis (ALS).
  • Thalidomide (THL), an anti-inflammatory agent, demonstrated increased lifespan in ALS transgenic mice.
  • THL was proposed as a potential therapeutic intervention for ALS.

Purpose of the Study:

  • To assess the safety, feasibility, and preliminary efficacy of Thalidomide (THL) in patients with ALS.
  • To evaluate THL as a treatment for Amyotrophic Lateral Sclerosis.

Main Methods:

  • A pilot, randomized clinical trial involving patients with ALS.
  • Patients were randomized to receive THL with riluzole (n=18) or riluzole alone (n=19).
  • THL dosage escalated from 100 mg/day to 400 mg/day over 6 weeks, planned for a total of 18 weeks.

Main Results:

  • 50% of patients (9/18) receiving THL developed bradycardia (heart rate < 60 bpm) within 12 weeks.
  • Mean heart rate decreased by 17 bpm in the THL group; one patient experienced severe bradycardia (30 bpm).
  • The study was prematurely terminated due to safety concerns, including one sudden unexpected death.

Conclusions:

  • Bradycardia was the most frequent adverse event associated with THL treatment in ALS patients.
  • THL-induced bradycardia may be linked to autonomic nervous system dysfunction in ALS.
  • The observed cardiac toxicity precludes further clinical trials and compassionate use of THL for ALS.