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Mechanism of Cardiac Arrhythmias

Mechanism of Cardiac Arrhythmias

Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.

Cardiac Action Potential

Cardiac Action Potential

Cardiac action potentials are essential for proper heart function, enabling the rhythmic contractions needed for adequate blood circulation. Nodal cells and Purkinje fibers, specialized for electrical conduction, generate these action potentials.
The cardiac action potential process involves a series of phases characterized by the movement of ions across the cardiac cell membranes, leading to the depolarization and repolarization of the cardiac myocytes.
Ionic Basis of Cardiac Action Potentials

Depolarizing Blockers: Mechanism of Action

Depolarizing Blockers: Mechanism of Action

Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because...

ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias

ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias

Arrhythmia is a condition characterized by an irregular heart rhythm, with ECG changes that differ based on its origin and nature. The types of arrhythmias discussed below include atrial, junctional, and ventricular arrhythmias.Atrial ArrhythmiasPremature Atrial Complexes (PACs): PACs are early atrial beats caused by stress, caffeine, alcohol, electrolyte imbalances, hypoxia, hyperthyroidism, or certain medications (e.g., bronchodilators and decongestants). The ECG shows early P waves with an...

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Related Experiment Video

Updated: May 5, 2026

Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples

Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples

Published on: April 21, 2014

Active Colitis Attenuates Ventricular Excitation-Contraction Coupling by T-Tubular Remodeling.

Edward J Ouille V¹, Carlos H Pereira¹, Ygor Marinho¹

¹Department of Internal Medicine/Cardiology, Rush University Medical Center, 1750 W. Harrison St., Chicago, IL 60612, USA.

|May 4, 2026

Summary

Inflammatory bowel disease (IBD) impairs heart function by affecting calcium handling and t-tubules in heart cells. Angiotensin II signaling exacerbates this, but ACE inhibition may offer cardiac protection in IBD patients.

Keywords:

angiotensin II calpain inflammatory bowel disease junctophilin-2 t-tubular remodeling ventricular contraction

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Last Updated: May 5, 2026

Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples

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Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing

Published on: December 11, 2017

Area of Science:

Cardiology
Gastroenterology
Cell Biology

Background:

Inflammatory bowel disease (IBD) is linked to cardiac issues like reduced ventricular function and arrhythmias.
The precise mechanisms underlying IBD-induced cardiac dysfunction remain unclear.

Purpose of the Study:

To investigate the cellular mechanisms of cardiac dysfunction in a mouse model of IBD-induced colitis.
To explore the role of angiotensin II (AngII) signaling in IBD-related cardiac changes.

Main Methods:

Utilized a dextran sodium sulfate-induced colitis mouse model.
Assessed cardiac function in isolated ventricular myocytes (VMs) measuring cell shortening, intracellular calcium ([Ca2+]i), reactive oxygen species (ROS), and t-tubular density.
Examined the effects of angiotensin-converting enzyme (ACE) inhibition (Perindopril) on cardiac parameters.

Main Results:

Colitis led to reduced VM cell shortening and altered Ca2+ handling, with prolonged Ca2+ transients and decreased t-tubular density.
T-tubular loss correlated with increased ROS, calpain-2 (CAPN2) expression, junctophilin-2 (JPH-2) cleavage, and autophagy.
ACE inhibition mitigated CAPN2, ROS, autophagy, and t-tubular remodeling but did not fully restore JPH-2.

Conclusions:

IBD-induced cardiac dysfunction involves AngII-mediated loss of t-tubular integrity and impaired Ca2+ handling.
Suppression of AngII-dependent CAPN2 and autophagy may prevent cardiac manifestations in IBD.
Targeting AngII signaling could be a therapeutic strategy for cardiac complications in IBD patients.