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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.

Decreased pulse rate

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...

Mutations

Mutations

Mutations

Mutations

Mutations

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...

Dysrhythmias IV: Characteristics of Bradyarrhythmias

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: May 16, 2026

Dual-Dye Optical Mapping of Hearts from RyR2R2474S Knock-In Mice of Catecholaminergic Polymorphic Ventricular Tachycardia

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Published on: December 22, 2023

Not very funny: how a single mutation causes heritable bradycardia.

Zafir Buraei¹, Jian Yang

¹Deparment of Biology and Health Sciences, Pace University, New York, NY 10038, USA. zburaei@pace.edu

Structure (London, England : 1993)

|December 11, 2012

Summary

Cardiac HCN channels regulate heart rhythm via cAMP modulation. A new study reveals an arrhythmia mutation disrupts this by altering channel structure and weakening cAMP binding.

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Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice

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Published on: July 5, 2021

Area of Science:

Cardiovascular Physiology
Molecular Biology
Structural Biology

Background:

Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are crucial for cardiac pacemaking.
Cyclic adenosine monophosphate (cAMP) is a key modulator of HCN channel function, influencing heart rate.

Discussion:

This study investigates the structural basis of HCN channel modulation by cAMP.
The research focuses on how mutations in HCN channels can lead to cardiac arrhythmias.
The entry-exit pathway of the HCN channel is identified as a critical region for cAMP interaction.

Key Insights:

An arrhythmia-causing mutation weakens cAMP binding to HCN channels.
This weakening is due to alterations in the local structure of the channel's entry-exit pathway.
The findings provide a structural explanation for the link between HCN channel mutations and cardiac arrhythmias.

Outlook:

Understanding these structural changes can inform the development of targeted therapies for arrhythmias.
Further research could explore other mutations affecting HCN channel function and their structural underpinnings.
This work highlights the importance of structural dynamics in channelopathies.