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Understanding How a Heart Attack Can Trigger Ventricular Fibrillation

Understanding How a Heart Attack Can Trigger Ventricular Fibrillation

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Discover how a heart attack can disrupt the heart's protective mechanisms and lead to dangerous ventricular fibrillation, with new insights into potential therapies to prevent this life-threatening arrhythmia.

2 min read

A heart attack, or myocardial infarction, often leads to severe complications, including the potentially fatal ventricular fibrillation (VF). Recent research from the University of Freiburg and Dalhousie University has shed light on why this arrhythmia occurs following a heart attack. The study reveals that during a heart attack, the natural protective mechanism that prevents mechanically induced arrhythmias becomes impaired. This mechanism involves the coordination between the heart's electrical and mechanical relaxation processes, which normally work in harmony to ensure proper heart function.

When a heart attack occurs, the coupling between electrical excitation and mechanical relaxation is disrupted. This disturbance results in a shortened electrical repolarization phase, causing the heart's mechanical actions to lag or become uneven. Such incoordination can create a vulnerable period during which abnormal electrical impulses may trigger ventricular fibrillation—a chaotic electrical activity that prevents the heart from pumping effectively.

The researchers demonstrated at the molecular level that structural and electrical changes during a heart attack contribute to this failure of the protective mechanism. Specifically, shortened electrical signals and uneven contractions increase the risk of electrical misfires. This discovery opens new avenues for targeted therapies, aiming to prevent VF by addressing these molecular disruptions.

Potential therapeutic options include blocking specific ion channels, buffering calcium levels, or reducing oxidative stress with antioxidants. These interventions could help restore the injured heart's natural protective coupling, thereby reducing the incidence of arrhythmias after a heart attack.

The findings are based on animal models, primarily rabbits, and underline the importance of further studies in larger animals and humans. The ultimate goal is to develop medications that can be administered during or after a heart attack to reduce the risk of life-threatening ventricular fibrillation, thereby improving patient outcomes.

This research highlights the intricate interplay between electrical signals and mechanical function in the heart, emphasizing the importance of maintaining this balance to prevent arrhythmias in cardiac patients.

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