May fever trigger ventricular fibrillation?

Area of Science:

• Cardiology
• Electrophysiology
• Infectious Disease

Background:

• Clinical precipitants of ventricular fibrillation (VF) are not fully understood.
• Factors like hypoxemia, acidosis, drug toxicity, and viral myocarditis are linked to sudden cardiac death, especially in structural heart disease.
• Febrile illness is known to unmask Brugada syndrome and increase VF propensity.

Purpose of the Study:

• To review the phenomenon of febrile illnesses triggering ventricular fibrillation (VF) in patients with and without structural heart disease.
• To explore the potential mechanisms underlying fever-induced polymorphic ventricular tachycardia and VF.
• To enhance understanding of infectious triggers for cardiac arrhythmias.

Main Methods:

• Literature review of studies investigating febrile illnesses and cardiac arrhythmias.
• Analysis of case reports and clinical data linking infections to ventricular fibrillation and polymorphic ventricular tachycardia.
• Exploration of proposed pathophysiological mechanisms.

Main Results:

• Febrile illnesses of infectious etiology have been associated with polymorphic ventricular tachycardia or VF in patients with structurally normal hearts.
• This association occurs even in the absence of known repolarization abnormalities.
• Fever appears to be a significant trigger for life-threatening arrhythmias in susceptible individuals.

Conclusions:

• Febrile illnesses represent a critical, often overlooked, precipitant for ventricular fibrillation.
• Understanding the mechanisms of fever-induced arrhythmias is crucial for managing sudden cardiac death risk.
• Further research is needed to elucidate the precise pathways linking infection, fever, and cardiac electrical instability.