How does infection cause ventricular tachycardia (VTach)?

From the Guidelines

Infection can trigger ventricular tachycardia through several mechanisms, including the release of cytokines that alter electrolyte balance and disrupt normal cardiac conduction, direct damage to heart muscle and conduction pathways, and metabolic derangements that destabilize cardiac membrane potentials. Systemic infections cause inflammatory responses that directly affect cardiac tissue, leading to the release of cytokines that alter electrolyte balance and disrupt normal cardiac conduction. Specific cardiac infections like myocarditis or endocarditis directly damage heart muscle and conduction pathways, creating arrhythmogenic substrates. Sepsis-induced hypotension and decreased cardiac perfusion can lead to myocardial ischemia, triggering VTach. Infections also cause metabolic derangements including fever, electrolyte abnormalities (particularly potassium, calcium, and magnesium), and acidosis that destabilize cardiac membrane potentials. Additionally, some infections release toxins that directly affect cardiac ion channels. In patients with pre-existing heart disease, these infection-related stressors can more easily trigger VTach. The body's sympathetic response to infection, including increased catecholamine release, further predisposes to arrhythmias by increasing heart rate and contractility.

According to the 2015 ESC guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death 1, myocarditis is a significant cause of ventricular tachycardia, and the diagnosis of myocarditis should be based on established histological, immunological, and immunohistochemical criteria. The guidelines also recommend that patients with myocarditis and ventricular arrhythmias should be treated with antiarrhythmic medications and device therapy, including implantable cardioverter-defibrillators (ICDs).

Some specific infections, such as Lyme disease and Chagas disease, can also cause ventricular tachycardia through different mechanisms. Lyme disease can cause AV block, while Chagas disease can cause ventricular tachyarrhythmias and AV block 1.

Treatment should address both the underlying infection with appropriate antimicrobials and provide cardiovascular support, including correction of electrolyte abnormalities, antipyretics for fever, and antiarrhythmic medications if necessary. The use of antiarrhythmic medications, such as amiodarone, and device therapy, including ICDs, can be effective in treating ventricular tachyarrhythmias in patients with myocarditis and other cardiac infections.

From the Research

Infection and Ventricular Tachycardia (VTach)

• Infection can lead to ventricular tachycardia (VTach) through various mechanisms, including sepsis-induced cardiac dysfunction 2, 3.
• Sepsis is a systemic inflammatory response to infection, which can cause cardiac dysfunction, including decreased ejection fraction and dilatation of ventricles 3.
• The mechanisms of sepsis-induced cardiac dysfunction include endothelial dysfunction, microcirculatory and mitochondrial dysfunction, and the role of circulating factors 2, 3.
• Inflammation plays a crucial role in cardiac dysfunction during sepsis, and can lead to adverse cardiac remodeling, including myocyte hypertrophy and death, fibrosis, and altered myocyte function 4.
• Viral infections, such as influenza, can also trigger cardiovascular events, including ventricular arrhythmia and heart failure, through the induction of pro-inflammatory cytokines and chemokines and recruitment of immune cells 5.

Key Factors Contributing to VTach

• Endothelial dysfunction and impaired myocardial oxygen consumption 2
• Microcirculatory and mitochondrial dysfunction 3
• Inflammation and the release of pro-inflammatory cytokines and chemokines 4, 5
• Abnormal nitric oxide and reactive oxygen species (ROS) signaling 4
• Abnormal excitation-contraction coupling and reduced calcium sensitivity at the myofibrillar level 4

Clinical Implications

• Patients with sepsis who develop cardiac dysfunction have significantly higher mortality, and thus cardiac dysfunction serves as a predictor of survival in sepsis 2.
• Understanding the mechanisms of sepsis-induced cardiac dysfunction and the role of inflammation in cardiac dysfunction can help improve treatment plans for patients with infection-related VTach 2, 3, 4, 5.