Cardiac Function Remains Impaired Despite Reversible Cardiac Remodeling after Acute Experimental Viral Myocarditis

Area of Science:

• Cardiology
• Virology
• Immunology

Background:

• Coxsackievirus B3 is a known cause of viral myocarditis.
• Viral myocarditis involves acute cardiac inflammation and potential long-term sequelae.
• Understanding the resolution of inflammation and its impact on cardiac fibrosis and function is crucial.

Purpose of the Study:

• To compare the acute and chronic phases of Coxsackievirus B3-induced myocarditis.
• To investigate the immediate effects of cardiac inflammation.
• To determine the long-term impact of resolved inflammation on cardiac fibrosis and function.

Main Methods:

• C57BL/6J mice were infected with Coxsackievirus B3.
• Hemodynamic function was assessed at 7 and 28 days post-infection.
• Cardiac viral burden, replication, cytokine, and matrix protein expression were analyzed.
• In vitro infection of cardiac fibroblasts assessed profibrotic signaling.

Main Results:

• Severe cardiac inflammation and fibrosis were observed during the acute phase.
• Cardiac inflammation and fibrosis significantly declined by day 28.
• Hemodynamic function remained impaired 28 days post-infection, despite resolved inflammation.
• Viral infection alone did not induce significant profibrotic signaling in cardiac fibroblasts.

Conclusions:

• Both cardiac inflammation and fibrosis associated with Coxsackievirus B3 infection are reversible.
• Impaired hemodynamic function persists even after viral myocarditis has healed.
• Long-term cardiac dysfunction may occur independently of persistent inflammation or fibrosis.