Can viral myocarditis lead to reduced ejection fraction?

Viral Myocarditis and Reduced Ejection Fraction

Yes, viral myocarditis definitively causes reduced ejection fraction through direct myocardial inflammation, necrosis, and subsequent scarring, with severity ranging from mild systolic dysfunction to fulminant heart failure with ejection fractions as low as 5-20%. 1

Mechanisms of Ejection Fraction Reduction

Viral myocarditis reduces ejection fraction through multiple pathophysiologic pathways:

• Acute inflammatory injury causes myocardial edema and necrosis, predominantly affecting the subepicardial layers of the lateral and inferolateral left ventricular walls, directly impairing contractility 1
• Extensive myocardial involvement leads to systolic dysfunction when inflammation is severe enough to cause sufficient myocardial damage 1
• Chronic viral persistence in the myocardium is associated with progressive cardiac dysfunction and declining left ventricular function over time 2

Clinical Spectrum and Severity

The degree of ejection fraction reduction varies dramatically based on disease severity:

• Mild cases may present with subclinical dysfunction or only abnormal ventricular strain patterns without overt heart failure 1
• Moderate cases typically present with acute heart failure and reduced systolic function 1
• Severe/fulminant cases demonstrate ejection fractions of 5-20% with overt sudden-onset heart failure requiring mechanical circulatory support 3, 4

A critical study of 68 patients with chronic myocarditis symptoms documented a mean ejection fraction of 27%, demonstrating the substantial impact of persistent viral inflammation 1

Acute vs. Chronic Presentations

Acute Phase

• Viral myocarditis may present with acute heart failure or "infarct-like" symptoms with ST-segment elevation, particularly in young men 1
• Up to 40% of hospitalized COVID-19 patients demonstrate myocardial dysfunction ranging from abnormal strain to overt left and right ventricular systolic dysfunction 1
• Fulminant myocarditis can cause cardiogenic shock, with COVID-19-associated myocarditis showing cardiogenic shock in 27% of cases 1

Chronic Phase

• New-onset heart failure typically reflects a previous episode of severe inflammatory injury with subsequent extensive scarring 1
• Late gadolinium enhancement (LGE) is present in up to 70% of patients with biopsy-proven chronic inflammation in the setting of heart failure 1
• Viral persistence is associated with progressive impairment of left ventricular ejection fraction over time 2

Prognostic Implications

The relationship between viral clearance and ejection fraction recovery is well-established:

• Spontaneous viral clearance (occurring in 36.2% of patients with single infections) is associated with significant improvement in LVEF from 50.2±19.1% to 58.1±15.9% 2
• Persistent viral genomes in the myocardium correlate with progressive decline in LV function (LVEF decreasing from 54.3±16.1% to 51.4±16.1%) 2
• Virus-specific clearance rates vary: enterovirus 50%, adenovirus 35.7%, parvovirus B19 22.2%, and HHV6 44.4% 2

Important Clinical Caveats

Symptom intensity does not correlate well with ejection fraction severity - patients may have severely reduced LVEF with minimal symptoms or vice versa 1. This dissociation means that:

• Echocardiographic assessment is mandatory regardless of symptom severity 1
• Cardiac biomarkers (troponin, BNP) also correlate poorly with the degree of systolic dysfunction 1
• CMR findings (increased T1/T2 signals, LGE) provide better assessment of inflammation severity and extent 1

Recovery Potential

While some patients experience complete recovery of ejection fraction, others develop persistent dysfunction:

• Aggressive immunosuppressive therapy in severe cases (LVEF 5-20%) can result in normalization to 50-74% within 2 weeks 3
• Combination therapy with CoQ10 and trimetazidine shows superior improvement in LVEF compared to either agent alone 5
• However, some patients develop persistently depressed LVEF (<35%) despite optimal medical therapy, requiring ICD implantation for primary prevention of sudden cardiac death 4

The key determinant of recovery appears to be viral clearance versus persistence, with persistent viral genomes predicting progressive deterioration of left ventricular function 2.