Hantavirus Cardiac Involvement: Pathophysiology and Outcomes

Cardiac involvement is a defining feature of Hantavirus Cardiopulmonary Syndrome (HCPS) and a significant complication in Hemorrhagic Fever with Renal Syndrome (HFRS). While historical views categorized the cardiac dysfunction as purely functional, modern evidence confirms a combination of direct viral effects and a profound cytokine-mediated inflammatory response that leads to myocardial depression and shock.

1. Pathophysiology and Mechanisms

The hallmark of cardiac involvement in hantavirus infection is increased microvascular permeability and myocardial depression without significant direct cytopathic damage to myocytes.

• “Typical” Myocarditis: Foundational studies identified hantaviral antigens and particles specifically within the cardiac endothelium and interstitial macrophages, accompanied by interstitial edema and myofiber necrosis.
• The Cytokine Storm: Myocardial depression is largely attributed to high levels of soluble mediators, including TNF-α, IFN-γ, and nitric oxide (NO). These cytokines impair endothelial function and directly inhibit myocardial contractility.
• Functional vs. Structural: The shock state is an “atypical septic shock” where low cardiac index (CI) and low stroke volume index (SVI) are accompanied by high systemic vascular resistance (SVR), mimicking cardiogenic shock.

2. Clinical and Hemodynamic Profile

Electrocardiographic (ECG) and Imaging Findings

• ECG Abnormalities: Patients often present with sinus tachycardia in some variants or bradycardia in other variants. Severe cases can mimic ST-elevation myocardial infarction (STEMI) due to diffuse ST-segment changes and wall motion abnormalities on echocardiography.
• Echocardiography: Typical findings include depressed Left Ventricular Ejection Fraction (LVEF) (often 35–40%) and pericardial effusion. Remarkably, myocardial function may recover fully in survivors within 2–4 weeks.

3. Long-Term Cardiovascular Outcomes

Survivors of severe hantavirus infection may face persistent cardiovascular and systemic burden:

• Persistent Symptoms: Up to 80% of survivors report long-term fatigue, and over 50% experience persistent dyspnea 3–6 months post-discharge, regardless of whether they required ECMO (Ares-Gómez et al., 2025).
• Late Complications: Long-term follow-up of survivors of certain variants has indicated an increased risk for acute myocardial infarction, hypertension, and venous thromboembolism (PMC8953343, 2022).

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References

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