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Accelerated Cardiac Allograft Vasculopathy in an Orthotopic Heart Transplant Recipient with Prior COVID-19
Neil U Parikh1, Neal M Dixit2, Austin B Churchill3
1Keck School of Medicine, University of Southern California (USC), Los Angeles, CA, USA.
Insights
Cardiac allograft vasculopathy (CAV) can accelerate after COVID-19. This case report highlights a heart transplant recipient who developed rapid CAV following SARS-CoV-2 infection, suggesting a potential new risk factor.
Area of Science:
- Cardiology
- Immunology
- Infectious Diseases
Background:
- Cardiac allograft vasculopathy (CAV) is a major complication after heart transplantation, characterized by intimal smooth muscle proliferation and immune responses.
- Viral infections are known contributors to CAV development, but the role of SARS-CoV-2 has not been previously reported.
Observation:
- A 48-year-old heart transplant recipient developed accelerated CAV two months after a mild COVID-19 infection.
- The patient presented with symptoms of heart failure and diffuse vasculopathy, unresponsive to standard treatments.
- Despite aggressive management including high-dose steroids and extracorporeal support, the patient experienced cardiac arrest and ultimately died.
Findings:
- The case demonstrates a potential link between SARS-CoV-2 infection and the rapid progression of cardiac allograft vasculopathy in a heart transplant recipient.
- This association was observed despite the absence of prior CAV indicators and a mild course of COVID-19.
Implications:
- Further research is warranted to investigate whether SARS-CoV-2 infection is a risk factor for developing CAV in organ transplant recipients.
- Understanding this potential link could inform post-transplant monitoring and management strategies for patients with a history of COVID-19.
Abstract:
BACKGROUND Cardiac allograft vasculopathy (CAV) is a post-orthotopic heart transplant (OHT) complication driven by intimal smooth muscle proliferation and immune hyperactivity to donor heart tissue. Accelerated CAV leads to allograft failure within 1 year after receiving a normal angiogram result. Viruses can contribute to CAV development, but CAV after SARS-CoV-2 infection has not been reported to date. CASE REPORT A 48-year-old man, 5 years after OHT for non-ischemic cardiomyopathy, was admitted to the Cardiac Care Unit with 3 days of abdominal pain, dyspnea, and palpitations. His medical history included hyperlipidemia and insulin-dependent diabetes. He was compliant with all medications. Two months prior, he had a mild COVID-19 case. An echocardiogram and coronary angiogram 6 and 9 months prior, respectively, were unremarkable. Right and left heart catheterization demonstrated increased filling pressures, a cardiac index of 1.7 L/ml/m², and diffuse vasculopathy most severe in the LAD artery. Flow could not be restored despite repeated ballooning and intra-catheter adenosine. Empiric ionotropic support, daily high-dose methylprednisolone, and plasmapheresis were started. A few days later, the patient had cardiac arrest requiring venoarterial extracorporeal membranous oxygenation. Given CAV's irreversibility, re-transplantation was considered, but the patient had an episode of large-volume hemoptysis and remained clinically unstable for transplant. The patient died while on palliative care. CONCLUSIONS Our patient developed accelerated CAV 2 months after having COVID-19. While CAV has known associations with certain viruses, its incidence after SARS-CoV-2 infection is unknown. Further research is needed to determine if prior SARS-CoV-2 infection is a risk factor for development of CAV in OHT recipients.
