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Accelerated Cardiac Allograft Vasculopathy in an Orthotopic Heart Transplant Recipient with Prior COVID-19.
Parikh, Neil U; Dixit, Neal M; Churchill, Austin B; Oliveira-Kowaleski, Andrea; Lau, Ryan P; Fishbein, Gregory A; Hsu, Jeffrey J.
Afiliação
  • Parikh NU; Keck School of Medicine, University of Southern California (USC), Los Angeles, CA, USA.
  • Dixit NM; Division of Cardiology, Department of Medicine, UC Davis Medical Center, Sacramento, CA, USA.
  • Churchill AB; David Geffen School of Medicine, University of California Los Angeles (UCLA), Los Angeles, CA, USA.
  • Oliveira-Kowaleski A; Department of Pathology, David Geffen School of Medicine, University of California Los Angeles (UCLA), Los Angeles, CA, USA.
  • Lau RP; Department of Pathology, David Geffen School of Medicine, University of California Los Angeles (UCLA), Los Angeles, CA, USA.
  • Fishbein GA; Department of Pathology, David Geffen School of Medicine, University of California Los Angeles (UCLA), Los Angeles, CA, USA.
  • Hsu JJ; Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles (UCLA), Los Angeles, CA, USA.
Am J Case Rep ; 24: e937955, 2023 Mar 01.
Article em En | MEDLINE | ID: mdl-36855283
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.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Transplante de Coração / COVID-19 Tipo de estudo: Risk_factors_studies Limite: Humans / Male / Middle aged Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Transplante de Coração / COVID-19 Tipo de estudo: Risk_factors_studies Limite: Humans / Male / Middle aged Idioma: En Ano de publicação: 2023 Tipo de documento: Article