SARS-CoV-2 infection in heart transplant recipients: a systematic literature review of clinical outcomes and immunosuppression strategies.

The impact of SARS-CoV-2 infection on heart transplant recipients is unknown. Literature is limited to case reports and series. The purpose of this study is to identify the clinical features, outcomes, and immunosuppression strategies of heart transplant recipients with COVID-19 infection. A systematic review was conducted using the search term "Coronavirus" or COVID," "SARS-CoV-2," "cardiac transplantation," and "heart transplant." Case reports and retrospective studies were gathered by searching Medline/PubMed, Google Scholar, CINAHL, Cochrane CENTRAL, and Web of Science. Thirty-three articles were selected for review. We identified 74 cases of SARS-CoV-2 infection in heart transplant and heart-kidney transplant recipients. The mean age was 60.5 ± 15.8 years, and 82.4% were males with median time from transplant of 6.5 years. Commonest symptoms were fever, cough, and dyspnea, but new left ventricular (LV) dysfunction was rare. Leukocytosis, lymphopenia, elevated inflammatory markers, and bilateral ground-glass opacities were common. Mortality was high, with particularly poor survival in patients who required intensive care unit (ICU) admission and older patients. Immunosuppression involved discontinuation of antimetabolites and steroids. COVID-19 infection in heart transplant (HT) recipients presents similarly to the general population, but new onset of LV dysfunction is uncommon. Immunosuppression strategies include increase in corticosteroids and discontinuation of antimetabolites.

Calcineurin-Inhibitor Induced Pain Syndrome in a Heart Transplant Patient.

Calcineurin-inhibitor induced pain syndrome (CIPS) also called the "symmetrical bone syndrome" is a condition describing reversible lower extremity pain in patients after organ transplantation who are receiving calcineurin inhibitors, especially tacrolimus. We present a case of CIPS after orthotopic heart transplant complicated with concurrent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. We emphasize the presentation; diagnostic evaluation, and findings. We then discuss the proposed pathophysiologic mechanisms of CIPS and conclude with discussion of management strategies. Additionally, we present a table to guide clinicians in assessing posttransplant bone pain syndromes. To our knowledge, this is the first article to describe a case of CIPS with concurrent SARS-CoV-2 infection.

Clinical variants of myocardial involvement in COVID-19-positive patients: a cumulative experience of 2020.

Myocardial injury, diagnosed by troponin elevation, is common in COVID-19 patients, but cardiac involvement with clinical manifestations occurs less frequently. We analyzed the literature on COVID-19 (2020) and systematically reviewed the cases where individual patient data were presented. We searched PubMed and Google Scholar for "COVID," "COVID-19," and "coronavirus" in combination with "myocarditis," "heart failure," "takotsubo," "cardiomyopathy," and "cardiogenic shock." We identified 90 cases of COVID-19 with myocardial involvement, mean age 52.9 ± 18.3 years, 54.5% males. Of them, 55 survived (61.1%), 20 died (22.2%), and in 15 (16.7%) the outcome was unknown at the time of publication. Among patients with known outcome, mortality was 26%. The nadir LVEF was 31.7 ± 13.1% and recovered to 50.1 ± 16.0%. Pericardial effusion was a common finding, reported in 21 (23.3%) of patients, including moderate size effusion in 8.9% and large in 7.8%. The effusion caused tamponade in 11 (12.2%) of patients. Out of 83 patients who experienced a decrease in LVEF, 30 could be classified as takotsubo syndrome. The takotsubo patients were older than those with myocarditis, and with relatively high proportion of males. About one third of the cases was complicated by cardiogenic shock. Myocardial involvement in COVID-19 patients most often presents as a new, rapid decrease in LVEF, although normal LVEF or takotsubo-like wall motion pattern does not rule out myocarditis. Moderate and large pericardial effusion is common, and cardiac tamponade occurs in 12.2% of patients. Cardiogenic shock develops in one third of the patients. Mortality appears to be high at 26%.

Fulminant myocarditis: COVID or not COVID? Reinfection or co-infection?

We describe a unique case of fulminant myocarditis in a patient with presumed SARS-CoV-2 reinfection. Patient had initial infection 4 months backand had COVID-19 antibody at the time of presentation. Endomyocardial biopsy showed lymphocytic myocarditis, that is usually seen in viral myocarditis. The molecular diagnostic testing of the endomyocardial biopsy for cardiotropic viruses was positive for Parvovirus and negative for SARS-CoV-2. Authors highly suspect co-infection of SARS-CoV-2 and Parvovirus, that possibly triggered the immune cascade resulting in fulminant myocarditis. Patient was hemodynamically unstable with ventricular tachycardia and was supported on VA ECMO and Impella CP. There was impressive recovery of left ventricular function within 48 h, leading to decannulation of VA ECMO in 72 h. This unique case was written by the survivor herself.