The first report on the impact of COVID-19 on heart transplant recipients has been published in The Journal of Heart and Lung Transplantation, outlining the management strategy by a team in Wuhan for two patients who contracted the virus in their native China.
Fei Li (Union Hospital, Huazhong University of Science and Technology, Wuhan, China) and colleagues report that the patients were managed with changes in immunosuppression and the selective use of antiviral and immunomodulatory therapy, and that both survived to discharge. One of the patients had a mild presentation; the other case was more severe and required prolonged hospitalisation.
In an accompanying editorial, Saima Aslam (Division of Infectious Diseases and Global Public Health, University of California, San Diego) and Mandeep R Mehra (Brigham and Women’s Hospital, and Harvard Medical School, Boston, USA) say that the findings “may provide insight into how the virus will impact transplant recipients around the world”.
Li et al report that one patient was a 51-year-old man who underwent a heart transplant in November 2003, and was receiving immunosuppression of tacrolimus 1mg twice daily plus mycophenolate mofetil 0.5g twice daily. He showed the symptoms of COVID-19 infection on 23 January 2020, complaining of intermittent fever, chills, fatigue, poor appetite and diarrhoea. Treatment included withholding baseline immunosuppression and treating with high dose corticosteroids and pooled immunoglobulin infusions. He was discharged on 27 February 2020. A second heart transplant male recipient aged 43-years presented to the outpatient clinic with fever for two days on 25 January, exhibited mild lung lesions on CT scan, but a nucleic acid test for 2019-nCoV was positive. The patient was quarantined at home and then admitted to the hospital on 6 February 2020; he was discharged on 11 February when two nucleic acid tests for 2019-nCoV tested negative. Laboratory findings for both mirrored those observed in non-transplant patients, with elevated C-reactive protein levels and lymphopaenia.
Discussing the findings, Aslam and Mehra hypothesise: “Whether transplantation related immunosuppression alters the predisposition to acquiring infection with SARS-CoV-2 or if the disease implications are modified for better or for worse remain uncertain. The novel coronavirus achieves its anchoring to the lung by using the angiotensin converting enzyme (ACE)-2 receptor. The pulmonary renin-angiotensin-aldosterone system via ACE-2 has been implicated in prevention of lung inflammation. When this system is overpowered by SARS-CoV-2, pulmonary inflammatory infiltrates emerge expressing the COVID-19 disease phenotype. It is unknown if heart transplant recipients have differential expression of pulmonary ACE-2 since a lower expression may result in less severe illness. Similarly, the anti-inflammatory effects of immunosuppression could diminish the clinical expression of disease as well. These speculative assumptions will require structured studies to enhance our understanding of this disease pathway and processes.”
Aslam and Mehra suggest advising transplant recipients to “ardently practice mitigation strategies such as social distancing, sanitisation, hand hygiene and avoidance of areas known to harbour potentially infected individuals”.
And they also highlight concerns around donor organs: “This will need to be debated and studied rapidly as more widespread testing becomes available,” they say. “At this time, it would be prudent to avoid transplanting organs from donors with a history of contact with someone at risk or diagnosed with COVID-19, as well as those with recent travel to an area with high density of infection.”