INTRODUCTION
The worldwide spread of the novel coronavirus disease 2019 (COVID-19) pandemic, first identified in Wuhan, China, has created unprecedented challenges in the diagnosis and medical treatment of affected patients as well as in public health management. Northern Italy was the first Western region to deal with COVID-19 and the first whose organ transplant population had to face the pandemic [1]. Despite the significant mitigating measures adopted, as of 4 May 2020, a total of 96,478 cases (46% of the total number of Italian cases) and 15,822 deaths (58%) have been reported in Lombardy and Veneto, respectively [2].
Data on patients with heart transplants in the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) era are still limited and mostly anecdotal [3–13]. Immunosuppression-related issues present the main concern in this special population. An abnormal inflammatory response has been hypothesized to play a crucial role in acquiring severe forms of COVID-19, mainly due to damage of one's own tissues and microcirculatory thrombophilia [14]. Importantly, it is well established that severe infections in the immunocompromised population dramatically influence both the care and prognosis of patients.
Asymptomatic carriers of the virus and patients with mild presentations of COVID-19 have been reported in the transplant recipient population, as have patients with more severe forms [3–13]. Despite the limited number of reported cases, significant heterogeneity dominates the clinical presentation patterns and challenges remain in fully characterizing risk factors. This uncertainty has opened up a great debate regarding immunomodulation interaction with the infection [15].
Immunomodulated recipients may present higher viral loads and shedding, resulting in greater infectivity and potential spread to other individuals and the transplant team. Moreover, drug–drug interactions with immunosuppressant medications need to be carefully evaluated and managed, particularly the interference of antiviral medications with calcineurin inhibitors and mammalian targets of rapamycin inhibitors metabolism [16].
Mortality data are only available from case reports and small case series. The scientific community still has no conclusive evidence as to whether or not outcomes in this population could be worse than those in immunocompetent patients.
Our goal was to report our single-centre experience related to the COVID-19-affected heart transplant population and our adopted strategies to mitigate the clinical presentation of the infection. Moreover, we investigated outcomes from balancing immunosuppression regimen and response to infection through our therapeutic management strategy.