Discussion:
Coronavirus 2019 (COVID-19) has rapidly spread from China all over the world due to its highly contagious nature. Symptoms mostly involve mild respiratory problems in the vast majority of COVID-19 patients, with complete recovery within a few weeks. However, about 14% of cases are severe and 5% are critical, with an estimated mortality ranging from 2.3% to 3.83% (1-3)
Few data is currently available regarding the incidence of late complications, viral persistence, or the prognoses in different categories of patients (4). There are few and conflicting data focusing on cardiac involvement in COVID 19 patients (5).
It is established that patients at highest risk of mortality are older and with additional comorbidities. (6,7).
For instance, as reported by Yang et al (8), patients with cardiovascular diseases are vulnerable to complications of COVID-19, that can lead to death. These data have been confirmed by two reports published by Shi (6) and Guo (7) who highlighted that patients with diabetes and cardiovascular comorbidities tend to have more severe acute COVID 19 illness and higher short-term mortality rate.
On the other hand, the virus itself might cause cardiac injury, with different mechanisms. Firstly, it has been suggested that the inflammatory response in COVID 19 patients could provoke plaque erosion or rupture in patients with coronary atherosclerosis. Secondly, the respiratory disease, causing hypoxemia, might be a trigger for atrial fibrillation and other arrhythmias (8).
To summarize, the virus is able to cause death through several mechanisms, among which the exacerbation of underlying cardiac disease could cause rapid worsening of patients’ clinical conditions. (6,7)
According to the first hypothesis, it can be assumed that, in presence of low cardiac output, the virus pathogenicity is favoured. In our two cases, no adverse events occurred, the hospital stay was uneventful (without multi-organ involvement) with hospital discharge in few days. Thus, although in the presence of more comorbidities, the maintenance of a valid support of the cardiovascular function seems to play a role on overcoming the SARS-CoV-2 infection.
Fried et al. (9) described the case of a COVID 19 patient with acute respiratory distress syndrome, who was initially supported with veno-venous extracorporeal membrane oxygenation (ECMO), then upgraded to veno-arterial. The authors concluded that “the addition of an arterial conduit might provide the necessary circulatory support without inducing left ventricular (LV) distension”.
This concept is even more empathized in LVAD patients where LV unloading is more granted than with ECMO.
The second hypothesis deals with the protective role of anticoagulation. Preliminary data suggest that SARS- CoV-2 infection could be a precipitant factor for acute venous thrombo-embolism (10). In this scenario, the compulsory anticoagulation needed in patients with LVAD can be a protective factor as well.
In this case report, we would like to highlight the unpredictable behaviour of SARS-CoV-2 infection. Up to now, the virus has been more aggressive in fragile individuals and our patients were at extremely high risk due to their multiple comorbidities.
We report that the presence of LVAD per se and the oral anticoagulation that VAD-required, might played a role in mitigating the cardiovascular complications of COVID 19.
References
  1. World Health Organization Coronavirus disease (COVID-2019) situation reports https://www.who.int/emergencies/diseases/ novel-coronavirus -2019/Situation - reports/. Accessed on June 10, 2020.
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  7. Guo T, Fan Y, Chen M, et al. Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19).JAMA Cardiol . Published online March 27, 2020. doi:10.1001/ jamacardio.2020.1017
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  10. Tang N, Bai H, Chen X, Gong J, Li D, Sun Z. Anticoagulant treatment is associated with decreased mortality in severe coronavirus disease 2019 patients with coagulopathy.J Thromb Haemost. 2020 Mar 27. doi: 10.1111/jth.14817. [Epub ahead of print]