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.
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