Clinical aspects SARS-CoV-2 (COVID-19) infection
A viral epidemic caused by a new coronavirus SARS-CoV-2 (COVID-19) began
in Wuhan (China) in November 2019. The epidemic quickly became a global
pandemic (1). Knowledges of this viral infection is evolving rapidly, to
date there are still no direct antivirals or effective vaccines and
therapeutic treatments are on an empirical basis. At the time of writing
this article, 10.7 million infected people and about 516,000 deaths are
reported. (2) SARS-CoV-2 is a family of RNA viruses capable of infecting
humans and causing severe respiratory tract infections that can be fatal
in some cases. (3) Studies have shown that SARS-CoV-2 has about 80% of
the SARS-CoV-like genome responsible for the 2003 outbreak. (4)
SARS-CoV-2 penetrates into cells using the S protein via the angiotensin
2 conversion enzyme receptor (ACE-2) on the cell surface, which is
widely present in the epithelial cells of the respiratory mucosa, (5).
ACE-2 is also a conversion enzyme with a key role in the
renin-angiotensin system (RAS). Clinical experts and scientists have
described SARS-CoV-2 infection in three stages: the first asymptomatic
or mildly symptomatic, the second moderately severe characterized by a
pulmonary inflammatory state, the third very severe stage characterized
by a generalized inflammatory state affecting all tissues causing
multi-organ dysfunction. (6) In the most severe stages of infection,
COVID-19 lung lesions are characterised by diffuse alveolar damage with
irregular inflammatory cellular infiltration consisting of the presence
of monocytes, macrophages and lymphocytes infiltrating the lung
interstitium, and presence of intravascular thrombosis. (7). Severe
inflammatory pulmonary infiltration prevents the exchange of alveolar
gases, moreover, the most serious cases develop significant
cardiovascular morbidity (8), (9). In this last direction, in fact data
that have recently emerged do not only identify COVID-19 viral infection
as a respiratory disease and risk of acute respiratory distress syndrome
but also with acute myocardial damage that can be a critical component
in the development of serious complications. These aspects are further
confirmed by studies that show that patients with a history of
cardiovascular disease are at increased risk of COVID-19 complications.
(10) In fact, in a recent study (11) it was found that 77% of the
deceased patients developed acute myocardial damage, other studies
confirm these data. (12) (13) Some pathophysiological bases have been
hypothesized, one of which is that the phenomenon of the ”cytokinic
storm” (14) which occurs in the most severe stages of COVID-19 infection
causes myocarditis which is the cause of acute heart failure, in
addition, TNF-α and some other pro-inflammatory cytokines are capable of
inducing typical cellular modifications of the decompensated heart, such
as down-regulation of the sarcoplasmic reticulum ATPasica calcic pump
(15), or decoupling of the beta-adrenergic receptors from activation of
cyclic intracellular AMP (16) or death of heart cells.