EDITORIAL
COVID-19 cardiac repercussions
Repercussões cardíacas
da COVID-19
Vinícius Afonso Gomes1,2,3,4
1CISVIVER, Salvador, BA,
Brazil
2Grupo de Pesquisa
Ciências da Saúde em Fisioterapia. Universidade Salvador (UNIFACS), Feira de
Santana, BA, Brazil
3Centro Universitário UNIRUY WYDEN,
Salvador, BA, Brazil
4Universidade Federal da
Bahia (UFBA), Salvador, BA, Brazil
Corresponding author: Vinícius Afonso
Gomes, Centro Universitário Uniruy/Wyden - Campus Paralela Av. Luís Viana, 3230 3° andar NAP,
Paralela 41720-200 Salvador BA
vinifisioterapia@yahoo.com.br
Although it is best known for damage to
the respiratory system, today we know that the new coronavirus (COVID-19) can
also compromise the heart [1]. This fact started to gain strength when a
retrospective study pointed out that 33% of deaths in these cases were
attributed to cardiorespiratory failure, and 7% to isolated heart failure [2].
A report of a previously healthy woman
who developed acute myopericarditis with systolic dysfunction during a COVID-19
condition, drew attention. In this case, it was possible to detect systemic
inflammatory responses associated with markers of myocardial injury, such as
elevated serum levels of highly sensitive troponin T and creatine kinase-MB.
Furthermore, abnormalities in ventricular contraction were found, without any
sign of obstruction of the acute coronary flow [3].
Despite the strong evidence, there is
still no proof of the presence of the virus within the myocardium, however the
occurrence of direct and indirect cardiac lesions attributed to it is
plausible. Indirect injuries can be caused by cardiac overload resulting from
hypoxemic respiratory failure and systemic inflammation. Whereas direct lesions
would be caused by successful tissue infection resulting in the death of
cardiomyocytes [4].
Another fact that suggests direct cardiac
injury by COVID-19 was the presence of an inflammatory infiltrate of
mononucleated cells found in autopsies in cardiac tissue [5]. In 2009, an
outbreak caused by a variation of the coronavirus led researchers to
investigate the presence of the viral genome in cardiac autopsies. Through the
real-time polymerase chain reaction (qPCR), it was possible to find the genome
in 35% of patients who died of acute respiratory syndrome [6]. This shows that
it is possible to expect similar behavior in cases of COVID-19, as the genomes
of both viruses are extremely similar [7].
Previous knowledge states that viral
respiratory infections can be the “trigger” for adverse effects of the heart [8].
In the case of arrhythmias, its manifestation can be observed in several ways,
ranging from “simple” isolated premature ventricular contractions, to the
successful ventricular fibrillation of asystole [9]. Regardless of the
condition that generates arrhythmias, it is known that episodes of hypoxemia,
sympathetic hyperactivity and pro-inflammatory effects, can make them more
frequent [8,9].
If in respiratory infections, healthy
hearts can develop arrhythmias, what to expect from those with some affection
already installed? The additional inflammation that is generated on the
atheromatous plaque, together with the increased demand for oxygen and the
reduction of its availability, increase the chances of myocardial infarction
[10,11]. The clot formed in cases where the plaque ruptures limits the passage
of blood, which causes ischemia and cardiac dysfunction [12].
Still about ischemia, it is necessary to
remember that pericytes are contractile, branched cells that have an important
role in reducing the permeability of blood vessels [13]. Infectious conditions
can promote lesions of these structures, thus causing ruptures of the
microcirculation, with subsequent myocardial ischemia [4]. It is true that this
process is still speculative, lacking studies that can confirm its hypothesis.
The chances of heart failure
decompensation in a COVID-19 infection are high. Its causes are also among
those that trigger arrhythmias and infarction, especially myocarditis [8]. The
risk of a heart with previous dysfunction deteriorating becomes greater when
trying to compensate someone's respiratory system with all the consequences of
a systemic inflammation [7]. Despite the relevance of decompensating heart
failure, there is another scenario that is even more worrying.
Retrospective cohorts have shown that
signs of cardiac injury, such as increased levels of troponin at the onset of
the disease, are associated with a worse prognosis [2,14]. In the study by Guo et
al. [7] the direct relationship between troponin T and the levels of highly
sensitive C-reactive protein (CRP) was proven, an important inflammatory marker
that reinforces the link between inflammation and myocardial injury. This fact
should not go unnoticed, as the risk of death in cases of myocardial injury
exceeds that of factors such as age, presence of diabetes mellitus, previous
chronic lung and heart disease [7,15].
In short, the heart can be greatly
affected in cases of COVID-19, contributing to a significant portion of cases
of morbidity and mortality. The worst outcomes seem to be associated with those
cases where the infectious process directly affects the heart, increasing the
levels of troponin T and CRP. We must emphasize that there are several
consequences, including arrhythmias, infarction and heart failure
decompensation, triggered mainly by the exacerbated inflammatory response and
myocarditis.