Discussion
There are growing links between COVID-19 and cardiovascular morbidity
(6). Although cardiac biomarkers such as
high-sensitivity troponin appear as good predictors of prognosis in
COVID-19 patients, data on echocardiographic abnormalities in these
individuals are scarce (10). To the best
of our knowledge, this is the first prospective health care workers
cohort with a long-term follow-up about the impact of COVID-19 and its
severity on echocardiographic indices. In this cohort follow-up report,
we demonstrated that although LV and RV function did not change
substantially over time in our cohort, various patterns of change were
seen based on the early echocardiogram.
In both severe and non-severe COVID-19 severity groups, among systolic
indices, 4DLVEDVI increased significantly, and in turn, 4DLVSVI and LVEF
increased significantly in the follow-up echocardiogram which may
indicate that in the early-time echocardiogram, patients had a higher
pulse rate in order to improve oxygenation in response to diseased lung
and after the lung recovery phase the heart rate slowed down and the
stroke volume increased naturally in response. An echocardiographic
study by Szekely et al. proved that patients with more COVID-19 clinical
severity had significantly higher heart rates, and the stroke volume was
reported non-significantly lower in the group with more severe
COVID-19(6).
In the severe COVID-19 group, 4DLVGLS increased significantly,
presenting that LV function is improved during the time, and the fall in
the 4DLVGLS in the early echocardiogram might have been a consequence of
the compensatory tachycardia mentioned above. It was expressed
previously in the ECHOVID study that LVGLS was lower in patients
hospitalized for COVID-19 compared to the healthy population
(11). Moreover, it was shown in Croft et
al. study that the LVGLS in hospitalized COVID-19 patients were lower
than the assumed lower limit of the normal range. They hypothesized that
the decrease in LVGLS associated with COVID-19 infection might be
attributable to a combination of causes. Direct and indirect processes
may cause myocardial damage. Viral invasion of the myocardium directly
results in cardiomyocyte death and inflammation. Indirect mechanisms
include cardiac stress caused by insults such as respiratory failure and
hypoxemia, as well as cardiac inflammation in the presence of
substantial systemic hyper inflammation
(12-14).
In the non-severe COVID-19 group, of the diastolic indices, lateral E’
decreased significantly in the normal range, indicating the
hyperactivity of LV in the early phase and relaxation of LV far after
COVID-19 relief.
Global RV function indicators demonstrate hyperactivity of RV during the
early COVID-19 recovery phase, as the 4DRVFAC in both non-severe and
severe COVID-19 groups decreased significantly in the follow-up
echocardiogram in comparison with the early echocardiogram while it
still lies within normal range. Furthermore, RVFWGLS decreased
significantly in the non-severe COVID-19 group. Among COVID-19 patients,
a cytokine storm is prevalent. Cardiac myofibroblasts and cardiomyocytes
are the major generators of various proinflammatory cytokines
(15). As a result of systemic
inflammation in COVID-19, the afterload increases
(16); thus, the rise in RVFWGLS in early
echocardiogram among the non-severe COVID-19 group demonstrates
hyperactivity of the RV in order to overcome the risen afterload.
A study of the right ventricle in COVID-19 proved that Interleukin 6
(IL-6) serum levels are associated with respiratory dysfunction, ARDS,
and poor clinical outcomes. The proinflammatory cytokine cascade may
lead to RV dysfunction through adverse inotropic effects on the
myocardium. Taken together, reduced RV contractility and abruptly high
pulmonary vascular resistance due to ARDS and pulmonary embolism in
COVID-19 may be fatal (15). The present
study’s findings showed no RV failure amongst patients as it was the
study of non-critically ill patients. It seems that in non-severe cases
of COVID-19, in the absence of a cytokine storm healthy heart will
increase its contractility during the acute phase. Although the higher
afterload is previously suggested to fail RV, in this circumstance was
not to an extent capable of failing the RV.
In a study of the prognostic value of RV strain, Li et al. stated that
non-survivors had RV enlargement and dysfunction. The SARS-CoV-2
infection has been shown to generate both pulmonary and systemic
inflammation, which may lead to RV failure via RV overload and direct
cardiomyocyte injury. This research reveals that RVLS is an independent
predictor of clinical outcomes in COVID-19 patients. Significantly, this
index may have more predictive value than other echocardiographic
markers. Therefore, individuals with COVID-19 should undergo an
examination of RV function by investigating RVLS for risk stratification
(17). In agreement with our findings, the
WASE-COVID study, which provided participants with a follow-up
echocardiogram, revealed an improvement in RVGLS in patients with
impaired RV function, which may be solid evidence of advancement in lung
function between the time of the baseline echocardiogram and the time of
the follow-up study (18).
Although TAPSE altered non-significantly in none of the COVID-19
severity groups, 4DRVFAC decreased significantly on the follow-up
echocardiogram in both severe and non-severe COVID-19 groups, suggesting
the RV hyperactivity to improve oxygenation against the COVID-19
affected lung in the early phase recovery period. Paternoster et al., in
a systematic review and meta-analysis, defined the RV dysfunction in
COVID-19 patients based on the recommended cut-offs of echocardiographic
guidelines that the cut-offs for RV failure determinants also assessed
in this study were FAC <35%, TAPSE < 17 mm and,
(PAP) > 25 mmHg. Thereafter, in line with the present
study, none of the mentioned indices in either severe or non-severe
groups had a significant alternation toward RV failure
(7, 19,
20).