According to the results of this study, LVSD was
associated with poor outcomes and it was found to
be an independent predictor of in-hospital mortality
and an approximately 2.6-fold increase in risk was
observed, after adjustment with multivariate analysis.
No significant difference was observed in mid-range
LVEF and reduced LVEF groups in terms of
in-hospital mortality, and the mortality risk increased
significantly in both groups in the regression analysis,
compared to the non-LVSD group.
Although COVID-19 infection begins as a
respiratory tract infection, pathological findings can
often occur in many organs and tissues, such as the
heart. In the studies conducted, the severe acute
respiratory syndrome-coronavirus 2 (SARS-CoV-2)
was seen in macrophages, endothelial cells, and
pericytes, and in the autopsy series, evidence of
viral replication in myocardial cells was obtained.[16]
Conditions such as the increased risk of MI, fulminant myocarditis, arrhythmias, venous thromboembolism,
and Takotsubo cardiomyopathy are the most common
CV complications identified in COVID-19 patients.[17]
In addition to direct myocardial damage caused by the
virus by binding to the angiotensin-converting enzyme
2 (ACE-2) receptor, which is important for cardiac
functions, causing ACE-2 receptor downregulation,
the release of inflammatory mediators, endothelial
dysfunction, and myocardial damage due to microand
macro-thrombi may play a role in the occurrence
of these complications.[18-20] Myocardial injury, defined
by the increased troponin levels, presented mortality
greater than those without myocardial injury, is an
independent risk factor for mortality.[15] In our study,
the myocardial injury was observed as the independent
predictor of mortality (OR=3.30, p<0.001). Arterial
and venous thrombosis can be seen in COVID-19.[21]
Studies have found that elevated D-dimer increases
the risk of mortality.[22] In our study, a significant
increase was observed in-hospital mortality risk with
elevated D-dimer. Also, age, DM, heart rate, and
oxygen saturation were other factors that significantly
increased the risk of in-hospital mortality.
Cardiovascular diseases are among the most
common comorbidities in patients hospitalized
with COVID-19 and are associated with poor
outcomes.[2] Heart failure is one of the important
causes of morbidity and mortality, particularly
in advanced ages. Conditions such as upper
respiratory tract infection and pneumonia may
cause decompensation in these patient groups.[7,8] It
has been observed that COVID-19 infection, which
is a respiratory tract infection, also predisposes to
decompensation.[9] In a small-scale study comparing
the patients hospitalized due to HF with and without
COVID-19 infection, mortality was approximately
five times higher in those with COVID-19
infection.[23] Again, in a study by Alvarez-Garcia
et al.,[14] the effect of HF on in-hospital death in
COVID-19 patients was examined and HF increased
mortality significantly, regardless of LVEF, and
mortality was observed at a rate of approximately 40%
in the group with HF. In our study, LVSD (both in
the mid-range LVEF and reduced LVEF groups) was
found to be an independent predictor of in-hospital
mortality, with a 2.6-fold increase in risk with
LVSD, and 42% of patients died during in-hospital
follow-up. According to the results of our study, the
frequency of myocardial injury was observed more in
the LVSD group, which is one of the predictors of mortality. The SARS-CoV-2 may predispose to stress
cardiomyopathy and cytokine-induced myocardial
dysfunction and, as a result, acute decompensation
of congestive heart failure may worsen subclinical
pre-existing injury in well-compensated patients.[24]
The increase in mortality in these patient groups may
be due to myocardial damage caused by the direct
effect of the virus, inflammatory response, hypoxia,
and endothelial dysfunction worsening LV systolic
functions and decompensation.
Heart failure patients are the groups that require
special care during hospitalization. Mortality was
found to be significantly higher in COVID-19
patients with HF, both with the results of other
studies and the results of our study. Perhaps due
to the density of hospitals caused by the pandemic,
the inability to pay close attention to these patients
may have contributed to the increase in mortality.
Among LVSD patients included in the study, the
number of patients who did not have optimal HF
treatment during hospitalization was not small. A
study showed that discontinuation of HF treatment
during hospitalization caused a significant increase
in in-hospital mortality.[9] Therefore, close follow-up
of patients hospitalized for COVID-19 with LVSD
and providing optimal treatment may reduce high
mortality rates.
This study has some limitations, including the
small number of LVSD patients from a single center
with a retrospective design. Another limitation is that
obesity and New York Heart Association (NYHA)
classes cannot be included in the multivariate analysis
due to insufficient data. As brain natriuretic peptide
levels were not studied and diastolic dysfunction
parameters were not evaluated in detail in most
patients, HF patients with preserved ejection fraction
could not be excluded from the study. The inability
to determine the intensive care admissions as the
outcome is another limitation. This is because severe
patients cannot be taken into intensive care due to
the lack of enough beds during the peak periods of
the disease.
In conclusion, LVSD was an independent
predictor of in-hospital mortality in our study. An
increased risk of in-hospital mortality was present in
both the mid-range LVEF and the reduced LVEF
group, separately. In addition, myocardial injury,
older age, DM, D-dimer, oxygen saturation, and
heart rate were other independent predictors of
in-hospital mortality.
Acknowledgment
I would like to acknowledge Ercan Taştan, Metin Okşul,
Burhan Aslan, Emrah Erdoğan, and İbrahim Halil Tanboğa
for their valuable contributions to the statistical analysis, data
collection, writing, and critical revision of the article.
Declaration of conflicting interests
The authors declared no conflicts of interest with respect
to the authorship and/or publication of this article.
Funding
The authors received no financial support for the research
and/or authorship of this article.
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