According to the results of the current study, male sex, old age, positive troponin, and a lower level of EF are all important factors that raise the risk of death following hospitalization for COVID-19. The pathogenic cause of COVID-19, a continuing worldwide pandemic, is SARS-CoV-2. Cardiovascular morbidity and mortality in this cohort are becoming increasingly recognized, along with expected respiratory mortality. The existence of cardiac injury has been attributed to in-hospital mortality in hospitalized COVID-19 patients. However, heart disease symptoms in COVID-19 patients frequently include indicators of myocardial injury. Similar associations have been noted regarding other coronavirus outbreaks, such as SARS and the Middle East respiratory illness, but there is still a crucial knowledge deficit regarding the possible effects of CVD and damage in COVID-19.
Patients with acute COVID-19 may exhibit a variety of cardiac clinical manifestations, including symptomatic heart disease, no clinical evidence of heart disease, and no symptoms but abnormal cardiac test results (e.g., elevated serum cardiac troponin or no symptoms but cardiac arrhythmias). Myocardial injury, heart failure, cardiac shock, and cardiac arrhythmias, including abrupt cardiac arrest, are all examples of cardiac problems. The general incidence of HF in COVID-19 patients may be linked to acute illnesses in people with known or undiscovered heart disease (such as coronary artery disease or hypertension), acute hemodynamic stress (such as acute pulmonary blindness), or acutely accelerated aging. Autopsy results obtained from examined cardiac tissues of 39 COVID-19 fatality patients revealed that SARS-CoV-2 was present in 62% of the specimens, indicating a high rate of viral presence in the myocardium. The direct viral damage and the systemic immune response brought on by infection remain the two fundamental questions regarding the cardiac injury and inflammation that have been observed so far [9].
A lower EF value was identified as an influential factor that increased the death rate in hospitalized COVID-19 patients. In line with another study, it was found that heart failure with reduced ejection fraction was significantly associated with in-hospital mortality [10]. Moreover, in another study, it was observed that myocarditis-induced heart failure with low ejection fraction and viral-induced cardiac inflammatory changes might occur [11]. The effects of right ventricular anomalies and left ventricular diastolic dysfunction were the two main findings of the echocardiographic assessments performed on hospitalized COVID-19 patients. Ninety percent of COVID-19 patients observed in Israel (mean age: 66 years) had normal left ventricular ejection fraction, and the most frequent anomalies were right ventricular enlargement (39%) and left ventricular diastolic dysfunction (16%)[12].
A comparison in the current study found an increasing level of IL-6 in dead patients. Freaney et al. revealed that proinflammatory cytokines, including IL-1 and IL-6, are released as a result of SARS-CoV-2 infection, having an impact not only on the respiratory system but also on the myocardium, both directly and indirectly. The role of inflammatory cells and pathways during an acute initial injury to the myocardium, such as an ischemic insult or a viral injury (e.g., influenza) contributing to heart failure with preserved ejection fraction (HFpEF), has been confirmed. Although case reports have described severe COVID-19 myocarditis that resulted in HFpEF, it is possible that the more typical manifestation in the COVID-19 era was HFpEF, which was caused primarily by the discovery of subclinical HFpEF and secondarily by the emergence of new HFpEF after SARS-CoV-2 infection. The identification of COVID-19 as a possible risk factor for HFpEF should induce screening and treatment to stop the progression of the condition and its unfavorable outcomes on an individual basis, thereby mitigating the rising morbidity, mortality, and inequalities of the condition [13].
The current research shows that positive troponin plays a significant role in COVID-19 deaths and increases the odds of mortality by 1.95 times. Consequently, high troponin levels are linked to high mortality in COVID-19 patients. During the current outbreak, troponin has served as a helpful indicator of the course and prognosis of the illness. As was seen in Guo et al.’s study, 16% of the patients who had underlying CVD but normal troponin levels had fairly good results. Myocardial biomarkers should be assessed in patients with CVD who acquire COVID-19 in order to risk-stratify patients and perhaps guide earlier and more aggressive therapies [14]. Similar results were found in another study showing that patients with troponin levels of 0.34 ng/mL had significantly higher atrial tachyarrhythmias, ventricular tachyarrhythmias, and 30-day in-hospital mortality than those with less severe troponin elevation [15].
High-sensitivity troponin plays a critical role in SARS-CoV-2. This suggests that the cardiovascular system is acutely involved in the most severe presentations. Additionally, it can prompt the consideration of an infectious cause of acute myocardial injury, which might help us make the best treatment decision and run follow-up diagnostic tests. Since patients who are suspected of having myocardial involvement should get a cardiac MRI and a myocardial biopsy to confirm the diagnosis, it is currently challenging to evaluate the correlation between COVID-19 and myocarditis by troponin dose alone.
A review of the potential effects of coronaviruses on the cardiovascular system was undertaken by Madjid et al. Viral pneumonia caused by COVID-19 with additional extra-pulmonary symptoms and consequences was confirmed in this research. In particular, immediate cardiac injury has been frequently observed in the most severe instances and has been linked to a greater mortality rate (indirectly demonstrated by high levels of high-sensitivity troponin)[16]. Additionally, as recently confirmed by Varga et al., a rise in troponin may be linked to clinical diseases that are not restricted to the heart, such as pulmonary embolism, renal failure, or the broad involvement of endothelial cells[17].
As was indicated, CRP and procalcitonin are two biomarkers with an increased level in dead patients. However, based on logistic regression results, no further information was found about the odds of death. According to another study, measurements of procalcitonin and CRP may help identify patients with subsequent bacterial infections and enable the targeted use of antibiotics, thus encouraging antibiotic stewardship. Therefore, it seems that critically ill COVID-19 patients develop secondary bacterial infections, which cause death[18].
Overall, it is suggested that further research should be conducted involving histological examinations of cardiac tissues in COVID-19 patients to determine the relationship between COVID-19 and myocardial injury. Since biopsy-proven myocarditis may occur in the absence of troponin release, autopsy studies of COVID-19 victims, regardless of troponin levels, will help clarify whether SARS-CoV-2 is a novel cause of viral myocarditis.
There are some limitations in the current study. The study’s main limitation is its non-randomized observational design, which means that all the registered cases involving the patients who were admitted to the hospital were included without taking the inclusion and exclusion criteria into account. The effects of several elements on the results were neglected due to a lack of information regarding some crucial data, such as body mass index, which could have a negative impact on the generalizability of the results. In addition, the studied patients had visited the hospital at different stages of their illness, and their case information and histories were related to the time of the visit, which caused differences in the results, the comparisons of the people, and the impacts of risk factors.