CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 20 AFRICA Our study revealed that patients with hypertension, diabetes mellitus, chronic renal failure, heart failure or COPD and patients who had had previous bypass surgery were more susceptible to cardiac injury. Such patients are more likely to develop severe pneumonia, myocardial ischaemia or cardiac dysfunction, which may ultimately lead to a sudden clinical deterioration. Parallel to our study, in a study by Yu Kang et al., pre-existing co-morbidities in patients, such as hypertension, diabetes and cardiovascular disease, were associated with a more severe course of COVID-19 and a higher mortality rate.20 Elderly patients with underlying diseases (especially hypertension, coronary heart disease and diabetes) are more likely to be infected with COVID19 and have a tendency to suffer the disease with higher severity.21 We also observed higher mortality rates for the older patients in our study. Acute inflammatory response can also lead to ischaemia in cases of pre-existing cardiovascular disease. The inflammatory activity in coronary atherosclerotic plaques is exacerbated during the systemic inflammatory response, making the plaques more prone to rupture.22 Inflammation causes endothelial dysfunction and increases the procoagulant activity of the blood. This may also contribute to the formation of an occlusive thrombus on a ruptured coronary plaque.23 Current guideline recommendations must be followed in terms of coronary intervention in patients with MI. Based on this evidence, we assume that an intense systemic inflammatory response that develops on the basis of pre-existing cardiovascular disease may accelerate the cardiac injury observed in patients with COVID-19 infection. In our study, daily troponin I values were monitored for 10 days. Regardless of the day, it was found that the troponin I value was related to the rate of ICU admission and mortality risk. This finding suggests that troponin I levels should be monitored not only on admission but also every few days in hospitalised patients. It was observed that the significant increase in troponin I levels, especially during the cytokine storm, was directly related to mortality rate. The pattern of increase in troponin I levels is important as it can be prognostic. Myocardial injury with DIC was reported in two critically ill patients with COVID-19.24 Both patients had significantly elevated serum troponin and brain natriuretic peptide levels. These patients returned to normal after treatment with heparin, mechanical ventilation and antiviral agents.24 Non-ischaemic mechanisms such as acute and fulminant myocarditis and stressinduced cardiomyopathy may also mediate myocardial injury in COVID-19 infection. Diagnosis can be made by cardiac magnetic resonance (MRI) or cardiac biopsy. Even after recovery from confirmed SARSCoV-2 infection, cardiac MRI showed left ventricle dilatation, low ejection fraction, myocardial oedema and inflammation in these patients.25 However, in a cohort study of 112 patients with COVID-19 disease, 14 patients had clinical abnormalities indicative of myocarditis but no evidence of cardiac injury on the ECG or echocardiogram. This finding led us to believe that cardiac injury was secondary to systemic effects rather than direct viral involvement.26 In a case report from Italy, a 53-year-old woman presented with severe fatigue and elevated cardiac biomarker levels, which is evidence of acute myopericarditis. There was widespread ST-elevation in her ECG and the MRI showed major abnormalities, including biventricular hypokinesia, ventricular interstitial oedema, peripheral pericardial effusion and left ventricular ejection fraction of 35%.27 In the autopsy series of 12 consecutive COVID-19 deaths, SARS-CoV-2 RNA was detected in the lungs of all patients and five patients showed high viral titres in the heart.15 Currently, the exact mechanism of action of cardiac injury by SARS-CoV-2 is not fully understood. Some evidence suggests an indirect effect of the virus, in which cardiac injury appears to be mostly associated with systemic inflammation and hypoxia. In a few cases, direct viral involvement of myocytes could lead to viral myocarditis.28 In a case series of 21 severe COVID-19 patients in the intensive care unit, one-third of patients developed new-onset cardiomyopathy with clinical signs of cardiogenic shock and globally reduced left ventricular ejection fraction on a transthoracic echocardiogram, with elevated CK or troponin I values.29 Several studies have reported takotsubo (stress-induced) cardiomyopathy as a complication of COVID-19.30,31 It has also been reported that cardiomyopathy can develop in COVID-19 with mild or no respiratory symptoms.32 Knowing the presence or absence of cardiomyopathy is important for managing patients in shock and determining the need for circulatory support and the type of extracorporeal membranous oxygenation. It has been shown that patients with high troponin levels are more likely to have malignant arrhythmias (ventricular tachycardia causing haemodynamic instability or ventricular fibrillation).32 Important aetiological factors in terms of cardiac injury are myocarditis, stress cardiomyopathy, acute heart failure and direct cardiac injury caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). However, it is likely that primary causes of most of the myocardial injury are primary non-cardiac conditions such as pulmonary embolism, severe inflammation and sepsis. Moderate or high elevation of fibrin-related markers (D-dimer and fibrin degradation products) has been reported in late stages of COVID-19 pneumonia and in all SARS-CoV-2 deaths; hence this suggests a common coagulation activation and secondary hyperfibrinolysis in these patients.33 Pathogenic mechanisms triggered by COVID-19 after entering the human body include inflammatory cascades, cytokine storms and activation of coagulation cascades. These processes are common in cases of systemic vasculitis and cause serious pulmonary, renal and cerebral complications apart from sepsis, DIC and acute cardiovascular events, and can be fatal. The prevalence of ultrasound-confirmed deep-vein thrombosis in COVID-19 patients is 22.7%,33 and 27% in patients in the ICU.11 In our study, daily D-dimer levels were measured for 10 days. It was found that high serum D-dimer levels were associated with ICU admission and higher mortality rates, regardless of the day of measurement. There was a correlation found between an increase in mortality rate and serum D-dimer levels higher than 1 µg/ml at hospital admission in a retrospective multi-centre cohort study.16 Patients with COVID-19 have been shown to have significantly higher levels of D-dimer, fibrin degradation products and fibrinogen compared to healthy controls.34 Additionally, higher levels of D-dimer have been shown in patients with severe COVID-19 infection.34 The elevation of D-dimer levels in COVID-19 patients may be associated with serious complications and death.34 Raised
RkJQdWJsaXNoZXIy NDIzNzc=