Cardiovascular Journal of Africa: Vol 32 No 6 (NOVEMBER/DECEMBER 2021)

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 32, No 6, November/December 2021 298 AFRICA Results There were a total of 10 patients in this preliminary report. Six of these patients were female and four were male. The minimum age was 17 years and the maximum was 79 years. The mean (SD) age was 52.5 ± 18.79 years. SARS-Cov-2 infection was diagnosed by RT-PCR assay in 60% and by serology in 40% of the patients. Sixty per cent of the patients had fever. About 70% of the patients were hypertensive and 50% were diabetic. All the patients with diabetes also had hypertension. Sixty per cent of the patients were obese. One patient had ischaemic heart disease with a previous history of myocardial infarction and stable chronic heart failure. One patient had no obesity, hypertension, diabetes mellitus or ischaemic heart disease. All patients had at least one elevated inflammatory marker. Elevated erythrocyte sedimentation rate (ESR) was seen in seven patients, while the three with normal ESR had elevated C-reactive protein (CRP). A D-dimer assay was done in six patients and was elevated in all. There was leucocytosis with neutrophilia in 30% of the patients, leucopaenia in 10%, relative lymphocytosis in 20% and moderate thrombocytopenia in 20%. Seven of the patients had elevated liver enzymes. Creatinine level was elevated in only one patient. Bilateral pneumonia was seen in four out of the 10 patients on either X-ray or CT scan of the chest. One of the cases presented in cardiogenic shock. He was 17 years and the youngest among the cases. In addition to cough and breathlessness, he also had pleuritic chest pain. The ECG showed sinus tachycardia and diffuse 1-mm ST-segment elevation. The echocardiography revealed mildly dilated cardiac chambers with normal left ventricular wall thickness. The left ventricular systolic function was severely depressed with left ventricular ejection fraction of 19.3%. Another case of a female patient of 54 years presentedwith chest tightness, cough and breathlessness. She had apical hypokinesia with bi-basal hyperkinesia, suggestive of stress cardiomyopathy on echocardiography. She was obese but not hypertensive or diabetic. Her ECG showed only sinus tachycardia. The high- sensitivity troponin I was undetectable. The echocardiographic findings returned to normal after three days. Five patients who presented with features of heart failure had left ventricular hypertrophy on echocardiography with good systolic function and grade 1 left ventricular diastolic dysfunction. One of the patients had asymmetric septal hypertrophy while the rest had concentric left ventricular hypertrophy. A normal-size hypocontractile left ventricle with mid-range left ventricular systolic function of 41% was seen in another patient who presented in heart failure. A 79-year-old patient among the cases who had ischaemic heart disease also presented in heart failure and the echocardiographic features were in keeping with ischaemic cardiomyopathy. The last of the cases had moderately dilated right heart with right ventricular overload, suggestive of pulmonary embolism. She was a known hypertensive and diabetic and she had delivered a live baby by cesarean section two months before presentation. A CT pulmonary angiogram could not be done owing to concern about infection control. Discussion At the start of the pandemic, COVID-19 was initially thought to be a respiratory disease with bilateral pneumonia, which can present as mild, moderate, severe or critical infection, with acute severe respiratory failure requiring mechanical ventilation. 13 It has however since been found to be a multi- systemic disease. 14 Some patients present with both pulmonary and cardiac manifestations, while others have only cardiac without pulmonary findings. 15,16 In this study, only four patients out of the 10 had pneumonia on X-ray or CT scan of the chest. Moreover, underlying cardiovascular co-morbidity also plays a role in the manifestation of SARS-Cov-2 infection. 11,17,18 Patients with cardiovascular co-morbidity have increased morbidity and mortality rates. 19 Hypertension was the commonest co-morbidity in this preliminary report, occurring in 70% of cases, followed by obesity in 60% of cases. It is not surprising that apart from the patient with fulminant myocarditis, all other patients had cardiovascular co-morbidity. Furthermore, cardiac involvement in COVID-19 is multi- factorial. Direct viral invasion of the myocardium or the effect of inflammatory mediators on the myocardium can cause myocarditis. 20 One patient in this study, 17 years of age, presented in cardiogenic shock due to fulminant myopericarditis or acute inflammatory cardiomyopathy. In fulminant myocarditis, direct viral invasion of the myocardium causes myocardial inflammation and oedema, whereas in acute inflammatory cardiomyopathy, the effect of inflammatory mediators on the myocardium, leading to increased capillary permeability, is believed to be responsible for the acute cardiomyopathy. 21-23 Cardiac magnetic resonance imaging (MRI) can be used for evaluation of suspected myocarditis but endomyocardial biopsy is still the gold standard in the evaluation of patients with myocarditis. 24 In addition, in some patients, heart failure has been reported to be the primary presentation of COVID-19. 25 Seven of the 10 patients seen in this study presented with heart failure. Six of these presented with de novo heart failure while one presented with de-compensated heart failure. Heart failure with preserved ejection fraction (HFpEF) was the predominant form seen in five of the seven patients who presented with heart failure. Infection with COVID-19 may unmask subclinical heart failure in patients with underlying risk factors. It may also exacerbate pre-existing heart failure. 26 The key link between heart failure and COVID-19 is their shared inflammatory pathophysiology. 26 The pro-inflammatory cytokines such as interleukin 1 and interleukin 6 that are released during infection with SARS-Cov-2 directly and indirectly affect the myocardium by causing endothelia dysfunction. Elevated inflammatory markers, most especially D-dimer, CRP and plasminogen activator inhibitors have been shown to be associated with higher risk of heart failure in the general population. 27 There are increasingnumbers of cases of stress cardiomyopathy during this pandemic. 28 This is most likely due to the psycho- socio-economic stress of the pandemic and not directly from the effects of the SARS-Cov-2 infection on the myocardium. 28 A patient in this study presented with features consistent with stress cardiomyopathy. There is a need for increased surveillance for this presentation in both infected and uninfected patients. However, it is also important to exclude myocarditis and acute coronary syndrome in such patients. Likewise, some studies have also shown that patients with COVID-19 are at an increased risk of venous thromboembolism, particularly pulmonary embolism. 29-31 This is due to systemic inflammation and elevated prothrombotic factors such as