CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 AFRICA 7 imaging and were classified into PE-positive (n = 33) and -negative groups. Physiological, radiological and biochemical parameters were compared and ROC curve analysis was conducted to determine a predictive D-dimer threshold. They proposed that in the absence of other clinical signs, a D-dimer threshold of 2 495 ng/ml could be used with high sensitivity and specificity to predict PE in hospitalised patients with COVID-19 (with 100% sensitivity and 90.6% specificity).22 In our study, the mean D-dimer value of all patients was 6.04 (IQR 9.06) and the cut-off point was 5.69 in patients who recieved thromboprophylaxis. Because of the prothrombotic state highlighted in COVID19, previous studies have reported that thrombus described by CTPA was in the majority of cases segmental or subsegmental during COVID-19-related PE. Some authors have suggested that a localised immunothrombosis process could contribute to the development of a thrombus within the lung inflammation area.23,24 For diagnostic accuracy and assessment of disease severity, in our study, the thrombus load was calculated from CTPA data using the Qanadli score.25 The mean Qanadli score was 11.29, which means that the distribution of thrombus localisation was mostly segmental and subsegmental. A study of 61 patients investigated the correlation between radiological and clinical–biochemical features in a cohort of hospitalised COVID-19 patients. PE was detected in only 14 patients and deep-vein thrombosis in five. The Qanadli score, RV/LV ratio, revised Geneva score and PESI were calculated in this patient group. It was found that the Qanadli score had a significant correlation with PESI, D-dimer, serum hs-troponin, serum albumin, arterial pressure of oxygen-to-inspired fraction of oxygen ratio (pO2/FiO2) and length of hospital stay. 26 In our study, there was a positive correlation between only the Qanadli and Geneva scores. Silva et al. evaluated the accuracy of the Wells and Geneva scores to predict PE in patients with SARS-CoV-2 infection in their study. There was no statically significant difference between the average Wells score in patients with and without PE (1.04 and 0.89, respectively, p = 0.733) and the AUC demonstrated that the Wells score had no discriminatory power (AUC = 0.5). The Geneva score of the groups was also similiar (4.20 vs 3.93, respectively, p = 0.420), with the AUC being 0.54.27 In our cohort, patients who developed PE had a pretest probability in the intermediate to low range, as confirmed by the Geneva score. The spectrum of mortality risk assessed by the PESI score ranged from Class I to III, but no patients died in our study. In the study of Wu et al., the median of the PESI was 88.1 (34–130).26 In our study, the mean of the PESI was 72.48 ± 24.62. This difference may have been due to the fact that our patients were younger. Although most of the hospitalised patients with COVID19 were on anticoagulant therapy, the incidence of PE was high. SARS-CoV-2 infection promotes endothelial dysfunction, prothrombotic events and pulmonary microthrombi, and the inflammatory host response leading to PE has been proven in autopsy studies.28 Poissy et al. showed that patients with COVID19 infection had a higher frequency of PE than patients infected with other infections.8 COVID-19 is now considered a pro-thrombotic disease with systemic inflammation. Post-mortem studies showed widespread alveolar damage and inflammation in patients. In the light of these data, it was determined that the pathogenic mechanism of PE was pulmonary intravascular coagulopathy.28,29 Despite prophylactic anticoagulation in patients with COVID-19, they can still develop thrombotic events. In a case series of 22 patients followed up in the ICU due to COVID-19 infection, PE was found in 20 patients, although all patients had received thromboprophylaxis.8 Similar results have been supported by other studies.30,31 In our study, 61% of the patients received at least one dose of anticoagulant treatment. There are several limitations to our study. It was a retrospective analysis of patients admitted with COVID-19 who underwent a CTPA, therefore, there may have been selection bias. In other words, the patients selected for CTPA were suspected of having a high pretest probability of PE. The sample size was small. There was a restriction on accessing different diagnostic tests and complex logistics to confirm PE, such as transthoracic echocardiography. Conclusion PE is seen frequently in patients with COVID-19 infection despite thromboprophylaxis. According to our results, traditional clinical prediction scores such as the PESI and Geneva score have little discriminatory power. A high D-dimer cut-off value should be considered a better measure to determine patients with PE. References 1. Grasselli G, Zangrillo A, Zanella A, Antonelli M, Cabrini L, Castelli A, et al. Baseline characteristics and outcomes of 1591 patients infected with SARS-CoV-2 admitted to ICUs of the Lombardy region, Italy. COVID-19 Lombardy ICU Network. J Am Med Assoc 2020; 323(16): 1574–1581. 2. Klok FA, Kruip MJHA, van der Meer NJM, Arbous MS, Gommers DAMPJ, Kant KM, et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19.Thromb Res 2020; 191(1): 145–147. 3. Goeijenbier M, van Wissen M, van de Weg C, Jong E, Gerdes VE, Meijers JC, et al. Viral infections and mechanisms of thrombosis and bleeding. J Med Virol 2012; 84(10): 1680–1696. 4. Ackermann M, Verleden SE, Kuehnel M, Haverich A, Welte T, Laenger F, et al. Pulmonary vascular endothelialitis, thrombosis, and angiogenesis in Covid-19. N Engl J Med 2020; 383(2): 120–128. 5. Edler C, Schröder AS, Aepfelbacher M, Fitzek A, Heinemann A, Heinrich F, et al. Dying with SARS-CoV-2 infection – an autopsy study of the first consecutive 80 cases in Hamburg, Germany. Int J Legal Med 2020; 134(5): 1275–1284. 6. Leonard-Lorant I, Delabranche X, Severac F, Helms J, Pauzet C, Collange O, et al. Acute pulmonary embolism in COVID-19 patients on CT angiography and relationship to D-dimer levels. Radiology 2020; 296(3): E189–E191. 7. Klok FA, Kruip MJHA, van der Meer NJM, Arbous MS, Gommers DAMPJ, Kant KM, et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thromb Res 2020; 191: 145–147. 8. Poissy J, Goutay J, Caplan M, Parmentier E, Duburcq T, Lassalle F, et al. Pulmonary embolism in COVID-19 patients: awareness of an increased prevalence. Circulation 2020; 142(2): 184–186. 9. Danzi GB, Loffi M, Galeazzi G, Gherbesi E. Acute pulmonary embolism and COVID-19 pneumonia: a random association? Eur Heart J 2020; 41(19): 1858.
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