ABC | Volume 115, Nº1, July 2020

Case Report Passos et al. Pulmonary Thromboembolism in COVID-19 Arq Bras Cardiol. 2020; 115(1):142-145 48 mmHg); d) degenerative changes of aortic and mitral valves; e) absence of vegetations and/or thrombus. The hypothesis of myopericarditis was then raised, but both electrocardiographic findings and myocardial lesion markers were normal. Cardiac magnetic resonance imaging, which is a valuable test in these situations, was delayed due to ongoing infection. Subsequently, an exponential increase in D-dimer and C-reactive protein levels was observed, while troponin and NT- pro-BNP levels remained within normal ranges, as described in Table 1. It is worth pointing out that the negative RT-PCR may be explained, at least in part, by the fact that the specimens were collected on the ninth day of symptom onset, when virus release is known to be falling. Due to the high suspicion of COVID-19, the regimen of antibiotics was maintained; also, a serological test was ordered, which yielded a positive result for the disease (IgG - / IgM + SARS-Cov-2). Considering the echocardiographic changes and significant elevation of D-dimer (5,000 ug), a lower extremity venous duplex scan was performed to investigate venous thrombosis, and the result was negative. Computed tomography angiography of the chest was then carried out (Figure 2), which revealed filling defect of the distal right pulmonary artery, extending to segmental branches of the right upper lobe, compatible with pulmonary thromboembolism. Then, an anticoagulation was initiated with enoxaparin 120 mg/day for 72 hours, substituted with rivaroxaban 30 mg/day due to improvement in hemodynamics and mechanical ventilation weaning plan. From the eight day on, the patient showed progressive improvement with concomitant decrease in dimer-D levels, as shown in Figure 1. The patient was extubated on the tenth day of hospitalization. Four days after, the patient was discharged, with rivaroxaban 30mg/day for further 17 days and when 21 days are completed, 20mg/day for 3-6 months, according to outpatient follow-up visits. Discussion There have been remarkable and variable cardiovascular complications of the coronavirus infection. 5 In severe manifestations of COVID-19, increased D-dimer and its association with increased mortality have been observed. 5 Studies have suggested that an exacerbate systemic inflammatory response plus hypoxia may cause endothelial dysfunction and increased procoagulant activity, contributing to thrombus formation. This prothrombotic state, associated with systemic infection, is commonly known as sepsis- induced coagulopathy. 6-9 It is worth mentioning that the data available on thrombotic risk are limited; most of the cases reported have been derived from case series in China, Holland and Fance. 10 However, most experts agree that one sign of increased thrombotic risk is sufficient to recommend pharmacological prophylaxis Figure 1 – Chest computed tomography without contrast on hospital admission. Ground-glass opacities, mainly in peripheral areas and more evidently in lower segments, affecting less than 50% of the pulmonary parenchyma. Table 1 – D-dimer, troponin, and NT-ProBNP levels during hospitalization Hospitalization day D-dimer (ug) Troponin (ug/ml) NT - ProBNP (ug/ml) Day 1 288 <0.012 - Day 2 449 < 0.012 Day 3 1220 < 0.012 Day 4 2310 Day 5 2240 Day 6 5000 Day 7 5000 < 0.012 111 Day 8 4030 104 Day 13 2210 Day 17 1590 416 143