ABSTRACT
The infection by the novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is associated with significant cardiovascular morbidity and mortality. Cardiac events require prompt diagnosis and management, also in the SARS-CoV-2 era. A 58-year-old male, heavy smoker and with known SARS-CoV-2 infection, abruptly developed severe hypotension and asthenia. At patients' home, emergency physicians found hemodynamic compromise with diffuse ST-elevation at electrocardiography. The patient was rapidly moved to the cardiac catheterization laboratory, and any contact with other health-care workers was avoided. Coronary angiography excluded coronary artery disease. At admission to the coronavirus disease-2019 unit, an increase in inflammatory markers and liver enzymes with normal troponin levels were observed. Bedside lung ultrasonography showed interstitial syndrome and bilateral pleural effusion, whereas echocardiography showed large and diffuse pericardial effusion with a swinging heart. The hemodynamic status improved after gentle fluid therapy such suggesting potential concomitant sepsis and pericardiocentesis was not performed. At this time, a computed tomography scan showed a widespread neoplasm in the right lung involving the subclavian artery and vein and the thoracic lymph nodes. The histology confirmed the diagnosis of a locally advanced pulmonary adenocarcinoma. One week after admission, the patient died for worsening respiratory failure. Not delayed primary PCI remains the standard of care for patients with suspected ST-elevation myocardial infarction (STEMI) in the SARS-CoV-2 era. A diagnostic deepening for potential STEMI-mimicker (known to be associated with SARS-CoV-2 infection and to patients' comorbidities) should be considered, and a multidisciplinary approach is needed in these patients.
ABSTRACT
INTRODUCTION: Emerging evidence points to an association between severe clinical presentation of COVID-19 and increased risk of thromboembolism. One-third of patients hospitalized due to severe COVID-19 develops macrovascular thrombotic complications, including venous thromboembolism, myocardial injury/infarction and stroke. Concurrently, the autopsy series indicate multiorgan damage pattern consistent with microvascular injury. PROPHYLAXIS, DIAGNOSIS AND TREATMENT: COVID-19 associated coagulopathy has distinct features, including markedly elevated D-dimers concentration with nearly normal activated partial thromboplastin time, prothrombin time and platelet count. The diagnosis may be challenging due to overlapping features between pulmonary embolism and severe COVID-19 disease, such as dyspnoea, high concentration of D-dimers, right ventricle with dysfunction or enlargement, and acute respiratory distress syndrome. Both macro- and microvascular complications are associated with an increased risk of in-hospital mortality. Therefore, early recognition of coagulation abnormalities among hospitalized COVID-19 patients are critical measures to identify patients with poor prognosis, guide antithrombotic prophylaxis or treatment, and improve patients' clinical outcomes. RECOMMENDATIONS FOR CLINICIANS: Most of the guidelines and consensus documents published on behalf of professional societies focused on thrombosis and hemostasis advocate the use of anticoagulants in all patients hospitalized with COVID-19, as well as 2-6 weeks post hospital discharge in the absence of contraindications. However, since there is no guidance for deciding the intensity and duration of anticoagulation, the decision-making process should be made in individual-case basis. CONCLUSIONS: Here, we review the mechanistic relationships between inflammation and thrombosis, discuss the macrovascular and microvascular complications and summarize the prophylaxis, diagnosis and treatment of thromboembolism in patients affected by COVID-19.