ABSTRACT
Background: COVID-19 disease is characterized by respiratory symptoms, but acute cardiovascular complications are reported in severe infections that adversely affect prognosis. Clinical Case: A patient is hospitalized for fever, chest pain, and dyspnoea. Clinical examination: pulmonary and peripheral congestion, low blood pressure values, oxygen saturation in ambient air 91%. Increased myocardiocytolysis and inflammatory indices. Nasopharyngeal swab: positive for COVID-19. Chest CT scan: interstitial pneumonia. ECG: sinus tachycardia, changes in ventricular repolarization. Echocardiogram: left ventricle dilated, hypertrophic and with severe global systolic dysfunction. Therapy: furosemide, high flow oxygen alternating CPAP, antiretrovirals, antibiotics, low molecular weight heparin, beta blocker. Cardiac MRI: focal edema of the anterior wall. Coronary angiography: moderate coronary artery disease. Control chest CT scan: resolution of pulmonary interstitial disease. Cardiac MRI after 2 months: improvement of the overall systolic function of the left ventricle. Conclusions: An entity defined as “acute myocardial damage” characterized by an increase in troponin with ECG and/or echocardiographic changes, is reported in COVID patients. These forms are not related to coronary artery disease but are the consequence of the septic state and the excessive activation of the infectious- inflammatory systems and can manifest themselves with myocarditis/stress myocardiopathy causing heart failure and left ventricular systolic dysfunction.
ABSTRACT
Background: CoViD-19 infection can induce myocardial damage and heart failure, potentially complicated by arrhythmias, both as a direct consequence of CoViD-19 infection on cardiac activity, and as an effect of prescribed drug therapies. In fact, drugs such as azithromycin or hydroxychloroquine, used in CoViD-19 infection, can lengthen the QT interval with the possible risk of arrhythmias. Description of the case: A 40-year-old patient hospitalized for CoViD complains of heartbeat and atypical chest pain. Normal vital signs. ECG: rapid ventricular response atrial fibrillation. Echocardiogram: normal. Chest x-ray: bibasal interstitial pneumonia. Elevated troponin. Conclusions: Arrhythmias in patients with CoViD -19 infection are probably the consequence of direct myocardial damage or may occur as a result of metabolic disorder, hypoxia, neuro-hormonal alterations or inflammatory stress in the context of acute viremia. The onset of an arrhythmia in the presence of elevated cardiac markers may be an indication of underlying myocarditis. Since hypoxia and electrolyte abnormalities that can facilitate the onset of arrhythmias are common in the acute phase of the disease, especially in the most severe pictures, the exact arrhythmic risk of patients with less severe pictures and of patients in the post-acute phase is currently unknown. Stratification of the long-term arrhythmic risk of patients who have experienced episodes of arrhythmias in the acute phase of the disease is essential for their correct management.
ABSTRACT
Background: SARS-CoV-2 disease may be associated with a state of hypercoagulability and an increased risk of both venous and arterial thromboembolism. Clinical and biological evidence has documented a high thromboembolic risk in the acute phase of the infection, but the incidence of the risk in the late phase of the disease requires further investigation. Description of the case: A hypertensive and diabetic patient comes to the emergency room for dyspnea and fever. It is hypotensive, tachycardic and hypoxemic. Elevated D-dimer and troponin. ECG: sinus tachycardia and right bundle branch block. Echocardiogram: hypertensive heart disease and right overload. Chest CT: bilateral interstitial pneumonia, with filling defects at the bifurcation of the right pulmonary artery. Nasopharyngeal swab for SARSCoV- 2: positive. Conclusions: SARS-CoV-2 is configured as a multidimensional disease whose characteristic physiopathological and clinical aspects are being defined: a) an increased immunological and inflammatory response with activation of a cytokine storm and consequent coagulopathy, which favours both venous thromboembolism events and thrombosis in situ in the pulmonary arterioles and alveolar capillaries;b) a high intrapulmonary shunt, which accounts for the severity of respiratory failure, attributed to a reduced hypoxic pulmonary vasoconstriction with pulmonary neoangiogenic phenomena. These patients may benefit from anticoagulant therapy initiated as early as the diagnosis of SARS-CoV-2 pneumonia.
ABSTRACT
Background: Patients with CoViD-19 are at high risk of thromboembolic events due to hemostatic changes directly related to the SARS-CoV-2 infection or to the consequence of cytokine storm. Anticoagulation with heparin is recommended to reduce the thrombotic risk. Spontaneous iliopsoas hematoma (IPH) is a potentially life-threatening complication of anticoagulation therapy described in CoViD-19 patients. Materials and Methods: We report two cases of association with IPH and SARS-CoV-2 pneumonia treated with heparin. Results: Over a 5-month period (November 2020-April 2021) 252 subjects with SARS-CoV-2 infection were admitted to our CoViD hospital. We found two cases of spontaneous IPH during the clinical course of CoViD-19. Diagnosis of IPH was made by CT angiogram. Coagulation parameters and platlet count were normal. One patient (an 83-year-old woman) was on prophylactic low weight molecular heparin (LWMH). The other patient (a 79-yearold man) received a therapeutic dosage with LWMH for pulmonary thrombosis and died, after urgent transarterial embolization, because of hemorrhagic hypovolemic shock. Conclusions: Although case reports are scarce for conclusion, our two cases, in addition to previous reports, suggest that CoViD-19 patients treated with anticoagulants are at risk of IPH. Given the indications to prescribe anticoagulation in CoViD-19 and the lack of solid evidences on the optimal dose and duration, it is important to be aware of IPH as a potentially serious complication. Rapid diagnosis and timely intervention are crucial to ensure good patient outcomes.
ABSTRACT
Background: Emerging evidence indicates that SARS-CoV-2 infection may cause neurological complications.Case Report: 63-year-old male was admitted for acute progressive symmetric ascending weakness. He denied fever, cough, respiratory symptoms and his past medical history wasunremarkable. Physical examination showed normal blood pressure, oxygen saturation 98% on air, temperature 36,4°C, heartrate 96 bpm and severe weakness in all limbs. Chest X-ray,echocardiogram and abdominal ultrasonography were normal;ECG showed sinus rhythm (96 bpm). Cervical and brain magneticresonance revealed enhancement of the nerve roots. Abnormallaboratory tests were: PCR 447 mg/L, ferritin 1857 ng/mL, Ddimer 935 ng/mL, fibrinogen 1013 mg/dL, platelet count69000/μ L and lymphocytopenia (260/μ L). Viral serologies andautoimmune markers were negative. Cerebrospinal fluid analysisshowed normal cell count and lack of albumin-cytological dissociation. Guillain-Barrè Syndrome (GBS) was suspected and therapy by intravenous immunoglobulin and steroid was started. Anasopharyngeal swab was performed, which resulted positive toSARS-CoV-2 on RT-PCR assay. The patient was transferred to Infectious Diseases Unit to begin treatment by tocilizumab, hydroxychloroquine and plasmapheresis. Conclusions: GBS is immune-mediated disease often triggeredby various infections. Since SARS-Cov-2 may lead to a massiverelease of inflammatory cytokines, it could be hypothesized thatan aberrant immune response to SARS-CoV-2 infection inducesinflammatory damage in peripheral nerves with molecular mimicryreaction.