ABSTRACT
76-year-old man, hypertensive, suffering from permanent atrial fibrillation in treatment with Apixaban 5mg x 2/day. Hyperpiressia for a few days, treated with broad- spectrum antibiotic therapy. For the appearance of dyspnea and constricting retrosternal pain of about 20 minutes, he accessed to the emergency room of “San Paolo” Hospital in Bari. Electrocardiogram showed high ventricular response atrial fibrillation, while echocardiogram hypokinesia of the apical segments and moderate left ventricular dysfunction. Blood tests showed an increase in myocardial troponines. Chest angio CT highlited bilateral ground glass pulmonary thickening and pleural effusion, in the absence of signs of pulmonary thromboembolysm. The first molecular swab for SARS COV2 resulted negative. Subsequent admission to Cardiology Unit. During the hospitalization, coronary artery showed non-significant atheromasia of the epicardic branches and slow run-off of the anterior interventricular artery and right coronary artery. Subsequent pneumological evaluation made the indication to therapy with cephalosporins and corticosteroids and clinical- instrumental follow-up. The patient was discharged after a few days with a diagnosis of ACS-NSTEMI. After 8 days, new access to the emergency room due to worsening of dyspnea. For high D- dimer values, he underwent a new chest angio CT which showed pulmonary embolism and confirmed the presence of pulmonary parenchymal thickening already described. The new molecular swab documented positivity for SARS-COV2. Therefore, the patient wea hospitalized in the COVID department. After a few hours, weakness of the right arm appeared;skull CT and neurological evaluation concluded for probable cerebral ischemic episode. SARS-COV2 disease could lead to a multi-organ hyperergic inflammatory response. In this clinical case, there was the involvement of multiple vascular districts (cardiac, pulmonary), and in addition, a brain perfusion deficit of a probably cardioembolic nature, despite adequate oral anticoagulant therapy with DOAC that had been taken for some time. Currently, the effectiveness of DOACs is not known in patients with SARS-COV2 infection and, above all, whether these drugs are able to counteract the hypercoagulation tendency associated with systemic vasculitis that accompanies the most complex clinical infection.
ABSTRACT
SARS-COV2 causes a large inflammatory response. The effects on the cardiac and vascular system are still being studied. Clinical Case: A 50-year-old man came to the emergency room of our hospital for fever and asthenia. For the positivity for SARS-COV2 and radiographic finding of bilateral interstitial pneumonia, he was hospitalized at the U.O. COVID, where for hypoxemic respiratory insufficiency he was subjected to ventilotherapy with CPAP. The improvement in respiratory failure and the negativization of the nasopharyngeal swab for SARS-COV2 indicated discharge. The patient underwent a pre-discharge ECG which showed negative T waves in the inferior site and from V3-V6 not present in the previous one. Dosage of cardiac cytonecrosis indices showed troponin T HS (34, ng/l v.n. <14 ng/l) slightly increased;blood chemistry tests show CRP equal to 26 mg/dl and normal leukocyte number and formula. The 2d color Doppler echocardiogram reported: “Akinesia of the mid-apical portion of the septum, apex and lower wall, with an FE equal to 45%. Presence of a slight pericardial detachment of the lateral wall of the left ventricle.” The patient was transferred to our U.O. of Cardiology, who underwent coronary angiography showing normal coronaries. With the suspicion of SARS-COV2 myocarditis, the patient underwent cardiac MRI which confirmed the akinesias shown on the echocardiogram. Late enhancement in subendocardial disposition consistent with an acute ischemic injury in these sites was evident on T2- weighted sequences. Discussion: Normal coronary myocardial infarctions (MINOCA) are described in the literature and it is hypothesized that the inflammatory reaction and hypoxia caused by SARS-COV2 may play a central role in the pathogenesis of ischemic disorder. The district nature of the lesion compatible with a coronary atherosclerotic obstruction not detected on angiographic examination, however, needs to be clarified. The vasculitis resulting from the infection can explain the locality of the lesion on the echocardiogram and on the ECG but opens the discussion on therapeutic choices.
ABSTRACT
Background: Right ventricle involvement during sepsis is often misunderstood, although it is described that an altered performance of the right ventricle is present in 2/3 of cases of moderate to severe forms of sepsis. Clinical Case: 30 years old woman without known cardiovascular risk factors with a history of multiple psychiatric disorders. Access to the emergency departement of our hospital complaining asthenia and hypotension. The patient underwent cardiological evaluation with EKG findings of sinus tachycardia and diffuse ST-T anomalies and bidimensional echocardiogram negative for biventricular kinetic anomalies. Laboratory evidence of creatinine 2.07 mg/dl, slight increase in inflammation indices (CRP 38 mg/dl) and anemia (HB: 9.2 g/l). Swab for SARS-COV2 was negative. The patient was then admitted to the local department of Medicine. During hospitalization, evidence of hypotension and progressive worsening of inflammation indices. Due to addominal pain, the patient underwent EGDS showing hiatal hernia. Subsequent onset of fever, with negative urine culture and positive blood cultures for S. Epidermidis. In addition, due to the detection of involuntary movements of the limbs and eyelids she was subjected to cerebral MRI in suspicion of encephalitis, that was excluded. At a subsequent cardiological and echocardiographic evaluation, finding of “Hypocontractile right ventricle, volume overload of the right sections with paradoxical movement of the interventricular septum, PAPs: 50 mmHg”. On chestabdomen CT scan “absence of focal pulmonary lesions and bilateral pleural effusions, patent pulmonary circulation, absence of thrombotic filling defects”. The patient was therefore transferred to our cardiology departement with diagnosis of septic shock. During hospitalization, evidence of hypokalemia, long QT interval (> 500 msec) and self-limiting polymorphic ventricular tachycardia. After long-term therapy with inotropics and antibiotics, we found a significant clinical improvement with echocardiographic evidence of complete recovery of right ventricular performance. The case described is a paradigmatic example of reversible alteration of right ventricle systolic function during septic shock (severe sepsis). The different pathogenetic determinants, however, are still debated. There are two possible hypotheses: inflammatory myocardial right ventricle involvement (myocarditis) or vasculitic involvement of right ventricle, sustained by inflammatory stress and bacteremia.