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Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a heritable heart muscle disorder with fibro-fatty replacement that involves the right ventricle and in the advanced phases could become biventricular. Takotsubo syndrome (TTS) is characterized by reversible systolic dysfunction occurring after a stressful event and independent of the underlying coronary artery disease. A 70-year-old female with family history of sudden cardiac death and a previous diagnosis of biventricular ARVC presented to the emergency department after experiencing chest pain and elevation of myocardial enzymes. The ECG showed sinus bradycardia and negative T-waves from V1-V3. Coronary arteries were free from stenosing atheromatous lesions at coronary angiography. Transthoracic echocardiography showed severe biventricular dysfunction due to left ventricular apical/peri-apical akinesis with apical ballooning pattern. Cardiac magnetic resonance confirmed the presence of transmural biventricular edema in the mid-apical segments in T2 weighted sequences involving both ventricles along with fibro-fatty replacement in post-contrast sequences. At discharge, a cardioverter-defibrillator was implanted. This case report shows that TTS diagnosis is challenging for the clinician due to the presence of structural cardiomyopathy with biventricular involvement. Second-line imaging modalities could be useful to identify the presence of myocardial edema and to recognize those conditions associated with poor prognosis.

A 62-year-old male patient with a history of atypical chest pain ad dyspnea presented to the emergency room during the COVID-19 pandemic. On admission, the ECG showed sinus rhythm with diphasic T waves in lead V2. A high resolution computed tomography revealed signs suggestive of pulmonary infarction and a subsequent nasopharyngeal swab for SARS-CoV-2 was positive. An ECG performed in the absence of symptoms showed persistence of diphasic T waves in lead V2. In the suspect of Wellens syndrome, a coronary angiography study was performed and showed a subocclusion of the proximal left anterior descending artery.

Several studies suggested that the acute phase of SARS-CoV-2 infection may be associated with a hypercoagulable state and increased risk for venous thromboembolism but the incidence of thrombotic complications in the late phase of the disease is currently unknown. The present article describes three cases of patients with SARS-CoV-2 pneumonia and late occurrence of pulmonary embolism. Case 1: a 57-year-old man diagnosed with pulmonary embolism and type B aortic dissection after 12 days from SARS-CoV-2 pneumonia. Laboratory panel at the time of pulmonary embolism showed no signs of ongoing inflammation but only an elevated D-dimer. Case 2: a 76-year-old man with a diagnosis of SARS-CoV-2 pneumonia followed by pulmonary embolism 20 days later, high-resolution computed tomography on that time showed a partial resolution of crazy paving consolidation. Case 3: a 77-year-old man with SARS-CoV-2 pneumonia who developed a venous thromboembolic event despite thromboprophylaxis with low molecular weight heparin. Also in this patients no markers of inflammation were present at the time of complication.The present cases raise the possibility that in SARS-CoV-2 infection the hypercoagulable state may persist over the active inflammation phase and cytokine storm. These findings suggest a role for medium-long term therapeutic anticoagulation started at the time of SARS-CoV-2 pneumonia diagnosis.