Obesity is a current pandemic that sets all affected individuals at risk of heart failure (HF), and the majority of them will develop the clinical syndrome of HF with preserved ejection fraction (HFpEF). The diagnosis of HFpEF is challenging as it is based on the detection of subtle functional and structural remodeling of the heart that leads to diastolic dysfunction with increased left ventricular (LV) filling pressures and raised natriuretic peptides (NPs). The accurate diagnosis of HFpEF is even more challenging in patients who are obese, since the echocardiographic imaging quality may be suboptimal, the parameters for the evaluation of cardiac structure are indexed to the body surface area (BSA) and thus may underestimate the severity of the remodeling, and the NPs in patients who are obese have a lower normal threshold. Moreover, patients who are obese are prone to atrial fibrillation (AF) and pulmonary hypertension (PH), making the evaluation of diastolic dysfunction more strenuous. The current review aims to offer insights on the accurate diagnosis of HFpEF in patients who are obese in different clinical scenarios—patients who are obese in different clinical scenarios—such as in sinus rhythm, in atrial fibrillation, and in the case of pulmonary hypertension—by applying multimodality imaging and clinical diagnostic algorithms.

Remdesivir is an antiviral agent used as supportive care in adults with SARS-COV2-induced pneumonia. We report a case of an 81-year-old patient who developed hepatocellular acute liver injury 48 hours after initiating remdesivir. During the investigation, other causes of hepatotoxicity were excluded. A decrease in transaminases and international normalized ratio (INR) was observed 24 hours after cessation of remdesivir. An abdominal CT demonstrated hepatic congestion, retrograde hepatic venous opacification shortly after intravenous contrast injection, and dilatation of hepatic veins and inferior vena cava. We suggest congestive hepatopathy secondary to remdesivir as a possible component of liver injury.

A 3.5 cm diameter descending aorta focal aneurysm was incidentally found when a computed tomography (CT) was conducted due to persistent pyrexia in an 85-year-old woman hospitalized for a non-obstructive urinary tract infection. Ten days later, whilst fever subsided and inflammation markers decreased, she became hypoxic. CT revealed an aortic intramural hematoma (Stanford type B) increasing the diameter of the thoracic aorta aneurysm to 6.5 cm. A thoracic endovascular aortic repair (TEVAR) surgery was performed. Seven days after the operation she developed respiratory and hemodynamic compromise. CT depicted further enlargement of the aortic intramural hematoma, increasing the aortic diameter to 8 cm. Transthoracic echocardiography provided valuable information showing extrinsic compression of the left atrium and left ventricle inflow obstruction provoking obstructive shock.