BackgroundExcessive weight and obesity (EwO) are independent factors in the development of heart failure; they lead to a state of myocardiopathy via inflammatory and hormonal mechanisms. If excessively accumulated, epicardial fat favors a proinflammatory state. Ventricular asynchrony is a marker of heart failure progression and has been poorly studied in EwO. The objective was evaluate the relation between epicardial fat, body mass index (BMI) and mechanical synchrony measured by echocardiography, in healthy individuals with EwO.MethodsWe included 55 healthy individuals between the ages of 18 and 35, 17 had a BMI < 25 kg/m2 (30.9%) and 38 had a BMI > 25 kg/m2 (EwO group) (69.09%), anthropometric measurements, transthoracic echocardiogram and synchrony evaluation were obtained.ResultsLeft atrial volume, telediastolic and telesystolic left ventricular volumes and the baseline volume of the right ventricle were greater in the EwO group (20 mL/m2 vs. 15 mL/m2, p = 0.001; 106 mL vs. 82 mL, p = 0.0149 vs. 32 mL, p = 0.001 and 34 mm vs. 31 mm, p = 0.02, respectively). The Yu index also correlated with epicardial fat, r = 0.53, p < 0.01, whereby the greater the amount of epicardial fat, the greater the dispersion timing of ventricular activation. The systolic synchrony index also correlated with the BMI, p = 0.01.ConclusionMechanical intraventricular asynchrony is associated to EwO and the amount of epicardial fat; hence, asynchrony may be one more factor leading to heart failure in EwO individuals.

Aortic coarctation (AC) represents 7% of congenital heart disease. It is a reversible secondary cause of systemic hypertension, however up to 35% of patients remain hypertensive and 18% have cardiovascular complications such as aortic aneurysm, dissection or aortic valve disease. AC is associated with bicuspid aortic valve (BAV) in around 60%, both diseases alter aortic wall distensibility, stiffness and wall shear stress (WSS). Our objective was to compare these parameters in patients with AC according to the morphology or the aortic valve (either bicuspid or tricuspid).

Chagas disease is a parasitosis caused by the protozoan Trypanosoma cruzi. It is endemic in Latin America, nevertheless it has spread to other regions of the world due to migration. Up to 30% of the infected patients progress to the chronic phase, with a 5-year mortality of 50% due to heart failure or ventricular arrhythmias. We aimed to compare ventricular function and delayed enhancement (DE) according to the predominant clinical presentation in Chronic Chagas disease (CCD) either ventricular tachycardia (VT) or heart failure (HF), as well as to compare CCD with the undetermined and subclinical phases.