LAUSR

Obesity doubles the lifetime risk of developing heart failure. Current knowledge on the role of obesity in causing cardiac dysfunction is insufficient for optimal risk stratification. The aim of the study was first to identify the prevalence of subclinical cardiac dysfunction in obesity patients and second to investigate the underlying pathophysiology by comparing obesity patients with and without cardiac dysfunction. The CARDIOBESE-study is a cross-sectional multicentre study of 100 obesity patients (BMI ≥35 kg/m2) without known cardiovascular disease, and 50 age- and gender-matched non-obese controls (BMI ≤30 kg/m2). Echocardiography was performed, blood samples were collected and a Holter monitor was affixed. Cardiac dysfunction was defined as either reduced LV ejection fraction, decreased global longitudinal strain (GLS), diastolic dysfunction, sustained supraventricular or (non)sustained ventricular arrhythmia or an increased BNP. Figure 1a shows the characteristics of the obesity patients and the non-obese controls. 59 obesity patients (48 [42–50] years, 70% female) showed subclinical cardiac dysfunction: 57 patients had decreased GLS, 2 patients with normal GLS had either diastolic dysfunction or increased brain natriuretic peptide. Only 1 non-obese control had diastolic dysfunction, none had another sign of cardiac dysfunction. Figure 1b shows the characteristics of obesity patients with and without cardiac dysfunction. Multivariable logistic analysis identified male gender and SDNN-index, which is a heart rate variability parameter and thereby a measure of autonomic dysfunction, as independent significant risk factors for subclinical cardiac dysfunction in obesity patients. There was a high prevalence (61%) of subclinical cardiac dysfunction in obesity patients without known cardiovascular disease, which appeared to be best identified by GLS. Subclinical cardiac dysfunction in obesity was linked to autonomic dysfunction and male gender, and not to the presence of traditional cardiac risk factors, inflammation, increased cardiac filling pressure, cardiomyocyte damage or increased left ventricular mass. Figure 1 Type of funding source: Public Institution(s). Main funding source(s): Stichting BeterKeter