Effects of Catecholamine Stress on Diastolic Function and Myocardial Energetics in Obesity

Abstract

Background— Obesity is characterized by impaired cardiac energetics, which may play a role in the development of diastolic dysfunction and inappropriate shortness of breath. We assessed whether, in obesity, derangement of energetics and diastolic function is further altered during acute cardiac stress. Methods and Results— Normal-weight (body mass index, 22±2 kg/m 2 ; n=9–17) and obese (body mass index, 39±7 kg/m 2 ; n=17–46) subjects underwent assessment of diastolic left ventricular function (cine magnetic resonance imaging volume-time curve analysis) and cardiac energetics (phosphocreatine/ATP ratio; 31 P-magnetic resonance spectroscopy) at rest and during dobutamine stress (heart rate increase, 65±22% and 69±14%, respectively; P =0.61). At rest, obesity was associated with a 22% lower peak filling rate ( P <0.001) and a 15% lower phosphocreatine/ATP ratio (1.73±0.40 versus 2.03±0.28; P =0.048). Peak filling rate correlated with fat mass, left ventricular mass, leptin, waist-to-hip ratio, and phosphocreatine/ATP ratio. On multivariable analysis, phosphocreatine/ATP was the only independent predictor of peak filling rate (β=0.50; P =0.03). During stress, a further reduction in phosphocreatine/ATP occurred in obese (from 1.73±0.40 to 1.53±0.50; P =0.03) but not in normal-weight (from 1.98±0.24 to 2.04±0.34; P =0.50) subject. For similar levels of inotropic stress, there were smaller increases in peak filling rate in obesity (38% versus 70%; P =0.01). Conclusions— In obesity, cardiac energetics are further deranged during inotropic stress, in association with continued diastolic dysfunction. Myocardial energetics may play a key role in the impairment of diastolic function in obesity.