Effects of Catecholamine Stress on Diastolic Function and Myocardial Energetics in Obesity
Background—Obesity is characterized by impaired cardiac energetics that 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 (BMI 22 ± 2; n = 9-17) and obese subjects (BMI 39 ± 7; n=17-46) underwent assessment of diastolic LV function (cine-MRI volume-time curve analysis) and cardiac energetics (PCr/ATP ratio; 31P-MR 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 (PFR) (p<0.001) and a 15% lower PCr/ATP ratio (1.73 ± 0.40 vs 2.03 ± 0.28, p=0.048). PFR correlated with fat mass, LV mass, leptin, waist-hip ratio and with PCr/ATP ratio. On multivariable analysis, PCr/ATP was the only independent predictor of PFR (β=0.50, p=0.03). During stress, a further reduction in PCr/ATP occurred in obesity (from 1.73 ± 0.40 to 1.53 ± 0.50, p=0.03) but not in normals (from 1.98 ± 0.24 to 2.04 ± 0.34, p = 0.50). For similar levels of inotropic stress, there were smaller increases in PFR in obesity (38% vs 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.
- Received September 21, 2011.
- Accepted February 17, 2012.
- Copyright © 2012, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited