OBJECTIVES: A reduced myocardial phosphocreatine/adenosine triphosphate (PCr/ATP) ratio is linked to both diastolic dysfunction and heart failure. Although obesity is well known to cause diastolic dysfunction a link to impaired cardiac energetics has only recently been established. We assessed whether or not long-term weight loss in obesity, which is known to reduce mortality, is accompanied by both improved cardiac energetics and diastolicfunction.
METHODS: Normal weight (BMI 22 Â± 2; n = 18) and obese subjects (BMI 34 Â± 4; n = 13) underwent cine-MRI (1.5 Tesla) to determine left ventriculardiastolic function using volume-time curve analysis, and (31)P-MR spectroscopy (3 Tesla) to assess cardiac energetics (PCr/ATP ratio). Obese subjects (n = 13) underwent repeat assessment after 1 year of supervised weight loss.
RESULTS: Obesity, in the absence of identifiable cardiovascular risk factors, was associated with significantly impaired myocardial high energy phosphate metabolism (PCr/ATP ratio, normal; 2.03 Â± 0.27 vs. obese; 1.58 Â± 0.47, p = 0.002) and significantly lower peak diastolic filling rate (normal; 4.8 Â± 0.8 vs. obese; 3.8 Â± 0.7 EDV/s, p = 0.01). Weight loss (on average 9 kg, 55 % excess weight) over 1 year resulted in a 24 % increase in PCr/ATP ratio (p = 0.01) and an 18 % improvement in peak diastolicfilling rate (p = 0.01). Myocardial PCr/ATP ratio remained positively correlated with peak diastolic filling rate after weight loss (r = 0.63, p = 0.02).
CONCLUSIONS: In obesity, weight loss improves impaired cardiac energetics and myocardial relaxation. Improved myocardial energetics appear to play a key role indiastolic functional recovery accompanying weight loss. Malik Hooker Authentic Jersey