Department of Cardiovascular Medicine, John Radcliffe Hospital, Oxford Centre for Clinical Magnetic Resonance Research, University of Oxford, Oxford OX3 9DU, UK.
Int J Cardiovasc Imaging. 2013 Jun;29(5):1043-50. doi: 10.1007/s10554-012-0174-6. Epub 2012 Dec 27.
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 diastolic function. Normal weight (BMI 22 ± 2; n = 18) and obese subjects (BMI 34 ± 4; n = 13) underwent cine-MRI (1.5 Tesla) to determine left ventricular diastolic 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. 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 ± 0.27 vs. obese; 1.58 ± 0.47, p = 0.002) and significantly lower peak diastolic filling rate (normal; 4.8 ± 0.8 vs. obese; 3.8 ± 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 diastolic filling 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). In obesity, weight loss improves impaired cardiac energetics and myocardial relaxation. Improved myocardial energetics appear to play a key role in diastolic functional recovery accompanying weight loss.
心肌磷酰肌酸/三磷酸腺苷（PCr/ATP）比值降低与舒张功能障碍和心力衰竭均有关。虽然肥胖症众所周知会导致舒张功能障碍，但最近才发现其与心脏能量代谢受损有关。我们评估了肥胖症患者的长期减重（已知可降低死亡率）是否同时伴有心脏能量代谢和舒张功能的改善。正常体重（BMI 22 ± 2；n = 18）和肥胖患者（BMI 34 ± 4；n = 13）接受电影-MRI（1.5 Tesla），使用容积时间曲线分析来确定左心室舒张功能，并进行（31）P-MR 光谱（3 Tesla）评估心脏能量代谢（PCr/ATP 比值）。13 名肥胖患者在 1 年的监督减重后进行了重复评估。在不存在可识别的心血管危险因素的情况下，肥胖症与心肌高能磷酸代谢明显受损（PCr/ATP 比值，正常；2.03 ± 0.27 比肥胖；1.58 ± 0.47，p = 0.002）和峰值舒张充盈率明显降低（正常；4.8 ± 0.8 比肥胖；3.8 ± 0.7 EDV/s，p = 0.01）有关。1 年内体重减轻（平均 9 公斤，超重 55%）导致 PCr/ATP 比值增加 24%（p = 0.01），峰值舒张充盈率提高 18%（p = 0.01）。减肥后，心肌 PCr/ATP 比值与峰值舒张充盈率仍呈正相关（r = 0.63，p = 0.02）。在肥胖症中，体重减轻可改善受损的心脏能量代谢和心肌松弛。改善的心肌能量代谢似乎在伴随体重减轻的舒张功能恢复中发挥关键作用。
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