Dávila-Román Víctor G, Vedala Giridhar, Herrero Pilar, de las Fuentes Lisa, Rogers Joseph G, Kelly Daniel P, Gropler Robert J
Cardiovascular Imaging and Clinical Research Core Laboratory, Cardiovascular Division, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.
J Am Coll Cardiol. 2002 Jul 17;40(2):271-7. doi: 10.1016/s0735-1097(02)01967-8.
The purpose of this study was to determine whether patients with idiopathic dilated cardiomyopathy (IDCM) exhibit alterations in myocardial fatty acid and glucose metabolism.
Alterations in myocardial metabolism have been implicated in the pathogenesis of heart failure (HF); however, studies of myocardial metabolic function in human HF have yielded conflicting results. Animal models of HF have shown a downregulation of the expression of enzymes of fatty acid beta-oxidation that recapitulates the fetal energy metabolic program, in which fatty acid metabolism is decreased and glucose metabolism is increased.
Seven patients with IDCM (mean left ventricular ejection fraction 27 +/- 8%) and 12 normal controls underwent positron emission tomography for measurements of myocardial blood flow (MBF), myocardial oxygen consumption (MVO(2)), myocardial glucose utilization (MGU), myocardial fatty acid utilization (MFAU) and myocardial fatty acid oxidation (MFAO).
The systolic and diastolic blood pressures, plasma substrates and insulin levels, MBF and MVO(2), were similar between groups. The rates of MFAU and MFAO were significantly lower in IDCM than in the normal control group (MFAU: 134 +/- 44 vs. 213 +/- 49 nmol/g/min, p = 0.003; and MFAO: 113 +/- 50 vs. 205 +/- 49 nmol/g/min, p = 0.001) and the rates of MGU were significantly higher in IDCM than the normal control group (MGU: 247 +/- 63 vs. 125 +/- 64 nmol/g/min, p < 0.001).
Patients with IDCM exhibit alterations in myocardial metabolism characterized by decreased fatty acid metabolism and increased myocardial glucose metabolism, a pattern similar to that shown in animal models of HF. Whether alterations in myocardial metabolism constitute an adaptive response or mediate the development of HF remains to be determined.
本研究旨在确定特发性扩张型心肌病（IDCM）患者的心肌脂肪酸和葡萄糖代谢是否存在改变。
心肌代谢改变与心力衰竭（HF）的发病机制有关；然而，关于人类HF心肌代谢功能的研究结果相互矛盾。HF动物模型显示脂肪酸β氧化酶表达下调，重现了胎儿能量代谢程序，即脂肪酸代谢减少，葡萄糖代谢增加。
7例IDCM患者（平均左心室射血分数27±8%）和12名正常对照者接受正电子发射断层扫描，以测量心肌血流量（MBF）、心肌氧耗量（MVO₂）、心肌葡萄糖利用率（MGU）、心肌脂肪酸利用率（MFAU）和心肌脂肪酸氧化（MFAO）。
两组间收缩压和舒张压、血浆底物和胰岛素水平、MBF和MVO₂相似。IDCM患者的MFAU和MFAO速率显著低于正常对照组（MFAU：134±44对213±49 nmol/g/min，p = 0.003；MFAO：113±50对205±49 nmol/g/min，p = 0.001），IDCM患者的MGU速率显著高于正常对照组（MGU：247±63对125±64 nmol/g/min，p < 0.001）。
IDCM患者表现出心肌代谢改变，其特征是脂肪酸代谢减少，心肌葡萄糖代谢增加，这一模式与HF动物模型相似。心肌代谢改变是构成适应性反应还是介导HF的发展仍有待确定。
