Aims We sought to determine if myocardial energetics could distinguish obesity cardiomyopathy as a distinct entity from dilated cardiomyopathy. Methods and results Sixteen normal weight participants with dilated cardiomyopathy (DCMNW), and 27 with DCM and obesity (DCMOB), were compared to 26 normal weight controls (CTLNW). All underwent cardiac magnetic resonance imaging and 31P spectroscopy to assess function and energetics. Nineteen DCMOB underwent repeat assessment after a dietary weight loss intervention. Adenosine triphosphate (ATP) delivery through creatine kinase (CK flux) was 55% lower in DCMNW than in CTLNW (P = 0.004), correlating with left ventricular ejection fraction (LVEF, r = 0.4, P = 0.015). In contrast, despite similar LVEF (DCMOB 41 ± 7%, DCMNW 38 ± 6%, P = 0.14), CK flux was two-fold higher in DCMOB (P < 0.001), due to higher rate through CK [median kf 0.21 (0.14) vs. 0.11 (0.12) s−1, P = 0.002]. During increased workload, the CTLNW heart increased CK flux by 97% (P < 0.001). In contrast, CK flux was unchanged in DCMNW and fell in DCMOB (by >50%, P < 0.001). Intentional weight loss was associated with positive left ventricular remodelling, with reduced left ventricular end-diastolic volume (by 8%, P < 0.001) and a change in LVEF (40 ± 9% vs. 45 ± 10%, P = 0.002). This occurred alongside a fall in ATP delivery rate with weight loss (by 7%, P = 0.049). Conclusions In normal weight, DCM is associated with reduced resting ATP delivery. In obese DCM, ATP demand through CK is greater, suggesting reduced efficiency of energy utilization. Dietary weight loss is associated with significant improvement in myocardial contractility, and a fall in ATP delivery, suggesting improved metabolic efficiency. This highlights distinct energetic pathways in obesity cardiomyopathy, which are both different from dilated cardiomyopathy, and may be reversible with weight loss.

中文翻译：

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肥胖改变扩张型心肌病的能量表型

目的 我们试图确定心肌能量学是否可以将肥胖型心肌病与扩张型心肌病区分开来。方法和结果 将 16 名患有扩张型心肌病 (DCMNW) 的正常体重参与者和 27 名患有扩张型心肌病 (DCMOB) 的参与者与 26 名正常体重对照者 (CTLNW) 进行比较。所有受试者都接受了心脏磁共振成像和 31P 光谱来评估功能和能量。十九名 DCMOB 在饮食减肥干预后接受了重复评估。DCMNW 中通过肌酸激酶（CK 通量）输送的三磷酸腺苷 (ATP) 比 CTLNW 低 55% (P = 0.004)，与左心室射血分数相关 (LVEF，r = 0.4，P = 0.015)。相比之下，尽管 LVEF 相似（DCMOB 41 ± 7%，DCMNW 38 ± 6%，P = 0.14），但 DCMOB 中的 CK 通量高出两倍（P < 0.001），因为通过 CK 的速率较高 [中位 kf 0.21] (0.14) 与 0.11 (0.12) s−1, P = 0.002]。在工作量增加期间，CTLNW 心脏使 CK 通量增加了 97%（P < 0.001）。相反，CK通量在DCMNW中没有变化，在DCMOB中下降(下降＞50％，P＜0.001)。有意减肥与积极的左心室重塑相关，左心室舒张末期容积减少（减少 8%，P < 0.001），并且 LVEF 发生变化（40 ± 9% vs. 45 ± 10%，P = 0.002） 。与此同时，ATP 输送率随体重减轻而下降（下降 7%，P = 0.049）。结论 在正常体重下，DCM 与静息 ATP 输送减少有关。在肥胖的 DCM 中，通过 CK 的 ATP 需求更大，表明能量利用效率降低。饮食减肥与心肌收缩力的显着改善和 ATP 输送量的下降有关，表明代谢效率得到提高。这凸显了肥胖型心肌病中独特的能量途径，它们与扩张型心肌病不同，并且可能随着体重减轻而逆转。