Rayner Jennifer J, Peterzan Mark A, Clarke William T, Rodgers Christopher T, Neubauer Stefan, Rider Oliver J
Oxford Centre for Clinical Magnetic Resonance Research (OCMR), Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Level 0, John Radcliffe Hospital, Oxford OX3 9DU, UK.
Wellcome Centre for Integrative Neuroimaging, FMRIB, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK.
Eur Heart J. 2021 Sep 20;43(9):868-77. doi: 10.1093/eurheartj/ehab663.
We sought to determine if myocardial energetics could distinguish obesity cardiomyopathy as a distinct entity from dilated cardiomyopathy.
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).
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.
我们试图确定心肌能量学是否能够将肥胖性心肌病作为一种独特的实体与扩张型心肌病区分开来。
将16名体重正常的扩张型心肌病患者（DCMNW）和27名患有扩张型心肌病且肥胖的患者（DCMOB）与26名体重正常的对照组（CTLNW）进行比较。所有人均接受了心脏磁共振成像和31P波谱分析以评估心脏功能和能量学。19名DCMOB患者在进行饮食减肥干预后接受了重复评估。通过肌酸激酶的三磷酸腺苷（ATP）输送量（CK通量）在DCMNW中比CTLNW低55%（P = 0.004），与左心室射血分数（LVEF，r = 0.4，P = 0.015）相关。相比之下，尽管LVEF相似（DCMOB为41±7%，DCMNW为38±6%，P = 0.14），但DCMOB中的CK通量高出两倍（P < 0.001），这是由于通过CK的速率更高[中位数kf为0.21（0.14）对0.11（0.12）s-1，P = 0.002]。在工作量增加时，CTLNW组心脏的CK通量增加了97%（P < 0.001）。相比之下，DCMNW中的CK通量未改变，而DCMOB中的CK通量下降（超过50%，P < 0.001）。有意减肥与左心室正向重构相关，左心室舒张末期容积减小（8%，P < 0.001），LVEF发生变化（40±9%对45±10%，P = 0.002）。这伴随着减肥导致的ATP输送速率下降（7%，P = 0.049）。
在体重正常的情况下，扩张型心肌病与静息ATP输送减少有关。在肥胖的扩张型心肌病患者中，通过CK的ATP需求更大，提示能量利用效率降低。饮食减肥与心肌收缩力的显著改善以及ATP输送的下降相关，提示代谢效率提高。这突出了肥胖性心肌病中独特的能量途径，其既不同于扩张型心肌病，且可能通过减肥而逆转。
