AbdelMassih Antoine Fakhry, Mostafa Fatma Alzahraa, Yassa Marianne Edward, Fouda Raghda, Abdelraouf Shereen, Ali Noha, Mira Marwa
Department of Pediatrics, Pediatric Cardiology Unit, Cairo University Children Hospital, Cairo University, Cairo, Egypt.
Department of Cardiac Sciences, Pediatric Cardiology Division, Sheikh Khalifa Medical City, Abu Dhabi, UAE.
J Cardiovasc Echogr. 2025 Apr-Jun;35(2):156-161. doi: 10.4103/jcecho.jcecho_3_25. Epub 2025 Jul 30.
Obesity impairs vascular compliance and myocardial functions; however, the intricate pathogenesis of this dysfunction is still elusive. There is conflicting evidence on serum nitric oxide (NOx) regulation in obesity, and some reports state that its bioavailability is reduced, while some others claim that it is upregulated. This study aimed to measure NOx status in obesity, to correlate it to vascular function, and to determine if myocardial function is tied to vascular dysfunction or not.
For this purpose, 20 obese patients underwent serum NOx testing, serum testing of postprandial C-peptide to glucose ratio (PCPRI), vascular function testing using conventional flow-mediated dilation (FMD) of brachial artery, and the advanced aortic strain rate (ASR), in addition to myocardial functions using speckle tracking echocardiography. The latter in addition to serum NO was benchmarked against 16 healthy controls.
Serum NOx was significantly higher in cases compared to controls (obesity group: 106 ± 14 vs. control group: 62 ± 9). The higher the insulin resistance (evidenced by high PCPRI), the higher was the NO level, denoting possibly a state of insulin-induced NO resistance. This NOx resistance was correlated with measures of vascular function, with ASR being more intimately related to serum NOx ( = 0.86 compared to an = 0.66 with FMD). Lower ASR was tied to lower myocardial functions as expressed by global longitudinal strain, notably the subendocardial layer ( = 0.56 and = 0.77, respectively).
Vascular dysfunction seen in obesity is probably orchestrated by a state of resistance to nitric oxide, induced by hyperinsulinemia. This vascular dysfunction seems to play a major role in reducing myocardial functions, especially the subendocardial component, which is known to be affected by impaired blood supply.
肥胖会损害血管顺应性和心肌功能；然而，这种功能障碍的复杂发病机制仍不清楚。关于肥胖患者血清一氧化氮（NOx）调节存在相互矛盾的证据，一些报告称其生物利用度降低，而另一些则声称其上调。本研究旨在测量肥胖患者的NOx状态，将其与血管功能相关联，并确定心肌功能是否与血管功能障碍相关。
为此，20名肥胖患者接受了血清NOx检测、餐后C肽与血糖比值（PCPRI）的血清检测、使用肱动脉传统血流介导的血管舒张（FMD）进行血管功能检测以及先进的主动脉应变率（ASR）检测，此外还使用斑点追踪超声心动图进行心肌功能检测。后者除血清NO外，还与16名健康对照进行了比较。
与对照组相比，病例组血清NOx显著更高（肥胖组：106±14 vs.对照组：62±9）。胰岛素抵抗越高（以高PCPRI为证据），NO水平越高，这可能表示存在胰岛素诱导的NO抵抗状态。这种NOx抵抗与血管功能指标相关，ASR与血清NOx的相关性更强（r = 0.86，而FMD的r = 0.66）。较低的ASR与较低的心肌功能相关，如整体纵向应变所表示，特别是心内膜下层（分别为r = 0.56和r = 0.77）。
肥胖中出现的血管功能障碍可能是由高胰岛素血症诱导的对一氧化氮的抵抗状态所导致。这种血管功能障碍似乎在降低心肌功能中起主要作用，特别是心内膜下层成分，已知其会受到血液供应受损的影响。
