Harada Haruhito, Ikeda Hisao, Nishiyama Yasuhiro, Niiyama Hiroshi, Katoh Atsushi, Kai Hisashi
Department of Cardiology, Kurume University Medical Center, Kurume, Japan.
Department of Physical Therapy, Faculty of Fukuoka Medical Technology, Teikyo University, Omuta, Japan.
Hypertens Res. 2020 Jun;43(6):534-542. doi: 10.1038/s41440-020-0404-6. Epub 2020 Feb 5.
Reduced skeletal muscle mass is the most important component of sarcopenia. Aging and chronic diseases, including chronic heart failure, are the causes of reduced skeletal muscle mass. However, little is known about the mechanism of skeletal muscle mass reduction in patients with cardiovascular disease (CVD). The purpose of this study was to assess the associations among skeletal muscle mass reduction, endothelial function, and other markers of advanced vascular damage in CVD patients. This was a retrospective cross-sectional analysis that included 310 inpatients with CVD in our hospital. Flow-mediated vasodilation (FMD) was performed to assess early vascular damage, i.e., endothelial dysfunction. The arterial velocity pulse index (AVI) and arterial pressure volume index (API) were assessed to reveal signs of advanced vascular damage, such as arterial stiffening and increased peripheral resistance. The bioelectrical phase angle (PA), as a marker of tissue damage, and the skeletal muscle index (SMI) were measured. Correlation analyses were performed among these parameters. Sarcopenia was diagnosed in 25.5% of patients according to the Asian Working Group for Sarcopenia criteria. Greater progression of arterial stiffness, shown by a higher AVI, and more severe tissue damage, shown by a narrower PA, were found in individuals with sarcopenia. Stepwise multivariate regression analysis showed that sex, age, PA, hypertension, and AVI were factors independently correlated with SMI. In conclusion, advanced vascular damage, such as increased arterial stiffness and peripheral resistance, might play an important role in the reduction in skeletal muscle mass, possibly through damage to skeletal muscle tissue in CVD patients.
骨骼肌质量减少是肌少症最重要的组成部分。衰老和包括慢性心力衰竭在内的慢性疾病是骨骼肌质量减少的原因。然而，关于心血管疾病（CVD）患者骨骼肌质量减少的机制知之甚少。本研究的目的是评估CVD患者骨骼肌质量减少、内皮功能和其他晚期血管损伤标志物之间的关联。这是一项回顾性横断面分析，纳入了我院310例CVD住院患者。采用血流介导的血管舒张功能（FMD）评估早期血管损伤，即内皮功能障碍。评估动脉速度脉搏指数（AVI）和动脉压力容积指数（API）以揭示晚期血管损伤的迹象，如动脉僵硬和外周阻力增加。测量作为组织损伤标志物的生物电阻抗相位角（PA）和骨骼肌指数（SMI）。对这些参数进行相关性分析。根据亚洲肌少症工作组标准，25.5%的患者被诊断为肌少症。在肌少症患者中发现，AVI越高表明动脉僵硬进展越明显，PA越窄表明组织损伤越严重。逐步多元回归分析表明，性别、年龄、PA、高血压和AVI是与SMI独立相关的因素。总之，晚期血管损伤，如动脉僵硬和外周阻力增加，可能在CVD患者骨骼肌质量减少中起重要作用，可能是通过损伤骨骼肌组织实现的。
