Takahashi Mao, Miyazaki Chikao, Xin Cao, Sato Shuji, Shimizu Kazuhiro, Chiba Tatsuo, Tsukuma Hisayuki, Komatsu Tetsuya, Aimoto Megumi, Nagasawa Yoshinobu, Takahara Akira, Shirai Kohji
Department of Cardiology, Sakura Hospital, Medical Center, Toho University, Chiba, Japan.
Mihama Hospital, Japan, Chiba.
Heart Vessels. 2023 May;38(5):740-748. doi: 10.1007/s00380-022-02223-8. Epub 2023 Jan 11.
Takotsubo cardiomyopathy (TCM) has been reported to occur after subarachnoid hemorrhage, and the involvement of a critical activity of catecholamines has been mentioned, but the details of its onset have not been fully clarified. Recently, proper arterial stiffness could be measured with cardio-ankle vascular index. Therefore, we aimed to clarify the role of arterial stiffness in onset of TCM using rabbits under infusion of noradrenaline and injection of blood into brain ventricle. Rabbits were divided into three groups: infusion of noradrenaline (group A), infusion of noradrenaline + injection of saline into the brain ventricle (group B), infusion of noradrenaline + injection of blood in the brain ventricle (group C). Aortic arterial stiffness beta (β) and femoral arterial stiffness beta (β) were defined according to definition of the cardio-ankle vascular index. Blood pressure (BP), β, β, and femoral vessel resistance (FVR) were measured. Left ventricular movement were monitored with echocardiography. BP increased uniformly in all three groups. β in the group A, B and C increased from 3.6 ± 3.2, 3.6 ± 3.6 and 3.9_ ± 4.2 to 15 ± 2, 17.9 ± 2.4, 34.8 ± 9.1 due to the ICP enhancements in addition to noradrenaline administration, respectively. β in groups B and C was significantly larger than that in group A. On echocardiography, a much higher akinesic area of the apex was observed in group C compared with group A and B. Cardiac movements similar to TCM were observed slightly in group B and definitely in group C. Noradrenaline administration infusion and blood injection into the brain ventricle induced TCM accompanying with enhanced femoral arterial stiffness. These results suggested that elevated arterial stiffness might be involved in the formation of TCM in addition to a critical activity of catecholamines and an increase in intracranial pressure with blood injection.
据报道,应激性心肌病(TCM)可发生于蛛网膜下腔出血后,且有人提及儿茶酚胺的关键活性参与其中,但其发病细节尚未完全阐明。最近,可通过心踝血管指数来测量合适的动脉僵硬度。因此,我们旨在通过给兔子输注去甲肾上腺素并向脑室注射血液,来阐明动脉僵硬度在TCM发病中的作用。将兔子分为三组:输注去甲肾上腺素组(A组)、输注去甲肾上腺素并向脑室注射生理盐水组(B组)、输注去甲肾上腺素并向脑室注射血液组(C组)。根据心踝血管指数的定义来定义主动脉动脉僵硬度β(β)和股动脉僵硬度β(β)。测量血压(BP)、β、β和股血管阻力(FVR)。用超声心动图监测左心室运动。三组的血压均均匀升高。由于除了给予去甲肾上腺素外还存在颅内压升高,A组、B组和C组的β分别从3.6±3.2、3.6±3.6和3.9±4.2增加到15±2、17.9±2.4、34.8±9.1。B组和C组的β明显大于A组。在超声心动图上,与A组和B组相比,C组观察到的心尖运动减弱区域要高得多。B组轻微观察到、C组明确观察到类似于TCM的心脏运动。去甲肾上腺素输注和向脑室注射血液会诱发TCM,并伴有股动脉僵硬度增强。这些结果表明,除了儿茶酚胺的关键活性以及注射血液导致的颅内压升高外,动脉僵硬度升高可能参与了TCM的形成。