Yuan Fangzhengyuan, Liu Chuan, Yu Shiyong, Bian Shizhu, Yang Jie, Ding Xiaohan, Zhang Jihang, Tan Hu, Ke Jingbin, Yang Yuanqi, He Chunyan, Zhang Chen, Rao Rongsheng, Liu Zhaojun, Yang Jun, Huang Lan
Institute of Cardiovascular Diseases of PLA, The Second Affiliated Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Department of Cardiology, The Second Affiliated Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Front Physiol. 2021 Apr 1;12:639761. doi: 10.3389/fphys.2021.639761. eCollection 2021.
Pulmonary artery pressure (PAP) is increased and right ventricular (RV) function is well preserved in healthy subjects upon exposure to high altitude (HA). An increase in PAP may trigger notching of the right ventricular outflow tract Doppler flow velocity envelope (RVOT notch), which is associated with impaired RV function in patients with pulmonary hypertension. However, whether HA exposure can induce RVOT notch formation and the subsequent impact on cardiac function in healthy subjects remains unclear.
A total of 99 subjects (69 males and 30 females) with a median age of 25 years were enrolled in this study; they traveled from 500 to 4100 m by bus over a 2-day period. All subjects underwent a comprehensive physiological and echocardiographic examination 1 day before ascension at low altitude and 15 ± 3 h after arrival at HA. The RVOT notch was determined by the presence of a notched shape in the RVOT Doppler flow velocity envelope. The systolic PAP (SPAP) was calculated as Bernoulli equation SPAP = 4 × (maximum tricuspid regurgitation velocity)+5 and mean PAP (mPAP) = 0.61 × SPAP+2. Cardiac output was calculated as stroke volume × heart rate. Pulmonary capillary wedge pressure (PCWP) was calculated as 1.9+1.24 × mitral E/e'. Pulmonary vascular resistance (PVR) was calculated as (mPAP-PCWP)/CO.
After HA exposure, 20 (20.2%) subjects had an RVOT notch [notch (+)], and 79 (79.8%) subjects did not have an RVOT notch [notch (-)]. In the multivariate logistic regression analysis, the SPAP, right ventricular global longitude strain (RV GLS), and tricuspid E/A were independently associated with the RVOT notch. The SPAP, mPAP, PVR, standard deviations of the times to peak systolic strain in the four mid-basal RV segments (RVSD4), peak velocity of the isovolumic contraction period (ICV), and the peak systolic velocity (s') at the mitral/tricuspid annulus were increased in all subjects. Conversely, the pulse oxygen saturation (SpO), RV GLS, and tricuspid annulus plane systolic excursion (TAPSE)/SPAP were decreased. However, the increases of SPAP, mPAP, PVR, and RVSD4 and the decreases of SpO, RV GLS, and TAPSE/SPAP were more pronounced in the notch (+) group than in the notch (-) group. Additionally, increased tricuspid ICV and mitral/tricuspid s' were found only in the notch (-) group.
HA exposure-induced RVOT notch formation is associated with impaired RV function, including no increase in the tricuspid ICV or s', reduction of RV deformation, deterioration in RV-pulmonary artery coupling, and RV intraventricular synchrony.
在健康受试者暴露于高海拔(HA)时,肺动脉压(PAP)会升高,而右心室(RV)功能则能得到良好维持。PAP升高可能会引发右心室流出道多普勒流速包络线切迹(RVOT切迹),这与肺动脉高压患者的RV功能受损有关。然而,HA暴露是否会导致健康受试者形成RVOT切迹以及随后对心脏功能的影响仍不清楚。
本研究共纳入99名受试者(69名男性和30名女性),中位年龄为25岁;他们在2天内乘坐巴士从海拔500米前往4100米。所有受试者在低海拔上升前1天以及到达HA后15±3小时接受了全面的生理和超声心动图检查。RVOT切迹通过RVOT多普勒流速包络线中是否存在切迹形状来确定。收缩期PAP(SPAP)根据伯努利方程计算为SPAP = 4×(最大三尖瓣反流速度)+5,平均PAP(mPAP)= 0.61×SPAP+2。心输出量通过每搏量×心率计算得出。肺毛细血管楔压(PCWP)根据1.9+1.24×二尖瓣E/e'计算得出。肺血管阻力(PVR)根据(mPAP-PCWP)/CO计算得出。
HA暴露后,20名(20.2%)受试者出现RVOT切迹[切迹(+)],79名(79.8%)受试者未出现RVOT切迹[切迹(-)]。在多因素逻辑回归分析中,SPAP、右心室整体纵向应变(RV GLS)和三尖瓣E/A与RVOT切迹独立相关。所有受试者的SPAP、mPAP、PVR、四个心底中部RV节段的收缩期应变峰值时间标准差(RVSD4)、等容收缩期峰值速度(ICV)以及二尖瓣/三尖瓣环处的收缩期峰值速度(s')均升高。相反,脉搏血氧饱和度(SpO)、RV GLS和三尖瓣环平面收缩期偏移(TAPSE)/SPAP降低。然而,切迹(+)组中SPAP、mPAP、PVR和RVSD4的升高以及SpO、RV GLS和TAPSE/SPAP的降低比切迹(-)组更明显。此外,仅在切迹(-)组中发现三尖瓣ICV和二尖瓣/三尖瓣s'升高。
HA暴露诱导的RVOT切迹形成与RV功能受损有关,包括三尖瓣ICV或s'无增加、RV变形减少、RV-肺动脉耦合恶化以及RV心室内同步性下降。