Holmes Anthony A, Taub Cynthia C, Garcia Mario J, Shan Jian, Slovut David P
aDepartment of Medicine bDivision of Cardiology cDepartment of Cardiovascular and Thoracic Surgery, Montefiore Medical Center, Bronx, New York, USA.
J Cardiovasc Med (Hagerstown). 2017 Feb;18(2):87-95. doi: 10.2459/JCM.0000000000000324.
Patients with paradoxical low-flow severe aortic stenosis (PLF-AS) reportedly have higher left ventricular hydraulic load and more systolic strain dysfunction than patients with normal-flow aortic stenosis. This study investigates the relationship of systolic loading and strain to PLF-AS to further define its pathophysiology.
One hundred and twenty patients (age 79 ± 12 years, 37% men) with an indexed aortic valve area (AVAi) of 0.6 cm/m or less and an ejection fraction of 50% or higher were divided into two groups based on indexed stroke volume (SVi): PLF-AS, SVi ≤ 35 ml/m, N = 46; normal-flow aortic stenosis, SVi > 35 ml/m, N = 74). Valvular and arterial load were assessed using multiple measurements, and strain was assessed using speckle-tracking echocardiography.
Patients with PLF-AS were found to have more valvular load (lower AVAi, P = 0.028; lower energy loss coefficient, P = 0.001), more arterial load [decreased arterial compliance and increased systemic vascular resistance (SVR), both P < 0.001] and more total hydraulic load [increased valvuloarterial impedance (Zva), P < 0.001]. Transvalvular gradients and arterial pressures were similar. Longitudinal strain was lower in PLF-AS (P < 0.001), but circumferential and rotation strains were similar. On adjusted regression, AVAi, SVR and longitudinal strain were associated with PLF-AS [odds ratio (OR) = 1.34, P = 0.043; OR = 1.31, P = 0.004; OR = 1.34, P = 0.011, respectively]. When SVR and AVAi were replaced with Zva, longitudinal strain and Zva (OR = 1.38, P = 0.015; OR = 1.33, P < 0.001 for both, respectively) were associated with PLF-AS.
Increased hydraulic load, from more severe valvular stenosis and increased vascular resistance, and longitudinal strain impairment are associated with PLF-AS and their interplay is likely fundamental to its pathophysiology.
据报道,矛盾性低流量严重主动脉瓣狭窄(PLF-AS)患者比正常流量主动脉瓣狭窄患者具有更高的左心室液压负荷和更多的收缩期应变功能障碍。本研究调查收缩期负荷和应变与PLF-AS的关系,以进一步明确其病理生理学。
120例患者(年龄79±12岁,男性占37%),其主动脉瓣面积指数(AVAi)为0.6cm/m²或更小,射血分数为50%或更高,根据每平方米体表面积的每搏量(SVi)分为两组:PLF-AS组,SVi≤35ml/m²,N = 46;正常流量主动脉瓣狭窄组,SVi>35ml/m²,N = 74)。使用多种测量方法评估瓣膜和动脉负荷,并使用斑点追踪超声心动图评估应变。
发现PLF-AS患者有更多的瓣膜负荷(AVAi更低,P = 0.028;能量损失系数更低,P = 0.001)、更多的动脉负荷(动脉顺应性降低和全身血管阻力增加,均P<0.001)以及更多的总液压负荷(瓣膜动脉阻抗增加,P<0.001)。跨瓣膜梯度和动脉压相似。PLF-AS患者的纵向应变更低(P<0.001),但圆周应变和旋转应变相似。在调整回归分析中,AVAi、全身血管阻力和纵向应变与PLF-AS相关[比值比(OR)分别为1.34,P = 0.043;OR = 1.31,P = 0.004;OR = 1.34,P = 0.011]。当用瓣膜动脉阻抗(Zva)替代全身血管阻力和AVAi时,纵向应变和Zva(OR分别为1.38,P = 0.015;两者OR均为1.33,P<0.001)与PLF-AS相关。
更严重的瓣膜狭窄和血管阻力增加导致的液压负荷增加以及纵向应变受损与PLF-AS相关,它们之间的相互作用可能是其病理生理学的基础。