高血压患者大动脉硬度与左心室收缩期心肌应变的相关性

Relationship between arterial stiffness and systolic deformation in patients with hypertension

目的探讨高血压患者大动脉硬度与左心室收缩期心肌应变的相关性。方法选取青岛大学附属医院2013年7月至2014年3月收治的原发性高血压患者60例,其中左心室正常构型(LVN)组25例,左心室肥厚(LVH)组35例。另选取同期健康体检者30名作为健康对照组。采用速度向量成像技术测量左心室收缩期峰值纵向、径向、环向应变及应变率,实时三维超声成像技术测量每搏量,并计算脉压/每搏量以评估大动脉硬度。采用方差分析比较健康对照组受试者、高血压LVN组、高血压LVH组患者脉压/每搏量、左心室收缩期峰值纵向、径向、环向应变及应变率差异,进一步组间两两比较采用SNK-q检验。采用多元线性回归分析筛选左心室收缩期峰值纵向应变的预测指标。采用Pearson相关分析分析体重指数、年龄、三酰甘油浓度、左心室射血分数(LVEF)、左心室质量指数(LVMI)、脉压/每搏量与左心室收缩期峰值纵向应变的相关性。结果健康对照组受试者、高血压LVN组、高血压LVH组患者的脉压/每搏量分别为(1.26±0.45)、(1.53±0.59)、(1.82±0.43)mm Hg·m2/ml(1 mm Hg=0.133 k Pa);左心室收缩期峰值纵向应变分别为(23.60±1.94)%、(19.69±2.56)%、(17.34±2.48)%,应变率分别为(1.64±0.17)、(1.52±0.14)、(1.38±0.18)s-1;径向应变分别为(28.69±5.2)%、(30.81±4.14)%、(26.53±3.50)%,应变率分别为(2.51±0.56)、(2.60±0.45)、(2.00±0.41)s-1;环向应变分别为(24.50±5.21)%、(24.01±4.60)%、(21.00±3.70)%,应变率分别为(1.38±0.38)、(1.30±0.30)、(1.10±0.26)s-1。高血压LVH组患者脉压/每搏量高于健康对照组受试者、高血压LVN组患者,高血压LVN组患者脉压/每搏量高于健康对照组受试者,且差异均有统计学意义(q值分别为6.56、3.22、2.90,P均<0.05);高血压LVH组患者左心室收缩期峰值纵向、径向、环向应变及应变率均低于健康对照组受试者、高血压LVN组患者,且差异均有统计学意义(纵向应变:q值分别为15.22、5.43;纵向应变率:q值分别为8.88、4.54;径向应变:q值分别为2.85、5.36;径向应变率:q值分别为6.10、6.81;环向应变:q值分别为4.42、3.61;环向应变率:q值分别为5.04、3.42;P均<0.05);高血压LVN组患者左心室收缩期峰值纵向应变及应变率均低于健康对照组受试者,且差异均有统计学意义(q值分别为8.73、3.77,P均<0.05);高血压LVN组患者左心室收缩期峰值径向、环向应变及应变率均低于健康对照组受试者,但差异均无统计学意义。多元线性回归分析结果表明,LVMI、脉压/每搏量可预测左心室收缩期峰值纵向应变。Pearson相关分析结果显示,体重指数、三酰甘油浓度、年龄、LVMI、脉压/每搏量与左心室收缩期峰值纵向应变呈负相关(r=-0.10、-0.09、-0.14、-0.42、-0.56、P均<0.05);LVEF与左心室收缩期峰值纵向应变呈正相关(r=0.13,P<0.05)。结论大动脉硬度是高血压患者左心室收缩功能的重要影响因素,对原发性高血压患者左心室收缩功能具有预测价值。

Objective To investigate the effect of arterial stiffness on systolic deformation in hypertensive disease. Methods Sixty essential hypertensive patients were enrolled, including 25 cases with left ventricular normal geometric（group LVN） and 35 cases with left ventricular hypertrophy（group LVH） in the Affiliated Hospital of Qingdao University during July 2013 to March 2014. Thirty patients in the control group were enrolled in the same period. The peak systolic strains and strain rates were determined by using velocity vector imaging. Stroke volume was obtained by using real-time three-dimensional echocardiography. And pulse pressure/stroke volume was used as a surrogate index of arterial stiffness. Pulse pressure/stroke volume, the differences of strain and strain rate in three groups were compared by analysis of variance, and SNK-q test was used for further comparison between two groups. Multiple linear regression was performed to estimate predictors for systolic longitudinal deformation. Pearson＇s correlation was used to analysis the relevance of systolic longitudinal strain and body mass index, triglyceride, left ventricular ejection fraction, age, left ventricular mass index, pulse pressure/stroke volume. Results Pulse pressure/stroke volume were（1.26±0.45） mm Hg·m2·ml-1,（1.53±0.59） mm Hg·m2·ml-1,（1.82±0.43） mm Hg·m2·ml-1（1 mm Hg=0.133 k Pa） in the control group, LVN, LVH respectively. The systolic strains and strain rates in the control group, LVN, LVH were recorded as follows：systolic longitudinal strains were（23.60±1.94）%,（19.69±2.56）%,（17.34±2.48）%, the systolic longitudinal strain rates were（1.64±0.17） s-1,（1.52±0.14） s-1,（1.38±0.18） s-1; the systolic radial strains were（28.69±5.2）%,（30.81±4.14）%,（26.53±3.50）%, the systolic radial strain rates were（2.51±0.56） s-1,（2.60±0.45） s-1,（2.00±0.41） s-1; the circumferential strains were（24.50±5.21）%,（24.01±4.60）%,（21.00±3.70）%, the circumferential strain rates were（1.38±0.38） s-1,（1.30±0.30） s-1,（1.10±0.26） s-1. Pulse pressure/stroke volume was higher in LVN and was more pronounced in the LVH group compared with the control（LVN/LVH with the control group： q=2.90, 6.56, LVN with LVH： q=3.22, all P〈0.05）. The strains and strain rates in LVH were lower than those of LVN and the control group, and the differences were statistically significant.（longitudinal strains： q=15.22, 5.43; longitudinal strain rates： q=8.88, 4.54; radial strains： q=2.85, 5.36; radial strain rates： q=6.10, 6.81; circumferential strains： q=4.42, 3.61; circumferential strain rates： q=5.04, 3.42; all P〈0.05）. The strains and strain rates in LVN were lower than the normal group, the significant differences of the longitudinal strains and longitudinal strain rates were found（q=8.73, 3.77, both P〈0.05） while there were no statistically significant differences of radial strains and radial strain rates, circumferential rates and circumferential strain rates. In a multivariate analysis, LVMI and AS were found to be predictors for systolic longitudinal strain. Body mass index, triglyceride, left ventricular ejection fraction, age, left ventricular mass index and pulse pressure/stroke volume were negatively related to systolic longitudinal strain（r=-0.10,-0.09,-0.14,-0.42,-0.56, all P〈0.05） by Pearson＇s correlation, while LVEF was positively related to mean systolic longitudinal strain（r=0.13, P〈0.05）. Conclusion Arterial stiffness is suitable as an predictor for left ventricular systolic deformation in hypertensive disease.