Aurigemma Gerard P, Devereux Richard B, De Simone Giovanni, Roman Mary J, O'Grady Michael J, Koren Michael, Alderman Michael, Laragh John
Division of Cardiology, Department of Medicine, University of Massachusetts Medical Center, Worcester, Mass 01655, USA.
Am Heart J. 2002 Mar;143(3):546-51. doi: 10.1067/mhj.2002.119764.
It has been hypothesized that the level of end-systolic wall stress (sigma(m)) is a feedback signal that regulates the level of hypertrophy. Thus, low levels of sigma(m) may signify inappropriate hypertrophy.
To characterize left ventricular (LV) structure and systolic function in hypertensive subjects with low levels of sigma(m), we studied 763 patients. LV function was studied by midwall stress-shortening analysis. Partition values for sigma(m) were derived from a separate group of normal subjects, and the study population was divided into low stress (group I, n = 136), high stress (group III, n = 157), and intermediate stress group II (n = 470). LV chamber and myocardial function were characterized by relating shortening at the endocardium and at the midwall, respectively, to stress.
As expected, group III patients had the highest values for systolic blood pressure and LV cavity size but the lowest values for wall thickness and relative wall thickness. Surprisingly, however, there were no significant differences among stress groups with regard to age or body mass index. Contrary to the hypothesis that low levels of stress are indicative of excessive hypertrophy, there were no significant differences among the 3 groups with regard to LV mass or any form of LV mass index. Furthermore, despite lower mean values for afterload, group I patients had significantly lower values for midwall shortening, and this finding was indicative of reduced myocardial function; stress-shortening plots demonstrated that 28% of group I patients fell below 95% CI compared with 10% of group II and only 5% of group III patients.
Hypertensive subjects with low values for sigma(m) have more concentric LV geometry (higher relative wall thickness) and, on average, reduced myocardial function.
有假说认为,收缩末期壁应力(σ(m))水平是调节心肌肥厚程度的反馈信号。因此,低水平的σ(m)可能意味着不适当的心肌肥厚。
为了描述σ(m)水平较低的高血压患者的左心室(LV)结构和收缩功能,我们研究了763例患者。通过室壁应力-缩短分析研究左心室功能。σ(m)的划分值来自另一组正常受试者,研究人群分为低应力组(I组,n = 136)、高应力组(III组,n = 157)和中间应力组II(n = 470)。通过分别将心内膜和室壁中部的缩短与应力相关联来描述左心室腔和心肌功能。
正如预期的那样,III组患者的收缩压和左心室腔尺寸值最高,但壁厚度和相对壁厚度值最低。然而,令人惊讶的是,各应力组在年龄或体重指数方面没有显著差异。与低应力水平表明过度心肌肥厚的假说相反,三组在左心室质量或任何形式的左心室质量指数方面没有显著差异。此外,尽管I组患者的后负荷平均值较低,但其室壁中部缩短值显著较低,这一发现表明心肌功能降低;应力-缩短图显示,I组28%的患者低于95%可信区间,而II组为10%,III组仅为5%。
σ(m)值较低的高血压患者具有更向心性的左心室几何形状(相对壁厚度更高),并且平均而言心肌功能降低。