title: Myocardial function and geometry in hypertensive subjects with low levels of afterload.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  Hypertensive subjects with low values for sigma(m) have more concentric LV geometry (higher relative wall thickness) and, on average, reduced myocardial function.
authors.affiliation: Division of Cardiology, Department of Medicine, University of Massachusetts Medical Center, Worcester, Mass 01655, USA. aurigemg@ummhc.org
authors.forename: Gerard P
authors.initials: GP
authors.lastname: Aurigemma
authors.forename: Richard B
authors.initials: RB
authors.lastname: Devereux
authors.forename: Giovanni
authors.initials: G
authors.lastname: De Simone
authors.forename: Mary J
authors.initials: MJ
authors.lastname: Roman
authors.forename: Michael J
authors.initials: MJ
authors.lastname: O'Grady
authors.forename: Michael
authors.initials: M
authors.lastname: Koren
authors.forename: Michael
authors.initials: M
authors.lastname: Alderman
authors.forename: John
authors.initials: J
authors.lastname: Laragh
mesh_terms: D000465:Algorithms; D000704:Analysis of Variance; D001794:Blood Pressure / Q000502:physiology; D004452:Echocardiography; D004562:Electrocardiography; D005260:Female; D006801:Humans; D006973:Hypertension / Q000473:pathology* / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*; D013599:Systole; D018487:Ventricular Dysfunction, Left / Q000473:pathology* / Q000503:physiopathology*; D016277:Ventricular Function, Left