title: Increased end diastolic wall stress precedes left ventricular hypertrophy in dilative heart failure--use of the volume-based wall stress index.
abstract: BACKGROUND
  To examine a potential interrelation of left ventricular (LV) wall stress and hypertrophy, we assessed increased wall stress in patients with suspected non-ischemic dilative cardiomyopathy and addressed the question whether increased LV wall stress is involved in the development of LV hypertrophy.
  
  
  METHODS
  We studied 502 consecutive patients in whom LV mass, LV enddiastolic (LVEDV) and endsystolic volume (LVESV) was determined using cardiac magnetic resonance (CMR). Based on a thick-walled sphere, we introduced a myocardial and cavity volume-based wall stress index. Follow up CMR examinations were obtained in a representative subgroup of 71 patients.
  
  
  RESULTS
  LV mass was correlated with LVEDV (r=0.517, P<0.001) and LVESV (r=0.510, P<0.001). Despite LV hypertrophy, LV mass was not sufficient to compensate for LV dilatation resulting in an increased wall stress. Increased LV enddiastolic wall stress was found in 227 patients (45 %) and increased endsystolic wall stress in 198 (39 %). In patients with normal LV enddiastolic wall stress ≤ 4 kPa at time of enrolment, no changes of LV mass occurred during follow up (142 ± 46 g vs. 141 ± 47 g). In contrast, patients with initially increased LV enddiastolic wall stress >4 kPa developed greater LV hypertrophy (141 ± 48 g vs. 158 ± 60 g, P=0.0247).
  
  
  CONCLUSIONS
  LV wall stress can be derived from CMR measurements of LV myocardium and cavity using the volume-based wall stress index. Increased LV enddiastolic wall stress leads to LV hypertrophy. Beyond a certain degree of LV dilatation, the extent of hypertrophy does not compensate LV dilatation. The ensuing increased wall stress promotes dilatation and consecutively hypertrophy with an unfavorable prognosis. It is proposed to use the volume-based wall stress index as new diagnostic criterion in heart failure.
authors.affiliation: Internal Medicine-Cardiology, Philipps University, Marburg, Germany. alter@staff.uni-marburg.de
authors.forename: Peter
authors.initials: P
authors.lastname: Alter
authors.forename: Heinz
authors.initials: H
authors.lastname: Rupp
authors.forename: Florian
authors.initials: F
authors.lastname: Stoll
authors.forename: Philipp
authors.initials: P
authors.lastname: Adams
authors.forename: Jens H
authors.initials: JH
authors.lastname: Figiel
authors.forename: Klaus J
authors.initials: KJ
authors.lastname: Klose
authors.forename: Marga B
authors.initials: MB
authors.lastname: Rominger
authors.forename: Bernhard
authors.initials: B
authors.lastname: Maisch
mesh_terms: D000328:Adult; D002311:Cardiomyopathy, Dilated / Q000175:diagnosis* / Q000503:physiopathology; D003971:Diastole / Q000502:physiology*; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000175:diagnosis* / Q000503:physiopathology; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000175:diagnosis* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies