title: Regional wall stress predicts ventricular remodeling after anteroseptal myocardial infarction in the Healing and Early Afterload Reducing Trial (HEART): an echocardiography-based structural analysis.
abstract: BACKGROUND
  Increased left ventricular (LV) wall stress after myocardial infarction (MI) has been implicated in LV remodeling. However, the relationship between LV wall stress and LV remodeling is incompletely defined.
  
  
  METHODS
  We prospectively studied the relationship between regional wall stress and LV remodeling by application of the finite element method to end-systolic LV models from patients enrolled in the Healing and Early Afterload Reducing Therapy (HEART) Trial. Individual LV models were constructed from orthogonal apical echocardiographic views obtained at day 14 after anteroseptal MI in 64 patients. Of these, 31 patients received low-dose (0.625 mg) ramipril and 33 patients received full-dose (10 mg) ramipril. LV wall stress was calculated by the finite element method and correlated with change in LV volume from day 14 to day 90 after MI.
  
  
  RESULTS
  Among all patients, increases in apical regional wall stress were associated with LV volume changes (P -trend =.015). The relationship between apical regional wall stress and change in LV volume was strongest in the low-dose ramipril group (r = 0.53, P =.002) and remained significant after adjustment for end-diastolic volume, infarct size, ejection fraction, and systolic blood pressure yet was attenuated in the full-dose ramipril group.
  
  
  CONCLUSIONS
  Apical regional wall stress is an independent predictor of subsequent LV remodeling after MI. The relationship between increased apical wall stress and LV dilatation appears to be attenuated by full-dose angiotensin-converting enzyme inhibition.
authors.affiliation: Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis St., Boston, MA 02115, USA.
authors.forename: Y
authors.initials: Y
authors.lastname: Aikawa
authors.forename: L
authors.initials: L
authors.lastname: Rohde
authors.forename: J
authors.initials: J
authors.lastname: Plehn
authors.forename: S C
authors.initials: SC
authors.lastname: Greaves
authors.forename: F
authors.initials: F
authors.lastname: Menapace
authors.forename: M O
authors.initials: MO
authors.lastname: Arnold
authors.forename: J L
authors.initials: JL
authors.lastname: Rouleau
authors.forename: M A
authors.initials: MA
authors.lastname: Pfeffer
authors.forename: R T
authors.initials: RT
authors.lastname: Lee
authors.forename: S D
authors.initials: SD
authors.lastname: Solomon
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D004311:Double-Blind Method; D004452:Echocardiography; D005260:Female; D020342:Finite Element Analysis; D006346:Heart Septum; D006352:Heart Ventricles / Q000000981:diagnostic imaging* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000503:physiopathology*; D011379:Prognosis; D011446:Prospective Studies; D017257:Ramipril / Q000627:therapeutic use; D012449:Safety; D013312:Stress, Physiological / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D013318:Stroke Volume / Q000187:drug effects; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D020257:Ventricular Remodeling / Q000187:drug effects
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D017257:Ramipril