title: Pathophysiologic significance of left ventricular hypertrophy in dilated cardiomyopathy.
abstract: OBJECTIVE
  Patients with dilated cardiomyopathy (DCM) with left ventricular hypertrophy (LVH) have been found to have a better prognosis than patients without LVH. However, the pathophysiologic mechanism for that has not been investigated. We sought to clarify the pathophysiologic significance of LVH in DCM.
  
  
  METHODS
  We performed isoproterenol infusion echocardiography (0.02 micrograms/kg/min) in 17 patients with DCM, and measured plasma epinephrine and norepinephrine levels at rest and at the end of ergometer exercise in 14 of the 17 patients. Patients were classified into groups according to the presence (9 patients) (LVH+) or absence (8 patients) (LVH-) of LVH. Left ventricular hypertrophy was defined as an inter-ventricular thickness or posterior wall thickness > or = 13 mm.
  
  
  RESULTS
  Although there was no significant difference between groups in fractional shortening at rest during isoproterenol infusion, fractional shortening was significantly higher in the LVH(+) group than in the LVH(-) group (29 +/- 9 vs. 17 +/- 8%; p < 0.025). Although there was no significant difference in plasma norepinephrine level, it was significantly lower in the LVH(+) group than in the LVH(-) group (233 +/- 169 vs. 519 +/- 258 pg/ml; p < 0.05) at the end point of the exercise.
  
  
  CONCLUSIONS
  Systolic reserve, represented by the response to isoproterenol, is greater in patients with DCM with LVH than in those without LVH, and a lower plasma level of norepinephrine is needed to activate the myocardium during exercise in patients with DCM with LVH. This pathophysiologic characteristic could be one of the mechanisms which explain a better prognosis in patients with DCM with LVH.
authors.affiliation: Department of Internal Medicine, University of Tsukuba, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Iida
authors.forename: M
authors.initials: M
authors.lastname: el Sersi
authors.forename: K
authors.initials: K
authors.lastname: Fujieda
authors.forename: S
authors.initials: S
authors.lastname: Kawano
authors.forename: F
authors.initials: F
authors.lastname: Tabei
authors.forename: Y
authors.initials: Y
authors.lastname: Iwasaki
authors.forename: T
authors.initials: T
authors.lastname: Masumi
authors.forename: I
authors.initials: I
authors.lastname: Yamaguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Sugishita
mesh_terms: D000328:Adult; D000368:Aged; D002311:Cardiomyopathy, Dilated / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D002316:Cardiotonic Agents; D002395:Catecholamines / Q000097:blood; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D007545:Isoproterenol; D008297:Male; D008875:Middle Aged; D011379:Prognosis
chemical_list: D002316:Cardiotonic Agents; D002395:Catecholamines; D007545:Isoproterenol