title: Diastolic compliance of hypertrophied ventricle is not acutely altered by pharmacologic agents influencing active processes.
abstract: OBJECTIVE
  To test, by studying the acute effects of drugs that influence active processes, the hypothesis that in humans with marked ventricular hypertrophy, reduced chamber compliance is primarily caused by passive structural changes.
  
  
  METHODS
  An uncontrolled (before-after) study.
  
  
  METHODS
  University Medical Center.
  
  
  METHODS
  Fourteen patients with ventricular hypertrophy (19 +/- 4.5-mm diastolic-wall thickness) and normal resting systolic function were studied while they had invasive cardiac catheterization.
  
  
  METHODS
  Intravenous beta-blocker (esmolol) or calcium channel blocker (verapamil) or both.
  
  
  METHODS
  Left ventricular function was determined by pressure-volume relations. Volume was measured using conductance catheter, providing a continuous voltage signal proportional to chamber volume. Pressure was measured by micromanometer. Cardiac-specific assessment of change in chamber contractility and diastolic compliance due to each drug was determined.
  
  
  RESULTS
  Both drugs lowered contractility by approximately 30% (P < 0.01). Esmolol slowed relaxation and reduced early peak filling rate, whereas verapamil delayed the time to peak filling (all P < 0.05). In contrast to the effects of both drugs on active contraction and early diastole, late-diastolic compliance was unaltered, and end-diastolic pressure-volume relations were almost identical.
  
  
  CONCLUSIONS
  Neither beta-receptor nor calcium channel blockade acutely alters left ventricular compliance despite substantial active effects manifest in systole and early diastole. This supports the notion that chamber compliance is principally determined by passive structural elements in the heart rather than by active processes.
authors.affiliation: Johns Hopkins Medical Institutions, Baltimore, Maryland.
authors.forename: D A
authors.initials: DA
authors.lastname: Kass
authors.forename: M R
authors.initials: MR
authors.lastname: Wolff
authors.forename: C T
authors.initials: CT
authors.lastname: Ting
authors.forename: C P
authors.initials: CP
authors.lastname: Liu
authors.forename: M S
authors.initials: MS
authors.lastname: Chang
authors.forename: W
authors.initials: W
authors.lastname: Lawrence
authors.forename: W L
authors.initials: WL
authors.lastname: Maughan
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D002312:Cardiomyopathy, Hypertrophic / Q000473:pathology / Q000503:physiopathology*; D003187:Compliance / Q000187:drug effects; D003971:Diastole / Q000187:drug effects; D006352:Heart Ventricles / Q000187:drug effects / Q000473:pathology; D006439:Hemodynamics / Q000187:drug effects; D011412:Propanolamines / Q000494:pharmacology*; D016277:Ventricular Function, Left / Q000187:drug effects*; D014700:Verapamil / Q000494:pharmacology*
chemical_list: D000319:Adrenergic beta-Antagonists; D011412:Propanolamines; D014700:Verapamil; C036604:esmolol