title: Functional impact of an increase in ventricular mass after myocardial damage and its attenuation by converting enzyme inhibition.
abstract: BACKGROUND
  A increase in left ventricular mass after ventricular damage has been identified as an initial response to injury. However, the functional significance of this response has not been clearly established and is the focus of this study.
  
  
  RESULTS
  Twelve mongrel dogs underwent transmyocardial direct current shock to produce transmural left ventricular damage. Six were assigned to converting enzyme inhibitor therapy initiated 24 hours after damage and continued for 4 weeks. The remaining six dogs served as a control group. Left ventricular structure (mass and end diastolic volume) and systolic function (regional and global ejection fraction at rest and during afterload stress) were assessed by magnetic resonance imaging before damage and at the end of the 4-week period. After myocardial damage, left ventricular mass increased from 93.6 +/- 4.0 to 107.5 +/- 3.4 gm in the control group (P < .01) with no change in ventricular volume. Ramipril-treated dogs displayed a reduction in mass (83.2 +/- 2.2 to 74.6 +/- 2.9 gm, P < .05). In the control group, there was greater reduction in global ejection fraction in response to afterload stress at 4 weeks compared with baseline (-16 +/- 4 vs -4 +/- 3%, P = .03). Ejection fraction response to afterload stress was maintained at 4 weeks in the converting enzyme inhibitor-treated group (-5 +/- 3 vs - 1 +/- 4%) and was different at 4 weeks from the control group (-1 +/- 4 vs -16 +/- 4%, P = .004).
  
  
  CONCLUSIONS
  The increase in left ventricular mass noted after direct current shock was associated with the impairment of systolic function during afterload stress. Inhibition of this mass increase results in preservation of function, thus further supporting the concept that attenuation of ventricular remodeling should be a therapeutic goal.
authors.affiliation: Department of Medicine, University of Minnesota, Minneapolis, USA.
authors.forename: K M
authors.initials: KM
authors.lastname: McDonald
authors.forename: A
authors.initials: A
authors.lastname: D'Aloia
authors.forename: T
authors.initials: T
authors.lastname: Parrish
authors.forename: J
authors.initials: J
authors.lastname: Mock
authors.forename: K
authors.initials: K
authors.lastname: Hauer
authors.forename: A E
authors.initials: AE
authors.lastname: Stillman
authors.forename: J N
authors.initials: JN
authors.lastname: Cohn
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D002302:Cardiac Output / Q000502:physiology; D004195:Disease Models, Animal; D004285:Dogs; D004597:Electroshock; D006335:Heart Injuries / Q000188:drug therapy; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology / Q000517:prevention & control*; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000503:physiopathology; D017257:Ramipril / Q000494:pharmacology* / Q000627:therapeutic use; D012016:Reference Values; D013314:Stress, Mechanical; D013318:Stroke Volume / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology / Q000517:prevention & control*; D020257:Ventricular Remodeling / Q000187:drug effects* / Q000502:physiology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D017257:Ramipril