Functional impact of an increase in ventricular mass after myocardial damage and its attenuation by converting enzyme inhibition

K. M. McDonald, A. D'Aloia, T. Parrish, J. Mock, K. Hauer, A. E. Stillman, J. N. Cohn

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


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. Methods and 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 convening 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). Conclusion: 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.

Original languageEnglish (US)
Pages (from-to)203-212
Number of pages10
JournalJournal of cardiac failure
Issue number3
StatePublished - 1998

Bibliographical note

Funding Information:
From the Cardiovascular Division, *Department of Medicine, and the *Department of Radiology, University of Minnesota, Minneapolis, Minnesota. Supported in part by Program Project Grant PO-132427 from the National Heart, Lung and Blood Institute. Manuscript received October 7, 1997; revised manuscript received June 1, 1998; revised manuscript accepted June 18, 1998. All editorial decisions for this article, including selection of reviewers, were made by a Guest Editor. This policy applies to all articles with authors from the University of Minnesota. Repdnt requests: Kenneth M. McDonald, MD, FRCPI, St. Vincents' Hospital, Elm Park, Dublin 4, Ireland.


  • Canine ventricular dysfunction
  • Convening enzyme inhibition
  • Myocardial necrosis
  • Ventricular mass
  • Ventricular remodeling


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