Circulation, Vol 89, 2219-2231, Copyright © 1994 by American Heart Association
L Hittinger, T Patrick, T Ihara, N Hasebe, YT Shen, B Kalthof, RP Shannon and SF Vatner
BACKGROUND: Ventricular hypertrophy begins as a physiological adaptation to
cardiac overload but progresses to a pathological state. We examined
whether the extent of hypertrophy influenced the response to exercise in
terms of its effects on regional and global ventricular function and
transmural myocardial blood flow distribution. METHODS AND RESULTS: Left
ventricular (LV) hypertrophy was induced by aortic banding in puppies. The
effects of treadmill exercise were compared in sham-operated control dogs
(n = 7) and in dogs with moderate LV hypertrophy (47% increase in LV
wt/body wt, n = 7) with normal baseline levels of LV systolic and diastolic
wall stress and dogs with severe LV hypertrophy (85% increase in LV wt/body
wt, n = 18), which exhibited elevated levels of LV systolic wall stress at
baseline. The dogs with severe LV hypertrophy were further subdivided into
those with either elevated or normal baseline levels of LV end-diastolic
pressure and wall stress. The response to exercise in dogs with moderate LV
hypertrophy was directionally similar to that of sham-operated control dogs
for systemic hemodynamics and global and regional LV function, ie, full and
subendocardial wall thickening rose, as did mean and diastolic arterial
pressures, shortening fraction, and Vcf. The endocardial/epicardial blood
flow ratio did not fall during exercise in these two groups. However,
relations comparing either LV shortening, Vcf, or wall thickening with LV
systolic wall stress during exercise demonstrated depressed myocardial
function in the dogs with moderate LV hypertrophy. In contrast, in dogs
with severe LV hypertrophy, exercise reduced LV shortening fraction, Vcf,
mean and diastolic arterial pressures, and full and subendocardial wall
thickening, and the endocardial/epicardial blood flow ratio fell to 0.73
+/- 0.07. There were no differences observed between the two subgroups with
severe LV hypertrophy, but the global and regional wall function responses
to exercise were more severely impaired than those in dogs with moderate LV
hypertrophy. CONCLUSIONS: Responses of global and regional LV function and
transmural myocardial blood flow distribution to exercise were clearly
abnormal in dogs with severe LV hypertrophy with elevated baseline levels
of LV systolic wall stress whether or not baseline levels of LV
end-diastolic wall stress were elevated. Thus, it required more severe LV
hypertrophy as well as elevated levels of LV wall stress to elicit
qualitatively abnormal regional and global hemodynamic responses to
exercise. However, even with moderate LV hypertrophy, which was well
compensated under baseline conditions, qualitatively impaired
contraction-afterload relations were observed during the stress of
exercise.
ARTICLES
Exercise induces cardiac dysfunction in both moderate, compensated and severe hypertrophy
Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, Mass.
This article has been cited by other articles:
 |
|
 |
|
  L. A. Nikolaidis, A. Doverspike, R. Huerbin, T. Hentosz, and R. P. Shannon Angiotensin-Converting Enzyme Inhibitors Improve Coronary Flow Reserve in Dilated Cardiomyopathy by a Bradykinin-Mediated, Nitric Oxide-Dependent Mechanism Circulation, June 11, 2002; 105(23): 2785 - 2790. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Takeichi, M. Yokota, M. Iwase, H. Izawa, T. Nishizawa, R. Ishiki, F. Somura, K. Nagata, S. Isobe, and A. Noda Biphasic changes in left ventricular end-diastolic pressure during dynamic exercise in patients with nonobstructive hypertrophic cardiomyopathy J. Am. Coll. Cardiol., August 1, 2001; 38(2): 335 - 343. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. J. Grieve, P. A. MacCarthy, N. P. Gall, A. C. Cave, and A. M. Shah Divergent Biological Actions of Coronary Endothelial Nitric Oxide During Progression of Cardiac Hypertrophy Hypertension, August 1, 2001; 38(2): 267 - 273. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. H. M. de Groot, M. Schoenmakers, M. M. C. Molenschot, J. D. M. Leunissen, H. J. J. Wellens, and M. A. Vos Contractile Adaptations Preserving Cardiac Output Predispose the Hypertrophied Canine Heart to Delayed Afterdepolarization-Dependent Ventricular Arrhythmias Circulation, October 24, 2000; 102(17): 2145 - 2151. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. H. Desai, E. Schauble, W. Luo, E. Kranias, and D. Bernstein Phospholamban deficiency does not compromise exercise capacity Am J Physiol Heart Circ Physiol, April 1, 1999; 276(4): H1172 - H1177. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A. Vos, S. H. M. de Groot, S. C. Verduyn, J. van der Zande, H. D. M. Leunissen, J. P. M. Cleutjens, M. van Bilsen, M. J. A. P. Daemen, J. J. Schreuder, M. A. Allessie, et al. Enhanced Susceptibility for Acquired Torsade de Pointes Arrhythmias in the Dog With Chronic, Complete AV Block Is Related to Cardiac Hypertrophy and Electrical Remodeling Circulation, September 15, 1998; 98(11): 1125 - 1135. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Kozakova, C. Palombo, L. Pratali, G. Pittella, F. Galetta, and A. L'Abbate Mechanisms of Coronary Flow Reserve Impairment in Human Hypertension: An Integrated Approach by Transthoracic and Transesophageal Echocardiography Hypertension, February 1, 1997; 29(2): 551 - 559. [Abstract] [Full Text]
|
|
|
|
|
|
L. Hittinger, I. Mirsky, Y.-T. Shen, T. A. Patrick, S. P. Bishop, and S. F. Vatner Hemodynamic Mechanisms Responsible for Reduced Subendocardial Coronary Reserve in Dogs With Severe Left Ventricular Hypertrophy Circulation, August 15, 1995; 92(4): 978 - 986. [Abstract] [Full Text]
|
|