Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1982;66:129-134

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Litchfield, R. L.
Right arrow Articles by Marcus, M. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Litchfield, R. L.
Right arrow Articles by Marcus, M. L.

Circulation, Vol 66, 129-134, Copyright © 1982 by American Heart Association


ARTICLES

Normal exercise capacity in patients with severe left ventricular dysfunction: compensatory mechanisms

RL Litchfield, RE Kerber, JW Benge, AL Mark, J Sopko, RK Bhatnagar and ML Marcus

About one-third of patients who have severe left ventricular dysfunction can achieve normal levels of exercise. To elucidate the mechanisms that permit this to occur, we studied six patients with severe left ventricular dysfunction (average left ventricular ejection fraction 17 +/- 2.5% [mean +/- SEM]) who achieved nearly normal levels of exercise tolerance (greater than 11 minutes of treadmill exercise, Sheffield protocol). All patients had normal pulmonary function at rest and during exercise. Hemodynamics were measured at rest and during supine and upright exercise. The major mechanisms of the preserved exercise capacity in these patients were chronotropic competence, ability to tolerate elevated wedge pressures (33 +/- 3 mm Hg) without dyspnea, ventricular dilation, and increased levels of plasma norepinephrine at rest and during exercise. Also, whereas peripheral vascular resistance was unchanged during supine exercise, it decreased by 50% during similar levels of upright exercise. As a consequence, increases in cardiac output from rest to exercise were greater during upright than supine exercise (100% vs 50%, respectively) (p less than 0.05), and pulmonary wedge pressures were lower during upright than supine exercise (21 +/- 5 mm Hg vs 33 +/- 3 mm Hg). Thus, multiple mechanisms permit some patients with severe left ventricular dysfunction to achieve normal levels of exercise. These studies emphasize that left ventricular function must be assessed by direct means rather than inferring function of the left ventricle from the results of an exercise tolerance test.


This article has been cited by other articles:


Home page
J. Appl. Physiol.Home page
R. Isnard, P. Lechat, H. Kalotka, H. Chikr, S. Fitoussi, J. Salloum, J.-L. Golmard, D. Thomas, and M. Komajda
Muscular blood flow response to submaximal leg exercise in normal subjects and in patients with heart failure
J Appl Physiol, December 1, 1996; 81(6): 2571 - 2579.
[Abstract] [Full Text] [PDF]


Home page
ANN INTERN MEDHome page
J. Myers and V. F. Froelicher
Hemodynamic Determinants of Exercise Capacity in Chronic Heart Failure
Ann Intern Med, September 1, 1991; 115(5): 377 - 386.
[Abstract] [PDF]


Home page
Arch Intern MedHome page
D. A. Weiner
Evaluating the Conditions of Patients With Congestive Heart Failure by Exercise Testing
Arch Intern Med, October 1, 1983; 143(10): 1978 - 1980.
[Abstract] [PDF]