Author + information
- Received July 11, 1990
- Revision received October 24, 1990
- Accepted November 9, 1990
- Published online April 1, 1991.
- Dalane W. Kitzman, MD∗,1,
- Michael B. Higginbotham, MB,
- Frederick R. Cobb, MD,
- Khalid H. Sheikh, MD and
- Martin J. Sullivan, MD
- ↵∗Address for reprints: Dalane W. Kitzman, MD, Box 31219, Division of Cardialogy, Duke University Medical Center, Durham, North Carolina 27710.
Invasive cardiopulmonary exercise testing was performed in 7 patients who presented with congestive heart failure, normal left ventricular ejection fraction and no significant coronary or valvular heart disease and in 10 age-matched normal subjects. Compared with the normal subjects, patients demonstrated severe exercise intolerance with a 48% reduction in peak oxygen consumption (11.6 ± 4.0 versus 22.7 ± 6.1 ml/kg per min; p < 0.001), primarily due to a 41% reduction in peak cardiac index (4.2 ± 1.4 versus 7.1 ± 1.1 liters/mm per m2; p < 0.001).
In patients compared with normal subjects, peak left ventricular stroke volume index (34 ±9 versus 46 ± 7 ml/min per m2; p < 0.01) and end-diastolic volume index (56 ± 14 versus 68 ± 12 ml/min per m2; p < 0.08) were reduced, whereas peak ejection fraction and end-systolic volume index were not different. In patients, the change in end-diastolic volume index during exercise correlated strongly with the change in stroke volume index (r = 0.97; p < 0.0001) and cardiac index (r = 0.80; p < 0.03). Pulmonary wedge pressure was markedly increased at peak exercise in patients compared with normal subjects (25.7 ± 9.1 versus 7.1 ± 4.4 mm Hg; p < 0.0001). Patients demonstrated a shift of the left ventricular end-diastolic pressure-volume relation upward and to the left at rest. Increases in left ventricular filling pressure during exercise were not accompanied by increases in end-diastolic volume, indicating a limitation to left ventricular filling.
These data suggest that abnormalities in left ventricular diastolic function limited the patients' ability to augment stroke volume by means of the Frank-Starling mechanism, resulting in severe exercise intolerance. These findings provide a pathophysiologic rationale for symptoms of chronic fatigue and dyspnea on exertion, which are often present in patients with a history of congestive heart failure and preserved systolic function.
↵1 Dr. Kitzman is the recipient of American Heart Association, North Carolina Affiliate Grant-in-Aid 1988-89-A-24 and a research grant from the American Federation for Aging Research, New York, New York.
☆ This study was presented in part at the 61st Scientific Sessions of the American Heart Association. Washington. D.C., November 1988. It was supported in part by Grant HL-1760 from the National Heart. Lung, and Blood Institute. Bethesda, Maryland: by the Geriatric Research. Education, and Clinical Center (GRECC). Durham Veterans Administration Medical Center and the Duke University Aging Registry. Durham. North Carolina: and by Grant RR-30. Division of Research Resources. General Clinical Research Centers Program. National Institutes of Health.
- Received July 11, 1990.
- Revision received October 24, 1990.
- Accepted November 9, 1990.