This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Massie, B. M. Articles by Topic, N. Search for Related Content PubMed PubMed Citation Articles by Massie, B. M. Articles by Topic, N.

Circulation, Vol 69, 1135-1141, Copyright © 1984 by American Heart Association

ARTICLES

Lack of relationship between the short-term hemodynamic effects of captopril and subsequent clinical responses

BM Massie, BL Kramer and N Topic

The role of hemodynamic monitoring during the initiation of vasodilator therapy for heart failure remains to be defined, despite the tremendous potential socioeconomic and clinical ramifications. We therefore performed resting and exercise hemodynamic studies before and during the initial 48 hr of captopril therapy in 14 stable patients with New York Heart Association Class II or III chronic congestive heart failure. Their clinical response to therapy was determined by evaluating changes in clinical status and the measured changes in exercise tolerance, heart size, and ejection fraction after 3 months. Significant improvement in each of these indexes was found for the group as a whole, but the baseline hemodynamics and the hemodynamic responses to captopril differed little between the patients showing marked improvement and those exhibiting little or no change. Correlations between the hemodynamic measurements and the changes in clinical class, exercise tolerance, heart size, and ejection fraction were generally poor. Even when they achieved significance, these correlations were too loose to allow prediction of the clinical efficacy of captopril in individual subjects. These findings indicate that the routine use of invasive hemodynamic monitoring during the initiation of captopril is unnecessary and potentially misleading, although such measurements remain valuable for diagnosis, the management of patients with complex conditions, and for investigation. The response to captopril may be best evaluated by serial measurements of exercise tolerance and heart size in addition to clinical assessment.

This article has been cited by other articles:

				L. W. Stevenson, T. H. Le Jemtel, E. U. Alt, L. W. Stevenson, T. H. Le Jemtel, and E. U. Alt Hemodynamic Goals Are Relevant Circulation, February 21, 2006; 113(7): 1020 - 1033. [Full Text] [PDF]

				G.A. Cooke, S.G. Williams, P. Marshall, J.K. Al-Timman, J. Shelbourne, D.J. Wright, and L.-B. Tan A mechanistic investigation of ACE inhibitor dose effects on aerobic exercise capacity in heart failure patients Eur. Heart J., September 1, 2002; 23(17): 1360 - 1368. [Abstract] [Full Text] [PDF]

				C. A. J. Farquharson and A. D. Struthers Gradual reactivation over time of vascular tissue angiotensin I to angiotensin II conversion during chronic lisinopril therapy in chronic heart failure J. Am. Coll. Cardiol., March 6, 2002; 39(5): 767 - 775. [Abstract] [Full Text] [PDF]

				S. D. Katz, M. Radin, T. Graves, C. Hauck, A. Block, T. H. LeJemtel, and for the Ifetroban Study Group Effect of aspirin and ifetroban on skeletal muscle blood flow in patients with congestive heart failure treated with enalapril J. Am. Coll. Cardiol., July 1, 1999; 34(1): 170 - 176. [Abstract] [Full Text] [PDF]

				M. A. Munger, S. F. Gardner, and R. C. Jarvis Endocrinologic Warfare: The Role of Angiotensin-Converting Enzyme Inhibitors in Congestive Heart Failure Journal of Pharmacy Practice, January 1, 1990; 3(5): 318 - 331. [Abstract] [PDF]

				F. Bellandi, M. De Scalzi, V. de Leonardis, L. Arena, B. Belli, S. Barbagli, G. Morace, P. Cinelli, and G. Morace Muscular Blood Flow in Patients with Heart Failure Angiology, August 1, 1986; 37(9): 658 - 662. [Abstract] [PDF]