This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted 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 WIENER, L. Articles by COX, J. W. Search for Related Content PubMed PubMed Citation Articles by WIENER, L. Articles by COX, J. W.

(Circulation. 1968;38:240.)
© 1968 American Heart Association, Inc.

---

Left Ventricular Hemodynamics in Exercise-Induced Angina Pectoris

LESLIE WIENER M.D.¹; EDWARD M. DWYER JR. M.D¹; J. WILLIAM COX M.D., PH.D.¹

¹ From the Cardiopulmonary Branch, Department of Medicine, U. S. Naval Hospital, Philadelphia, Pennsylvania.

The sequence of events characterizing the onset and course of exercise-induced angina pectoris was studied in 10 patients with ischemic heart disease during cardiac catheterization. Exercise produced a precipitous rise in left ventricular end-diastolic pressure prior to the onset of angina and electrocardiographic ischemia. A corresponding abnormal increase in pulmonary artery pressure occurred. Cardiac output increased commensurate with the degree of exertion and was accompanied by a slight reduction in stroke volume. Left ventricular work and stroke work paralleled the changes in cardiac output and stroke volume. Determinants of myocardial oxygen consumption, that is, heart rate, left ventricular systolic pressure, and left ventricular first derivative, were monitored continuously and noted to increase by 43%, 20%, and 38%, respectively, prior to angina. Ischemic ST-segment depression corresponded closely in time with angina. Angina and electrocardiographic and hemodynamic abnormalities persisted throughout exercise. Two minutes after exercise, hemodynamic values returned to normal along with a reduction in intensity of angina; ST-segment abnormalities persisted until 4 minutes after exercise. Pathophysiological mechanisms occurring during angina are described, and differences from typical heart failure are discussed.

Key Words: Coronary artery disease • Exercise

This article has been cited by other articles:

				M. K. Batur, A. Yildirir, O. Onalan, G. Kabakci, L. Tokgozoglu, and A. Oto Angioplasty induced myocardial ischaemia prolongs the signal-averaged P-wave duration in single vessel coronary artery disease Europace, January 1, 2002; 4(3): 289 - 293. [Abstract] [PDF]

				M. D. Guazzi, A. Polese, F. Magrini, M. T. Olivari, P. Moruzzi, and C. Fiorentini Echocardiographic and Hemodynamic Correlates in Prinzmetal Angina Pectoris: A Case Report Angiology, January 1, 1979; 30(10): 708 - 715. [PDF]

				S. J. Schang, C. J. Pepine, and C. R. Bemiller Anomalous Coronary Artery Origin and Bicuspid Aortic Valve Vascular and Endovascular Surgery, March 1, 1975; 9(2): 67 - 72. [Abstract] [PDF]

				Y. Z. Yuceoglu, S. Rubler, K. P. Eshwar, V. Tchertkoff, and A. Grishman Pulmonary Edema Associated With Pulmonary Embolism: a Clinicopathological Study Angiology, September 1, 1971; 22(9): 501 - 510. [PDF]