Author + information
- Received December 17, 1992
- Revision received April 12, 1993
- Accepted May 19, 1993
- Published online November 1, 1993.
- Thomas R. Porter, MD, FACCa,∗,
- David O. Taylor, MD, FACCa,
- Alan Cycan, RNa,
- Jennifer Fields, RNa,
- Cynthia W. Bagley, RPha,
- Natesa G. Pandian, MD, FACC† and
- Pramod K. Mohanty, MD, FACCa
- ↵∗Present address and address for correspondence: Thomas R. Porter, MD, Section of Cardiology, University of Nebraska Medical Center, 600 South 42nd Street, Omaha, Nebraska 68198-2265.
Objectives. The purpose of this study was to determine whether pulmonary artery responses to acetylcholine are abnormal in patients with chronic heart failure.
Background. Defective pulmonary artery endothelium-dependent responses have been observed in chronic heart failure models in animals. However, pulmonary artery endothelial response in humans with chronic heart failure are unknown.
Methods. Twenty-two patients with chronic treated heart failure (12 with secondary pulmonary hypertension, Group I; 10 with normal pulmonary artery pressure, Group II) and 8 control patients constituted the study groups. Intravascular ultrasound measurements of pulmonary artery area just beyond the tip of an 8F infusion sheath were obtained in response to acetylcholine (10−6, 10−5and 10−4mol/liter). The 10−6mol/liter infusion was repeated after methylene blue infusion. Indomethacin (5 μg/ml) was sequentially added to this combination in 17 patients.
Results. There were no significant differences among the three groups in vascular area responses to the lowest concentration (10−6and 10−5mol/liter) of acetylcholine, but the 10−4mol/liter infusion resulted in significant constriction in Group II patients (p < 0.05, analysis of variance [ANOVA]). Pretreatment with methylene blue in Group II also resulted in significant pulmonary artery vasoconstriction to even the 10−6mol/liter acetylcholine infusion (10.4 ± 7.8% in Group II vs. 1.7 ± 3.9% in the control group and 0.1 ± 4.3% in Group I, p < 0.05, ANOVA). The addition of indomethacin resulted in reversal of the constriction in Group II patients.
Conclusions. These responses indicate that the pulmonary artery endothelium may play a significant role in inhibiting vasoconstriction in patients with chronic heart failure who maintain normal pulmonary artery pressure.
☆ This study was supported in part by funds from Veterans Affairs Research Services, Washington, D.C. and Lipman Foundation and was presented in part at the 41st Annual Scientific Session of the American College of Cardiology, Dallas, Texas, April 1992.
- Received December 17, 1992.
- Revision received April 12, 1993.
- Accepted May 19, 1993.