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(Circulation. 1999;100:e141.)
© 1999 American Heart Association, Inc.

Circulation Electronic Pages

Hemodynamic Interaction of Aspirin With Enalapril

Marco Guazzi, MD, PhD

Istituto di Cardiologia Universita degli Studi di Milano, Milan, Italy

	Introduction

 
To the Editor:

I am writing regarding the report by Spaulding et al that appeared in Circulation.¹ These authors investigated the acute systemic and pulmonary hemodynamic response to 10 mg of enalapril in 20 patients with congestive heart failure; the patients were randomly assigned to receive either aspirin or ticlopidine. Enalapril, given after 1 week of such treatment, caused a significant reduction in systemic vascular resistance and mean systemic arterial pressure only in patients receiving ticlopidine; total pulmonary resistance and wedge pulmonary pressure (PWP) decreased significantly in both groups. The authors concluded that "a negative aspirin-enalapril interaction on prostaglandin synthesis presumably alters vasodilatation in systemic vessels, whereas prostaglandin-independent actions of ACE inhibition such as pulmonary arterial vasodilatation are maintained."

One concern is the small number of patients in the study and the imbalance that existed between the groups: there were 33% fewer patients in the aspirin group than in the ticlopidine group. Another concern is the obvious importance of blood pressure in the calculation of systemic vascular resistance; a slight change in the reading may importantly alter calculated resistance and the significance of changes with enalapril. Blood pressure was taken with the cuff method, apparently without a random zero method, and no information was provided concerning variability.

Regarding the results, 2 points are difficult to interpret. First, according to the conclusive statement, the pulmonary circulation seems to be a selective target of the angiotensin II–mediated vasoconstriction. This argues, without any supporting evidence, against the systemic angiotensinergic vasodilator activity of . . . [Full Text of this Article]

Christian Spaulding, MD; Bernard Charbonnier, MD; Alain Cohen-Solal, MD, PhD; Yves Juillière, MD; Eckhard Peter Kromer, MD; Khaldoun Benhamda, MD; Romain Cador, MD; Simon Weber, MD

Department of Cardiology, Cochin Hospital, René Descartes University, Paris, France