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European Heart Journal 2004 25(22):2034-2039; doi:10.1016/j.ehj.2004.09.003
Copyright © 2004 by the European Society of Cardiology.
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Clinical research

Alpha-adrenergic receptor blockade and hyperaemic response in patients with intermediate coronary stenoses

Emanuele Barbatoa, Jozef Bartuneka, Wilbert Aarnoudseb, Marc Vanderheydena, Frank Staelensa, William Wijnsa, Guy R. Heyndrickxa, Nico H.J. Pijlsb and Bernard De Bruynea,*

a Cardiovascular Center Aalst, Onze Lieve Vrouw Clinic, Moorselbaan 164, B-9300 Aalst, Belgium
b Division of Cardiology, Catharina Hospital – Eindhoven, The Netherlands

Received May 31, 2004; revised August 15, 2004; accepted September 9, 2004 * Corresponding author. Tel.: +32 53 724447; fax: +32 53 724550 (E-mail: bernard.de.bruyne{at}olvz-aalst.be).

See page 1970 for the editorial comment on this article (doi:10.1016/j.ehj.2004.09.005)

BACKGROUND: Maximal hyperaemia is paramount in the diagnosis of patients with coronary artery disease. However in these patients, enhanced α-adrenergic microvascular vasoconstriction may preclude adenosine to induce maximal hyperaemia.

AIM: To assess the presence and the clinical relevance of residual microvascular resistance after administration of adenosine.

METHODS AND RESULTS: Fractional flow reserve (FFR, calculated by coronary pressure measurements during adenosine-induced hyperaemia) was assessed in 85 patients with an intermediate coronary stenosis (mean diameter stenosis of 50±1%) and normal left ventricular function which were divided into the following three groups: (a) 33 patients before and after IC bolus of phentolamine, an α1-, α2-adrenergic blocker; (b) 32 patients before and after IC bolus of urapidil, a selective α1-adrenergic blocker; (c) 20 patients before and after IC bolus of saline.

Since minimal luminal diameter remained unchanged before and after phentolamine (1.46±0.06 vs. 1.47±0.06 mm, ns), urapidil (1.46±0.06 vs. 1.39±0.08, ns), and saline (1.56±0.08 vs. 1.55±0.08, ns), changes in FFR reflects changes in microvascular resistance.

Overall, phentolamine and urapidil induced a slight but significant decrease in FFR (phentolamine: 0.79±0.02 vs. 0.77±0.02, p<0.05; urapidil: 0.78±0.02 vs. 0.75±0.02, p<0.05). However, only 6 patients showed a change in FFR from ⩾0.75 to <0.75 and no patients showed a change in FFR from ⩾0.80 to <0.75 that could have influenced clinical decision making. Saline did not induce any change in FFR. Phentolamine and urapidil induced only transient and negligible haemodynamic changes in heart rate and blood pressure.

CONCLUSIONS: The administration of α-adrenergic blockers in addition to adenosine unmasks a small, yet clinically irrelevant, degree of residual microvascular tone. The consequential changes in FFR values do not significantly affect clinical decision making.


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