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J Am Coll Cardiol, 1999; 33:1499-1505
© 1999 by the American College of Cardiology Foundation
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Alpha-adrenoceptor blockade prevents exercise-induced vasoconstriction of stenotic coronary arteries

Barbara K. Julius, MD*, Giuseppe Vassalli, MD*, Lazar Mandinov, MD{dagger} and Otto M. Hess, MD{dagger}

* Department of Internal Medicine, Cardiology, University Hospital, Zurich, Switzerland
{dagger} Department of Internal Medicine, Cardiology, Inselspital, Bern, Switzerland



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Figure 1 Quantitative coronary angiography of the left anterior descending coronary artery in a patient with moderate lesion in Aldrigde projection. Automatic evaluation of the stenotic segment was performed by computer analysis. The proximal and distal reference segments are marked with two lines. The minimal luminal diameter was 2.6 mm at Rest, 2.7 mm after intracoronary phentolamine (Reg), 2.6 mm during the first (Ex 1) and 2.6 mm during the second (Ex 2) exercise level, and amounted to 3.0 mm after sublingual nitroglycerin (NTG).

 


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Figure 2 Rate-pressure product (RPP) and mean pulmonary artery pressure (mPAP) at rest (R), after intracoronary administration of phentolamine (Drug), during two levels of supine bicycle exercise (Ex1; Ex2), and after sublingual nitroglycerin administration (NTG). Note the significant rise of both parameters during exercise. However, patients on chronic beta-blockade reached a lower rate-pressure product than did the two other groups. Open circles = alpha-blockers; solid circles = alpha- plus beta-blockers; solid triangles = control group. NTG = nitroglycerin. *p < 0.05 versus alpha- plus beta-blockers.

 


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Figure 3 Responses of normal and stenotic coronary arteries to dynamic exercise after intracoronary phentolamine administration in patients without ({alpha}; upper panel) and with chronic beta-blockade ({alpha} + ß; lower panel). For comparison purposes, data are shown also for controls (C). Coronary cross-sectional area (CSA) is expressed in percent of resting luminal area. Normal vessel size remained unchanged after phentolamine administration and increased during exercise both before and after administration of phentolamine or nitroglycerin. The CSA of the stenotic vessel segments also remained unchanged after phentolamine administration. However, in phentolamine-treated patients with or without chronic beta-blockade, paradoxical stenosis vasoconstriction was prevented during exercise. Coronary vasoconstriction was reversible after nitroglycerin administration.

 





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