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Effects of selective alpha1- and alpha2-adrenergic blockade on coronary flow reserve after coronary stenting
Luisa Gregorini1, Jean Marco, Bruno Farah
1Experimental Surgery and Transplantation Institute, Ospedale Maggiore IRCCS, University of Milano, Italy. Luisa.Gregorini@unimi.it
Insights
Alpha-adrenergic vasoconstriction limits coronary flow reserve (CFR) after stenting. Blocking alpha-adrenergic receptors with urapidil or yohimbine improved CFR, suggesting the adrenergic system
Area of Science:
- Cardiovascular physiology
- Interventional cardiology
- Pharmacology
Background:
- Coronary flow reserve (CFR) is often suboptimal post-coronary stenting.
- Alpha-adrenergic coronary vasoconstriction is hypothesized to limit CFR.
Purpose of the Study:
- To investigate the role of alpha-adrenergic vasoconstriction in limiting coronary flow reserve (CFR) after coronary stenting.
- To assess the effects of alpha-adrenergic antagonists on CFR post-stenting.
Main Methods:
- Assessed coronary blood flow velocity and cross-sectional area in 46 patients undergoing stenting.
- Induced hyperemia with adenosine before and after stenting.
- Administered alpha(1)-antagonist urapidil or alpha(2)-antagonist yohimbine with adenosine.
Main Results:
- Stenting did not alter CFR, but it decreased post-procedure.
- Yohimbine and urapidil improved CFR in patients with reduced CFR post-stenting.
- Both antagonists enhanced the vasodilator effect of adenosine and increased blood flow velocity.
Conclusions:
- Alpha-adrenergic blockade with urapidil and yohimbine attenuated CFR impairment after stenting.
- The adrenergic system significantly limits the coronary circulation's ability to dilate.
- Targeting the adrenergic system may improve coronary blood flow post-revascularization.
Background:
Coronary flow reserve (CFR) is not normalized shortly after coronary stenting. We hypothesized that alpha-adrenergic coronary vasoconstriction acts to limit CFR.
Methods And Results:
We assessed flow velocity by Doppler wires and cross-sectional area by angiography in 46 patients undergoing coronary culprit lesion stenting (81+/-4% stenosis). Hyperemia was induced by adenosine (24 micro g IC or 140 micro g/kg per minute IV) before and after stenting. Finally, either the alpha(1)-antagonist urapidil (10 mg IC) or the alpha(2)-antagonist yohimbine (3 mg IC) was randomly combined with adenosine. In 8 subjects with angiographically normal coronary arteries, CFR was increased from 3.21+/-0.30 to 3.74+/-0.43 by yohimbine and to 4.58+/-0.65 by urapidil, respectively (P=0.0001). Patients were divided according to the cutoff of CFR > or =3.0 (n=18) or <2.5 (n=28). Revascularization per se did not change CFR. However, 15 minutes after stenting, CFR decreased to 2.05+/-0.55 from CFR 3.64+/-0.58, whereas in patients with CFR 2.39+/-0.51, it remained unchanged. Yohimbine improved CFR to 3.26+/-0.42 and to 3.41+/-0.58 in patients with >3.0 and <2.05+/-0.55 baseline CFR, respectively. Urapidil improved CFR to 3.52+/-0.30 and 3.98+/-1.07, respectively.
Conclusions:
Urapidil and yohimbine attenuated the CFR impairment occurring after revascularization by increasing both the epicardial vasodilator effect of adenosine and the blood flow velocity, thus suggesting that the adrenergic system plays an important role in limiting the capacity of the coronary circulation to dilate.
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