January 11, 2005Circulation
Role of β 2 Adrenergic Receptors in Human Atherosclerotic Coronary Arteries
Why the study?
Does intracoronary salbutamol alter lumen diameter and coronary blood flow differently in normal, mildly atherosclerotic, and stenotic human coronary arteries?
Population
Human coronary arteries categorized as normal, mildly atherosclerotic, and stenotic.
Comparison
Intracoronary infusion of increasing doses of… vs Responses compared across normal, mildly…
Design
Cross-sectional
Follow-up
Acute (during infusion)
Authors
Discussion
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Implication
May precipitate ischemia via paradoxical vasoconstriction in stenotic vessels; hypothesis-generating for beta2-adrenergic dysfunction in advanced atherosclerosis.
Key Points
- To evaluate the vasomotor role of beta-2 adrenergic receptors across normal, mildly atherosclerotic, and stenotic human coronary arteries.
- Assessed lumen diameter using quantitative coronary angiography across 34 normal, 55 mildly atherosclerotic, and 42 stenotic coronary artery segments during intracoronary infusion of salbutamol (0.15–0.6 µg/min) and acetylcholine (1–10 µg/min).
- Measured average peak velocity and coronary blood flow via Doppler flow wire in 11 normal, 10 mildly atherosclerotic, and 11 stenotic arteries, repeating protocols with phentolamine in 6 stenotic arteries and L-NMMA in 6 normal arteries.
- In normal vessels, salbutamol significantly increased lumen diameter (11 ± 2%, P<0.05), average peak velocity (53 ± 17%, P<0.05), and coronary blood flow (57 ± 17%, P<0.05), with blood flow responses blunted by L-NMMA (29 ± 6%, P<0.05).
- In stenotic vessels, salbutamol induced paradoxical reductions in lumen diameter (-6 ± 2%, P<0.05), average peak velocity (-15 ± 9%, P<0.05), and coronary blood flow (-15 ± 6%, P<0.05), an effect completely abolished by phentolamine pretreatment.
- Acetylcholine increased coronary blood flow in normal arteries (67 ± 19%, P<0.05), produced no significant change in mildly atherosclerotic vessels (-10 ± 13%, P=NS), and reduced blood flow in stenotic arteries (-15 ± 6%, P<0.05).
Structured PICO
Does intracoronary salbutamol alter lumen diameter and coronary blood flow differently in normal, mildly atherosclerotic, and stenotic human coronary arteries?
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Population
Human coronary arteries categorized as normal (34 segments for lumen diameter [LD], 11 for average peak velocity [APV]/coronary blood flow [CBF]), mildly atherosclerotic (55 segments for LD, 10 for APV/CBF), and stenotic (42 segments for LD, 11 for APV/CBF).
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Intervention
Intracoronary infusion of increasing doses of the beta2-AR agonist salbutamol (0.15, 0.3, and 0.6 μg/min) and the endothelial vasodilator acetylcholine (1, 3, and 10 μg/min). Subsets also received intracoronary phentolamine or L-NMMA.
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Comparator
Responses compared across normal, mildly atherosclerotic, and stenotic coronary arteries.
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Outcome
Changes in lumen diameter (LD) measured by quantitative coronary angiography, and changes in average peak velocity (APV) and coronary blood flow (CBF) measured by Doppler flow wire.surrogate
Beta2-adrenergic vasodilatation is impaired in severely atherosclerotic coronary arteries, leading to paradoxical vasoconstriction that may precipitate ischemia during sympathetic activation.
Cite This Study
Barbato et al. (2005) studied this question.