Preserved Vasodilator Response to Acetylcholine in Atherosclerotic Coronary Arteries Before and After PTCA

ANDREA MACCHI, ROBERT G. XUEREB, MARIOSA XUEREB, GABRIELE VICEDOMINI, ALBERTO MARGONATO, ORAZIO CARANDENTE, SERGIO L. CHIERCHIA

Research output: Contribution to journalArticle

Abstract

The vascular response to local administration of acetylcholine is used, clinically, to assess endothelial function in vivo. However, whether this response predominantly reflects the functional state of the vascular endothelium, or rather results from smooth muscle reactivity per se is not clear. In 15 patients with chronic stable angina and angiographically significant coronary disease, we studied the effects of increasing doses of intracoronary acetylcholine (5, 10, 30, 50, and 80 μg) and nitroglycerin (200 μg) on coronary vascular tone. In three patients the protocol was perfrnned at the time of diagnostic coronary angiographv and 7 and 24 hours after angioplasty. The remaining five underwent acetylcholine administration before and after percutaneous transluminl coronary angioplasty (PTCA). We quantitatively assessed the diameter of 54 coronary arterial segments; 12 stenotic segments, 13 post‐PICA segments with residual irregularities, 18 reference segments of the ranee arteries taken proximal to the stenosis or to the dilatation site, and II remote segments ofnonstenotic vessels. They all showed a bimodal response to acetylcholine. At the lowest concentration (5 μg) the agent invariably caused dilatation (9.22 ± 6.55%), which was not significantly different in the various segments and was always less than that induced by nitroglycerin (24.56 ± 12.82%, P < 0.0001). At the highest doses (50 or 80 μg) acetylcholine always induced vasoconstriction, which was significantly more pronounced in the post‐PTCA (‐31.54 ± 10.65%) and stenotic segments (‐23.08 ± 11.88%) than in the reference and remote segments (respectively, ‐14.88 + 7.63% and ‐ 18.67 + 8.37%, P < 0.05). We conclude that: (l) some degree of endothelial dependent vasodilatation is preserved even in the presence of atheroma and intimal injury induced by angioplasty; (2) atheroma and especially acute intimal injury augment the vasoconstrictor response to high dose acetylcholine, the effect being most probably mediated by primary smooth muscle supersensivity: (3) since acetylcholine has direct and endothelium‐mediated vasoactive effects, this agent may not be the ideal one for testing endothelial integrity. (J Interven Cardiol 1994; 7:57–64)

Original languageEnglish
Pages (from-to)57-64
Number of pages8
JournalJournal of Interventional Cardiology
Volume7
Issue number1
DOIs
Publication statusPublished - 1994

Fingerprint

Vasodilator Agents
Angioplasty
Acetylcholine
Coronary Vessels
Tunica Intima
Nitroglycerin
Atherosclerotic Plaques
Smooth Muscle
Blood Vessels
Dilatation
Stable Angina
Vascular Endothelium
Wounds and Injuries
Vasoconstrictor Agents
Vasoconstriction
Vasodilation
Coronary Disease
Pathologic Constriction
Arteries

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging
  • Cardiology and Cardiovascular Medicine

Cite this

MACCHI, ANDREA., XUEREB, ROBERT. G., XUEREB, MARIOSA., VICEDOMINI, GABRIELE., MARGONATO, ALBERTO., CARANDENTE, ORAZIO., & CHIERCHIA, SERGIO. L. (1994). Preserved Vasodilator Response to Acetylcholine in Atherosclerotic Coronary Arteries Before and After PTCA. Journal of Interventional Cardiology, 7(1), 57-64. https://doi.org/10.1111/j.1540-8183.1994.tb00890.x

Preserved Vasodilator Response to Acetylcholine in Atherosclerotic Coronary Arteries Before and After PTCA. / MACCHI, ANDREA; XUEREB, ROBERT G.; XUEREB, MARIOSA; VICEDOMINI, GABRIELE; MARGONATO, ALBERTO; CARANDENTE, ORAZIO; CHIERCHIA, SERGIO L.

In: Journal of Interventional Cardiology, Vol. 7, No. 1, 1994, p. 57-64.

Research output: Contribution to journalArticle

MACCHI, ANDREA, XUEREB, ROBERTG, XUEREB, MARIOSA, VICEDOMINI, GABRIELE, MARGONATO, ALBERTO, CARANDENTE, ORAZIO & CHIERCHIA, SERGIOL 1994, 'Preserved Vasodilator Response to Acetylcholine in Atherosclerotic Coronary Arteries Before and After PTCA', Journal of Interventional Cardiology, vol. 7, no. 1, pp. 57-64. https://doi.org/10.1111/j.1540-8183.1994.tb00890.x
MACCHI ANDREA, XUEREB ROBERTG, XUEREB MARIOSA, VICEDOMINI GABRIELE, MARGONATO ALBERTO, CARANDENTE ORAZIO et al. Preserved Vasodilator Response to Acetylcholine in Atherosclerotic Coronary Arteries Before and After PTCA. Journal of Interventional Cardiology. 1994;7(1):57-64. https://doi.org/10.1111/j.1540-8183.1994.tb00890.x
MACCHI, ANDREA ; XUEREB, ROBERT G. ; XUEREB, MARIOSA ; VICEDOMINI, GABRIELE ; MARGONATO, ALBERTO ; CARANDENTE, ORAZIO ; CHIERCHIA, SERGIO L. / Preserved Vasodilator Response to Acetylcholine in Atherosclerotic Coronary Arteries Before and After PTCA. In: Journal of Interventional Cardiology. 1994 ; Vol. 7, No. 1. pp. 57-64.
@article{6afd46b90ea248b5bfec42bb0aeb661e,
title = "Preserved Vasodilator Response to Acetylcholine in Atherosclerotic Coronary Arteries Before and After PTCA",
abstract = "The vascular response to local administration of acetylcholine is used, clinically, to assess endothelial function in vivo. However, whether this response predominantly reflects the functional state of the vascular endothelium, or rather results from smooth muscle reactivity per se is not clear. In 15 patients with chronic stable angina and angiographically significant coronary disease, we studied the effects of increasing doses of intracoronary acetylcholine (5, 10, 30, 50, and 80 μg) and nitroglycerin (200 μg) on coronary vascular tone. In three patients the protocol was perfrnned at the time of diagnostic coronary angiographv and 7 and 24 hours after angioplasty. The remaining five underwent acetylcholine administration before and after percutaneous transluminl coronary angioplasty (PTCA). We quantitatively assessed the diameter of 54 coronary arterial segments; 12 stenotic segments, 13 post‐PICA segments with residual irregularities, 18 reference segments of the ranee arteries taken proximal to the stenosis or to the dilatation site, and II remote segments ofnonstenotic vessels. They all showed a bimodal response to acetylcholine. At the lowest concentration (5 μg) the agent invariably caused dilatation (9.22 ± 6.55{\%}), which was not significantly different in the various segments and was always less than that induced by nitroglycerin (24.56 ± 12.82{\%}, P < 0.0001). At the highest doses (50 or 80 μg) acetylcholine always induced vasoconstriction, which was significantly more pronounced in the post‐PTCA (‐31.54 ± 10.65{\%}) and stenotic segments (‐23.08 ± 11.88{\%}) than in the reference and remote segments (respectively, ‐14.88 + 7.63{\%} and ‐ 18.67 + 8.37{\%}, P < 0.05). We conclude that: (l) some degree of endothelial dependent vasodilatation is preserved even in the presence of atheroma and intimal injury induced by angioplasty; (2) atheroma and especially acute intimal injury augment the vasoconstrictor response to high dose acetylcholine, the effect being most probably mediated by primary smooth muscle supersensivity: (3) since acetylcholine has direct and endothelium‐mediated vasoactive effects, this agent may not be the ideal one for testing endothelial integrity. (J Interven Cardiol 1994; 7:57–64)",
author = "ANDREA MACCHI and XUEREB, {ROBERT G.} and MARIOSA XUEREB and GABRIELE VICEDOMINI and ALBERTO MARGONATO and ORAZIO CARANDENTE and CHIERCHIA, {SERGIO L.}",
year = "1994",
doi = "10.1111/j.1540-8183.1994.tb00890.x",
language = "English",
volume = "7",
pages = "57--64",
journal = "Journal of Interventional Cardiology",
issn = "0896-4327",
publisher = "Wiley-Blackwell",
number = "1",

}

TY - JOUR

T1 - Preserved Vasodilator Response to Acetylcholine in Atherosclerotic Coronary Arteries Before and After PTCA

AU - MACCHI, ANDREA

AU - XUEREB, ROBERT G.

AU - XUEREB, MARIOSA

AU - VICEDOMINI, GABRIELE

AU - MARGONATO, ALBERTO

AU - CARANDENTE, ORAZIO

AU - CHIERCHIA, SERGIO L.

PY - 1994

Y1 - 1994

N2 - The vascular response to local administration of acetylcholine is used, clinically, to assess endothelial function in vivo. However, whether this response predominantly reflects the functional state of the vascular endothelium, or rather results from smooth muscle reactivity per se is not clear. In 15 patients with chronic stable angina and angiographically significant coronary disease, we studied the effects of increasing doses of intracoronary acetylcholine (5, 10, 30, 50, and 80 μg) and nitroglycerin (200 μg) on coronary vascular tone. In three patients the protocol was perfrnned at the time of diagnostic coronary angiographv and 7 and 24 hours after angioplasty. The remaining five underwent acetylcholine administration before and after percutaneous transluminl coronary angioplasty (PTCA). We quantitatively assessed the diameter of 54 coronary arterial segments; 12 stenotic segments, 13 post‐PICA segments with residual irregularities, 18 reference segments of the ranee arteries taken proximal to the stenosis or to the dilatation site, and II remote segments ofnonstenotic vessels. They all showed a bimodal response to acetylcholine. At the lowest concentration (5 μg) the agent invariably caused dilatation (9.22 ± 6.55%), which was not significantly different in the various segments and was always less than that induced by nitroglycerin (24.56 ± 12.82%, P < 0.0001). At the highest doses (50 or 80 μg) acetylcholine always induced vasoconstriction, which was significantly more pronounced in the post‐PTCA (‐31.54 ± 10.65%) and stenotic segments (‐23.08 ± 11.88%) than in the reference and remote segments (respectively, ‐14.88 + 7.63% and ‐ 18.67 + 8.37%, P < 0.05). We conclude that: (l) some degree of endothelial dependent vasodilatation is preserved even in the presence of atheroma and intimal injury induced by angioplasty; (2) atheroma and especially acute intimal injury augment the vasoconstrictor response to high dose acetylcholine, the effect being most probably mediated by primary smooth muscle supersensivity: (3) since acetylcholine has direct and endothelium‐mediated vasoactive effects, this agent may not be the ideal one for testing endothelial integrity. (J Interven Cardiol 1994; 7:57–64)

AB - The vascular response to local administration of acetylcholine is used, clinically, to assess endothelial function in vivo. However, whether this response predominantly reflects the functional state of the vascular endothelium, or rather results from smooth muscle reactivity per se is not clear. In 15 patients with chronic stable angina and angiographically significant coronary disease, we studied the effects of increasing doses of intracoronary acetylcholine (5, 10, 30, 50, and 80 μg) and nitroglycerin (200 μg) on coronary vascular tone. In three patients the protocol was perfrnned at the time of diagnostic coronary angiographv and 7 and 24 hours after angioplasty. The remaining five underwent acetylcholine administration before and after percutaneous transluminl coronary angioplasty (PTCA). We quantitatively assessed the diameter of 54 coronary arterial segments; 12 stenotic segments, 13 post‐PICA segments with residual irregularities, 18 reference segments of the ranee arteries taken proximal to the stenosis or to the dilatation site, and II remote segments ofnonstenotic vessels. They all showed a bimodal response to acetylcholine. At the lowest concentration (5 μg) the agent invariably caused dilatation (9.22 ± 6.55%), which was not significantly different in the various segments and was always less than that induced by nitroglycerin (24.56 ± 12.82%, P < 0.0001). At the highest doses (50 or 80 μg) acetylcholine always induced vasoconstriction, which was significantly more pronounced in the post‐PTCA (‐31.54 ± 10.65%) and stenotic segments (‐23.08 ± 11.88%) than in the reference and remote segments (respectively, ‐14.88 + 7.63% and ‐ 18.67 + 8.37%, P < 0.05). We conclude that: (l) some degree of endothelial dependent vasodilatation is preserved even in the presence of atheroma and intimal injury induced by angioplasty; (2) atheroma and especially acute intimal injury augment the vasoconstrictor response to high dose acetylcholine, the effect being most probably mediated by primary smooth muscle supersensivity: (3) since acetylcholine has direct and endothelium‐mediated vasoactive effects, this agent may not be the ideal one for testing endothelial integrity. (J Interven Cardiol 1994; 7:57–64)

UR - http://www.scopus.com/inward/record.url?scp=84993865992&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84993865992&partnerID=8YFLogxK

U2 - 10.1111/j.1540-8183.1994.tb00890.x

DO - 10.1111/j.1540-8183.1994.tb00890.x

M3 - Article

AN - SCOPUS:84993865992

VL - 7

SP - 57

EP - 64

JO - Journal of Interventional Cardiology

JF - Journal of Interventional Cardiology

SN - 0896-4327

IS - 1

ER -