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Platelet glycoprotein IIb/IIIa receptor blockade and coronary resistance in unstable angina

Authors :
Silvio Fedele
Roberto Testa
Mario Marzilli
Gianmario Sambuceti
Source :
Journal of the American College of Cardiology. 40(12):2102-2109
Publication Year :
2002
Publisher :
Elsevier BV, 2002.

Abstract

ObjectivesWe designed a study to explore the effect of glycoprotein (GP) IIb/IIIa blockade on the atherosclerotic plaque and distal coronary vasculature.BackgroundPlatelet GP IIb/IIIa blockers have been proven to be beneficial in acute ischemic syndromes. This effect has also been attributed to the prevention of microvascular obstruction, although the underlying mechanisms have not been fully defined.MethodsEighteen patients with unstable refractory angina pectoris underwent cardiac catheterization and angioplasty. Trans-stenotic and microvascular resistances to flow were measured at baseline, during hyperventilation, and after intracoronary adenosine. Measurements were repeated early after abciximab administration and after successful percutaneous transluminal coronary angioplasty.ResultsHyperventilation induced an ischemic attack in 12 of 18 patients and increased epicardial (12.8 ± 16.9 vs. 6.1 ± 6.1 mm Hg/ml per min, p < 0.05) and microvascular (9.9 ± 7.5 vs. 6.8 ± 5.8 mm Hg/ml per min, p < 0.05) coronary resistance. Abciximab had no significant effect on epicardial resistance, although it significantly reduced distal coronary resistance under all study conditions, including baseline (4.8 ± 4.8 mm Hg/ml per min, p < 0.01), hyperventilation (5.1 ± 5.4 mm Hg/ml per min, p < 0.01), and intracoronary adenosine (2.7 ± 3.0 vs. 4.3 ± 4.3 mm Hg/ml per min, p < 0.05). The hyperventilation test became negative in all patients after abciximab administration.ConclusionsThese observations confirm the immediate beneficial effects of platelet GP IIb/IIIa blockade with abciximab in acute ischemic syndromes and suggest that improvement of microvascular function may play a central role in the mechanism of action of this drug.

Details

ISSN :
07351097
Volume :
40
Issue :
12
Database :
OpenAIRE
Journal :
Journal of the American College of Cardiology
Accession number :
edsair.doi.dedup.....87214d0325c2d8fad3d90da887b9c32a
Full Text :
https://doi.org/10.1016/s0735-1097(02)02590-1