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Published on: May 28, 2019
Platelet glycoprotein IIb/IIIa receptor blockade and coronary resistance in unstable angina
Mario Marzilli1, Gianmario Sambuceti, Roberto Testa
1University of Siena, Italy. marzilli@unisi.it
Insights
Glycoprotein (GP) IIb/IIIa blockade with abciximab improved microvascular function in patients with acute ischemic syndromes. This suggests that enhanced microvascular function is a key mechanism behind the drug's beneficial effects.
Area of Science:
- Cardiology
- Vascular Biology
- Pharmacology
Background:
- Platelet GP IIb/IIIa blockers are effective in acute ischemic syndromes.
- Their role in preventing microvascular obstruction requires further elucidation.
Purpose of the Study:
- To investigate the impact of GP IIb/IIIa blockade on atherosclerotic plaque and distal coronary vasculature.
- To explore the mechanisms underlying the therapeutic effects of abciximab.
Main Methods:
- Eighteen patients with unstable angina underwent cardiac catheterization and angioplasty.
- Coronary resistances were measured at baseline, during hyperventilation, and after adenosine, before and after abciximab administration and angioplasty.
Main Results:
- Hyperventilation increased epicardial and microvascular coronary resistance.
- Abciximab significantly reduced distal coronary resistance under all conditions.
- Hyperventilation-induced ischemic attacks resolved after abciximab treatment.
Conclusions:
- Abciximab provides immediate benefits in acute ischemic syndromes.
- Improved microvascular function is a crucial mechanism of action for GP IIb/IIIa inhibitors.
Objectives:
We designed a study to explore the effect of glycoprotein (GP) IIb/IIIa blockade on the atherosclerotic plaque and distal coronary vasculature.
Background:
Platelet 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.
Methods:
Eighteen 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.
Results:
Hyperventilation 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.
Conclusions:
These 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.
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