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Measurement of Myocardial Lactate Production for Diagnosis of Coronary Microvascular Spasm
Published on: September 17, 2021
Platelet reactivity and coronary microvascular impairment after percutaneous revascularization in stable patients
Fabio Mangiacapra1, Mariano Pellicano2, Luigi Di Serafino2
1Cardiovascular Research Center Aalst, OLV Clinic, Aalst, Belgium; Unit of Cardiovascular Science, Department of Medicine, Campus Bio-Medico University, Rome, Italy.
Insights
Prasugrel significantly reduces platelet reactivity after percutaneous coronary intervention (PCI) compared to clopidogrel. This potent platelet inhibition may improve coronary microvascular function following PCI in patients with stable coronary artery disease.
Area of Science:
- Cardiology
- Pharmacology
- Interventional Cardiology
Background:
- Increased platelet reactivity (PR) and coronary microvascular impairment are observed in patients on clopidogrel post-PCI.
- Prasugrel offers stronger platelet inhibition than clopidogrel, but its effect on PCI-related platelet activation is unclear.
Purpose of the Study:
- To compare the effects of prasugrel versus clopidogrel on peri-procedural PR variations.
- To assess the correlation between platelet inhibition potency and PCI-induced coronary microvascular impairment.
Main Methods:
- Forty thienopyridine-naive patients were randomized to prasugrel (n=20) or clopidogrel (n=20) loading dose before elective PCI.
- Adenosine diphosphate (ADP)-induced PR and the index of microvascular resistance (IMR) were measured at baseline and post-PCI.
Main Results:
- ADP-induced PR was significantly lower in the prasugrel group versus the clopidogrel group at baseline and post-PCI (p < 0.001).
- A peri-procedural increase in PR occurred with clopidogrel (p=0.008) but not with prasugrel (p=0.822).
- A significant correlation was found between IMR and PR at baseline (r=0.458, p=0.003) and post-PCI (r=0.487, p=0.001).
Conclusions:
- Prasugrel loading dose attenuates PCI-related PR increase compared to clopidogrel in stable CAD patients undergoing PCI.
- This effect may contribute to prasugrel's benefit on peri-procedural coronary microvascular function.
Background And Aims:
Increased platelet reactivity (PR) associated with variable degree of coronary microvascular impairment has been reported in patients on clopidogrel after elective percutaneous coronary intervention (PCI). Prasugrel provides more potent platelet inhibition than clopidogrel, though it is unknown whether it might also prevent PCI-related platelet activation. In stable patients undergoing elective PCI, we compared: (1) the effects of prasugrel vs. clopidogrel on peri-procedural variations of PR and (2) the correlation of platelet inhibition potency with PCI-induced coronary microvascular impairment.
Methods:
Forty thienopyridine-naive patients were randomly assigned to a loading dose of either prasugrel 60 mg (n = 20) or clopidogrel 600 mg (n = 20) at least 12 h before PCI. At the time of PCI, we assessed adenosine diphosphate (ADP)-induced PR with the Multiplate Analyzer, and the pressure-derived index of microvascular resistance (IMR) in the treated coronary, both at baseline and post-procedure.
Results:
ADP-induced PR was significantly lower in the prasugrel compared with clopidogrel group both at baseline (16.0 ± 8.7 vs. 33.9 ± 18.0 aggregation units [AU], p < 0.001) and post-procedure (16.2 ± 9.0 vs. 39.0 ± 18.6 AU, p < 0.001). A significant peri-procedural increase in PR was observed in the clopidogrel group (p = 0.008), but not in the prasugrel group (p = 0.822). A significant correlation was found between IMR and PR both at baseline (r = 0.458, p = 0.003) and post-PCI (r = 0.487, p = 0.001).
Conclusions:
A loading dose of prasugrel compared with clopidogrel is able to attenuate PCI-related increase in PR in patients with stable CAD undergoing PCI, which might contribute to the beneficial effect of this drug on peri-procedural coronary microvascular function.
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