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Updated: May 18, 2026

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function
Published on: March 15, 2022
Periprocedural variations of platelet reactivity during elective percutaneous coronary intervention
F Mangiacapra1, J Bartunek, N Bijnens
1Cardiovascular Center Aalst OLV Hospital, Aalst, Belgium.
Insights
Percutaneous coronary intervention (PCI) increases platelet reactivity (PR) and this increase is linked to procedural complexity and vascular damage. This heightened PR is associated with periprocedural myocardial infarction (PMI).
Area of Science:
- Cardiovascular Medicine
- Interventional Cardiology
- Hematology
Background:
- Percutaneous coronary intervention (PCI) is known to influence platelet reactivity (PR).
- Understanding these modulations is crucial for managing patients undergoing these procedures.
Purpose of the Study:
- To evaluate periprocedural changes in platelet reactivity (ΔPR) following coronary interventions.
- To determine if ΔPR correlates with periprocedural myocardial infarction (PMI).
- To investigate the in vitro mechanisms underlying these PR variations.
Main Methods:
- Assessed PR using ADP, high-sensitivity ADP, and TRAP-6 tests in 65 patients before, immediately after, and 24 hours post-PCI.
- Measured E-selectin and ICAM-1 levels pre- and post-procedure.
- Conducted in vitro experiments using porcine carotid arteries and plastic tubes to simulate procedural conditions.
Main Results:
- Platelet reactivity (PR) increased significantly after PCI and rotational atherectomy (RA) compared to coronary angiography (CA) alone.
- ΔPR correlated directly with total inflation time and stent length in the PCI group.
- Increased PR was significantly associated with the occurrence of PMI and changes in E-selectin levels.
Conclusions:
- PCI impacts platelet function in proportion to procedural complexity and vascular injury, even with dual antiplatelet therapy.
- These findings highlight the importance of monitoring PR and managing vascular damage during PCI.
Background:
Percutaneous coronary intervention (PCI) modulates platelet reactivity (PR).
Objectives:
To assess: (i) the impact of coronary interventions on periprocedural variations (Δ) of PR; (ii) whether ΔPR correlates with periprocedural myocardial infarction (PMI); and (iii) the mechanisms of these variations in vitro.
Methods And Results:
We enrolled 65 patients on aspirin (80-100 mg day(-1)) and clopidogrel (600 mg, 12 h before PCI): 15 with coronary angiography (CA group), 40 with PCI (PCI group), and 10 with rotational atherectomy plus PCI (RA group). PR was assessed by ADP, high-sensitivity ADP and thrombin receptor activator peptide 6 tests prior to, immediately after and 24 h after the procedure. E-selectin and ICAM-1 were assessed prior to and immediately after the procedure. In vitro, PR was measured during pulsatile blood flow at baseline, after balloon inflation and after stent implantation in six porcine carotid arteries and five plastic tubes. PR declined in the CA group, but significantly increased in the PCI and RA groups immediately postprocedure, and decreased to baseline at 24 h. ΔPR increased across the three groups (P < 0.0001). In the PCI group, ΔPR was directly related to total inflation time (r = 0.435, P = 0.005) and total stent length (r = 0.586, P < 0.001). The change in E-selectin significantly and inversely correlated with ΔPR (P < 0.001). No correlation was found with sICAM-1. PR increased significantly more in patients with PMI than in patients without PMI (P = 0.013). In vitro, platelet activation was observed in the presence of carotid arteries but not in the presence of plastic tubes.
Conclusions:
Despite dual antiplatelet therapy, PCI affected platelet function proportionally to procedural complexity and the extent of vascular damage.
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