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Association between Antiplatelet Therapy and Changes in Intraplaque Hemorrhage in Patients with Mild to Moderate
Mohamed Kassem1,2, Geneviève A J C Crombag1,2, Jens Stegers1
1Department of Radiology and Nuclear Medicine, Maastricht University Medical Center, Maastricht, The Netherlands.
Insights
Starting antiplatelet therapy after a stroke or TIA did not increase intraplaque hemorrhage (IPH) or its progression over two years. Previous antiplatelet use was associated with baseline IPH, but new therapy initiation showed no link to IPH development or worsening.
Area of Science:
- Cardiovascular Medicine
- Neurology
- Radiology
Background:
- Carotid atherosclerotic intraplaque hemorrhage (IPH) is a predictor of stroke.
- Antiplatelet agents are crucial for secondary stroke prevention.
- Previous studies suggested a link between antiplatelet use and IPH.
Purpose of the Study:
- To investigate the impact of initiating versus continuing antiplatelet therapy on IPH.
- To analyze changes in IPH volume over two years in relation to antiplatelet use patterns.
Main Methods:
- Prospective study (PARISK) involving symptomatic carotid stenosis patients.
- Carotid plaque MRI at baseline and 2-year follow-up to assess IPH presence and volume.
- Categorization into new users (started therapy post-event) and continued users (pre-existing therapy).
Main Results:
- Baseline antiplatelet use was associated with the presence of IPH (OR=5.6).
- No significant changes in IPH volume were observed over 2 years in either new or continued antiplatelet users.
- New antiplatelet use was not associated with newly developed IPH or IPH volume progression.
Conclusions:
- The association between prior antiplatelet use and baseline IPH is confirmed.
- Initiating antiplatelet therapy following a stroke or TIA is not linked to new IPH or progression of existing IPH over two years.
Introduction:
Carotid atherosclerotic intraplaque hemorrhage (IPH) predicts stroke. Patients with a history of stroke are treated with antiplatelet agents to prevent secondary cardiovascular events. A positive association between previous antiplatelet use and IPH was reported in a cross-sectional analysis. We investigated the changes in IPH over 2 years in patients who recently started versus those with continued antiplatelet use.
Methods:
In the Plaque at Risk (PARISK) study, symptomatic patients with <70% ipsilateral carotid stenosis underwent carotid plaque magnetic resonance imaging (MRI) at the baseline and after 2 years to determine IPH presence and volume. Participants were categorized into new users (starting antiplatelet therapy following the index event) and continued users (previous use of antiplatelet therapy before the index event). The association between previous antiplatelet therapy and the presence of IPH at baseline MRI was investigated using multivariable logistic regression analysis. The IPH volume change over a period of 2 years, defined as the difference in volume between follow-up and baseline, was investigated in each group with a Wilcoxon signed-rank test. The IPH volume change was categorized as progression, regression, or no change. Using multivariable logistic regression, we investigated the association between new antiplatelet use and (1) newly developed ipsilateral or contralateral IPH and (2) IPH volume progression.
Results:
A total of 108 patients underwent carotid MRI at the baseline and follow-up. At the baseline, previous antiplatelet therapy was associated with any IPH (OR = 5.6, 95% CI: 1.3-23.1; p = 0.02). Ipsilateral IPH volume did not change significantly during the 2 years in patients who continued receiving antiplatelet agents (86.4 mm3 [18.2-235.9] vs. 59.3 mm3 [11.4-260.3]; p = 0.6) nor in the new antiplatelet users (n = 31) (61.5 mm3 [0.0-166.9] vs. 27.7 mm3 [9.5-106.4]; p = 0.4). Similar results of a nonsignificant change in contralateral IPH volume during those 2 years were observed in both groups (p > 0.05). No significant associations were found between new antiplatelet use and newly developed IPH at 2 years (odds ratio [OR] = 1.0, 95% CI: 0.1-7.4) or the progression of IPH (ipsilateral: OR = 2.4, 95% CI: 0.3-19.1; contralateral: OR = 0.3, 95% CI: 0.01-8.5).
Conclusion:
Although the baseline association between IPH and previous antiplatelet therapy was confirmed in this larger cohort, the new onset of antiplatelet therapy after transient ischemic attack/stroke was not associated with the newly developed IPH or progression of IPH volume over the subsequent 2 years.
