Abstract 153: Prior Statin Therapy is Not Associated With Cerebral Bleeding-prone Angiopathies in Patients With Ischemic Stroke Who Start Long-term Oral Anticoagulation

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Abstract

Introduction: Statin therapy might be associated with an increased risk of hemorrhagic stroke, which has been attributed to low LDL-cholesterol levels and antithrombotic effects.

Hypothesis: Previous statin therapy is associated with surrogate markers of amyloid and hypertensive angiopathies in patients with cardioembolic stroke who need to start long-term oral anticoagulation (OA).

Methods: A prospective multicenter study of patients included in the HERO study (Intracerebral Hemorrhage due to Oral Anticoagulants: Prediction of the Risk by Magnetic Resonance). Patients were naïve for OA and had an acute cardioembolic ischemic stroke (TIA or infarct). A MR examination was performed during admission to evaluate: 1) Microbleeds (-MB-, number, distribution, burden); 2) Leukoaraiosis (-LK- presence and degree); 3) Superficial siderosis (-SS-, presence). We collected data on the specific statin, the dose and the statin intensity (low, medium or high according to accepted classifications). We also recorded demographic data and traditional vascular risk factors.

Results: We studied 470 patients (age 77.5±6.4 years, 43.7% were men). A total of 193 (41.1%) patients received prior treatment with any statin, of whom 43.5% received simvastatin and 41.3% atorvastatin. Statin intensity was low in 14.5%, medium in 61.1%, high in 16.5% and unknown in 10.8%. LK was detected in 82.5% and was severe in 19.8%. SS was detected in 20 (4.3%) patients. MBs were detected in 140 (29.8%) patients and the distribution was lobar in 55%, deep in 30% and both in 15%. Of the MB group 74 (53%) had 1 MB, 66 (47%) had >1 MB, and 11.4% had >5 MBs. The presence of MB, LK or SS was not related to the pre-treatment with statin. The statin intensity was not related to the presence of SS, the presence/degree of LK, and the presence/distribution/burden of MBs. MBs were detected with increased frequency in hypertensive patients (p=0.09). LK presence and degree were increased in patients with MB (p=0.012) and SS (p=0.041).

Conclusion: In conclusion, prior treatment with statins is not associated with surrogate markers of bleeding-prone cerebral angiopathies in patients with cardioembolic stroke. Therefore previous statin treatment should not influence the decision to start long-term oral anticoagulation.

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