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Rosuvastatin prevents aortic arch plaque progression and improves prognosis in ischemic stroke patients
Kazuyoshi Kaneko1, Hiroki Saito1, Toshiki Sasaki1
1a Department of Cardiology , Kitamurayama Municipal Hospital , Higashine , Japan.
Insights
Rosuvastatin therapy prevented aortic arch plaque progression in patients with complicated aortic arch plaques (CAP), reducing major adverse cerebrovascular events (MACEs) and improving outcomes for ischemic stroke (IS) patients.
Area of Science:
- Cardiovascular Medicine
- Neurology
- Pharmacology
Background:
- Complicated aortic arch plaques (CAP) are linked to recurrent ischemic stroke (IS) and poorer prognosis.
- Understanding the impact of therapies on CAP progression is crucial for managing IS patients.
Purpose of the Study:
- To investigate the effects of rosuvastatin on the progression of complicated aortic arch plaques (CAP).
- To determine if rosuvastatin therapy improves the prognosis of ischemic stroke (IS) patients with CAP.
Main Methods:
- Retrospective analysis of 97 acute cerebral embolism patients.
- Transesophageal echocardiography (TEE) used to identify CAP (aortic wall thickness ≥4 mm or plaque ulceration).
- Comparison of outcomes between patients with CAP who received rosuvastatin and those who did not, alongside patients without CAP.
Main Results:
- Complicated aortic arch plaques (CAP) were present in 40% of patients.
- Not taking rosuvastatin was an independent risk factor for major adverse cerebrovascular events (MACEs) in patients with CAP (OR = 18.044, p < 0.01).
- Rosuvastatin therapy led to improved CAP diameter, better lipid profiles, and prevented plaque progression in 88% of treated patients, with 15 showing regression.
Conclusions:
- Rosuvastatin therapy effectively prevents the progression of aortic arch plaque in IS patients.
- Rosuvastatin may offer significant long-term clinical benefits for IS patients with CAP.
Objectives:
Complicated aortic arch plaques (CAP) and their progression are important for recurrent ischemic stroke (IS) and its prognosis. We investigated the effects and clinical benefits of rosuvastatin therapy on this pathophysiology. The purpose of this study was to investigate whether rosuvastatin prevention of aortic arch plaque progression improved the prognosis of IS patients.
Methods:
Ninety-seven consecutive acute cerebral embolism patients were retrospectively surveyed. All had transesophageal echocardiography (TEE) to assess the presence or absence of CAP, defined as aortic wall thickness ≥4 mm or plaque ulceration. Patients received conventional antithrombotic therapy as clinically indicated. All patients with CAP were recommended to receive 5 mg rosuvastatin/day, administered by their attending physicians; not all physicians followed this recommendation. Six-month follow-up TEEs were performed in patients with CAP who received rosuvastatin. Major adverse cerebrovascular events (MACEs) comprised recurrent IS and death.
Results:
CAP was detected in 39 patients (40%), and MACEs in 15. Multivariate regression analysis showed that patients with CAP not taking rosuvastatin was an independent risk factor for MACEs (odds ratio = 18.044; 95% confidential interval = 2.089-155.846, p < 0.01). When patients were divided into three groups: those with CAP taking rosuvastatin, those with CAP not taking rosuvastatin, and those without CAP, Kaplan-Meier analysis demonstrated that patients with CAP not taking rosuvastatin had significantly more MACEs than those in the other two groups (long-rank test; χ2 = 6.553, p < 0.05). Six-month TEE follow-ups in the 26 patients with CAP taking rosuvastatin showed significant improvement in CAP diameter with improved lipid profiles; 88% (23/26 patients) showed no morphological CAP progression; 15 of these showed CAP regression.
Discussion:
Rosuvastatin therapy prevented aortic arch plaque progression in IS patients with CAP, and may also have long-term clinical benefits.
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