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FRI086 Statin Use After Lobar Intracerebral Hemorrhage- Is It Safe?
Disclosure: D. Vedamurthy: None. M. Ambrosino: None. K. Suri: None. D. Soffer: None. D. Jacoby: None. Background: Observational studies and randomized clinical trials have yielded conflicting data on the role of statins in causing intracerebral hemorrhage. It is unclear whether it is safe to continu...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10555303/ http://dx.doi.org/10.1210/jendso/bvad114.600 |
Sumario: | Disclosure: D. Vedamurthy: None. M. Ambrosino: None. K. Suri: None. D. Soffer: None. D. Jacoby: None. Background: Observational studies and randomized clinical trials have yielded conflicting data on the role of statins in causing intracerebral hemorrhage. It is unclear whether it is safe to continue statins in patients who have atherosclerotic cardiovascular disease (ASCVD) when they sustain an intracerebral hemorrhage (ICH). It is also not clear whether this risk of ICH (if present) relates to statin use or “too low” levels of LDL-C. Case: 75-year-old female with history of hypertension, hyperlipidemia, and a coronary artery calcium score of 450, presented to the hospital with severe headache and was diagnosed to acute right ICH. She did not smoke, use street drugs or drink excess alcohol. She did not have a family history of premature ASCVD. Her other medication included amlodipine, rosuvastatin and aspirin. Her lipid panel at hospitalization was TC 130 mg/dl, HDL 38 mg/dl, TG 137 mg/dl and LDL-C 70 mg/dl. Imaging studies were negative for cortical venous thrombosis, reversible cerebrovascular constriction, vasculitis, aneurysm, or AV fistula as etiologies. TEE was negative for cardioembolic source. Her hypertension medications were optimized, and she was discharged without any statin therapy. She fortunately recovered with mild deficits. She enrolled in an open-label randomized study- SATURN- which aims to assess safety of statin use in recurrent ICH. Her lipid panel while off statins showed a TC 274 mg/dl, TG 159 mg/dl, markedly elevated LDL-C of 197 mg/dl, and HDL-C 47 mg/dl. She presents to the lipid clinic for risk reduction. Early studies suggested increased ICH related to very low LDL-C levels, especially in the East Asian population. Concerns about statin use and ICH sparked after post-hoc analyses of SPARCL. Data from mendelian randomization studies and meta-analysis have failed to show convincing associations between statin use and ICH. Certain genetic variants, especially related to Apo E, have been shown to enhance this risk for ICH. There is a diversity in management of patients who have sustained an ICH (especially the lobar type as opposed to deep). An open label randomized trial (SATURN) is currently recruiting patients to answer this unresolved question. The dilemma is compounded in patients who have comorbid ASCVD. There are signals that PCSK9 inhibitors may be safer in terms of less propensity to cause intracerebral hemorrhage, but more data is needed. Moreover, the very low LDL-C levels achieved with use of PCSK-9 inhibitors may be concerning. Conclusion: There are no clear major society guidelines to advice clinicians on the best way to manage patients who have sustained a lobar intracerebral hemorrhage and have a compelling reason to be on statins for lipid lowering therapy to treat ASCVD. There are no clear guidelines on how low is “too low” as far as LDL-C targets are concerned. We present this case study as a call for more robust and expedient research in this field. Presentation: Friday, June 16, 2023 |
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