How is hemorrhage prevented in cerebral amyloid angiopathy (CAA)?

Answer

Patients with cerebral amyloid angiopathy (CAA) have an increased risk of bleeding while taking warfarin, even when the level of anticoagulation is in the therapeutic range (ie, international normalized ratio, 2-3). The vasculopathic changes may predispose these patients to small bleeds. The use of anticoagulants may result in the enlargement of small hemorrhages that otherwise would have remained asymptomatic.

Withdrawal of anticoagulant agents is a prudent intervention to prevent recurrences in patients with prior lobar hemorrhages, particularly if GRE MRI suggests earlier petechial hemorrhages. Antiplatelet agents are a safer alternative.

Strong evidence regarding the relationship between CAA and antithrombotic therapy is lacking. Data suggested that GRE microbleeds were more prevalent among a cohort of aspirin users in the Rotterdam Scan Study; however, more research is needed to understand the dynamic between antithrombotic therapy and the risk of intracerebral hemorrhage and microbleed formation.^[19]

In the patient with coronary artery disease, cardiac stents, and/or ischemic stroke, the benefit of antithrombotic therapy is clear and withdrawal of antiplatelet therapy requires prudent consideration of multiple factors. Management must be tailored to each individual case, taking into account the risk of hemorrhage, the benefit of stroke prophylaxis, and the preferences of the patient.

Two studies support the treatment of hypertension to prevent hemorrhage recurrence in CAA. The first, an analysis of patients in the PROGRESS trial, showed that those on active therapy with perindopril had fewer recurrences of all types of hemorrhage than those in the control group.^[16] A second study, a single center cohort study of patients with lobar and nonlobar hemorrhages, suggested that inadequate blood pressure control during follow-up was associated with higher risk of lobar as well as nonlobar ICH recurrence.^[20]

Did this answer your question?

Yes No

Additional feedback? (Optional)

Thank you for your feedback!

Pezzini A, Del Zotto E, Volonghi I, Giossi A, Costa P, Padovani A. Cerebral amyloid angiopathy: a common cause of cerebral hemorrhage. Curr Med Chem. 2009. 16(20):2498-513. [Medline].
Chung YA, Hyun O J, Kim JY, Kim KJ, Ahn KJ. Hypoperfusion and Ischemia in Cerebral Amyloid Angiopathy Documented by 99mTc-ECD Brain Perfusion SPECT. J Nucl Med. 2009 Dec. 50(12):1969-74. [Medline].
Weller RO, Preston SD, Subash M, Carare RO. Cerebral amyloid angiopathy in the aetiology and immunotherapy of Alzheimer disease. Alzheimers Res Ther. 2009 Oct 12. 1(2):6. [Medline].
Eng JA, Frosch MP, Choi K, et al. Clinical manifestations of cerebral amyloid angiopathy-related inflammation. Ann Neurol. 2004 Feb. 55(2):250-6. [Medline].
Roy O Weller, Stephen D Preston, Malavika Subash and Roxana O Carare. Cerebral amyloid angiopathy in the aetiology and immunotherapy of Alzheimer disease. Alzheimers Res Ther (epub). 2009 Oct 12. 1(2):6-13. [Medline]. [Full Text].
Ellis RJ, Olichney JM, Thal LJ, Mirra SS, Morris JC, Beekly D, et al. Cerebral amyloid angiopathy in the brains of patients with Alzheimer's disease: the CERAD experience, Part XV. Neurology. 1996 Jun. 46(6):1592-6. [Medline].
Oh U, Gupta R, Krakauer JW, et al. Reversible leukoencephalopathy associated with cerebral amyloid angiopathy. Neurology. 2004 Feb 10. 62(3):494-7. [Medline].
Cano LM, Martinez-Yelamos S, Majos C, Alberti MA, Boluda S, Velasco R, et al. Reversible acute leukoencephalopathy as a form of presentation in cerebral amyloid angiopathy. J Neurol Sci. 2009 Oct 22. [Medline].
Greenberg SM. Cerebral amyloid angiopathy: prospects for clinical diagnosis and treatment. Neurology. 1998 Sep. 51(3):690-4. [Medline].
Neuraceq (florbetaben F 18) prescribing information. [package insert]. Matran Switzerland: Piramal Imaging, S.A. 2014.
Johnson KA, Gregas M, Becker JA, Kinnecom C, Salat DH, Moran EK, et al. Imaging of amyloid burden and distribution in cerebral amyloid angiopathy. Ann Neurol. 2007 Sep. 62(3):229-34. [Medline].
Blitstein MK, Tung GA. MRI of cerebral microhemorrhages. AJR Am J Roentgenol. 2007 Sep. 189(3):720-5. [Medline].
Chalela JA, Kang DW, Warach S. Multiple cerebral microbleeds: MRI marker of a diffuse hemorrhage-prone state. J Neuroimaging. 2004 Jan. 14(1):54-7. [Medline].
Greenberg SM, Eng JA, Ning M, Smith EE, Rosand J. Hemorrhage burden predicts recurrent intracerebral hemorrhage after lobar hemorrhage. Stroke. 2004 Jun. 35(6):1415-20. [Medline].
Chen YW, Gurol ME, Rosand J, Viswanathan A, Rakich SM, Groover TR, et al. Progression of white matter lesions and hemorrhages in cerebral amyloid angiopathy. Neurology. 2006 Jul 11. 67(1):83-7. [Medline].
Arima H, Tzourio C, Anderson C, Woodward M, Bousser MG, MacMahon S, et al. Effects of perindopril-based lowering of blood pressure on intracerebral hemorrhage related to amyloid angiopathy: the PROGRESS trial. Stroke. 2010 Feb. 41(2):394-6. [Medline].
Petridis AK, Barth H, Buhl R, Hugo HH, Mehdorn HM. Outcome of cerebral amyloid angiopathic brain haemorrhage. Acta Neurochir (Wien). 2008 Sep. 150(9):889-95. [Medline].
Izumihara A, Ishihara T, Iwamoto N, et al. Postoperative outcome of 37 patients with lobar intracerebral hemorrhage related to cerebral amyloid angiopathy. Stroke. 1999 Jan. 30(1):29-33. [Medline].
Vernooij MW, Haag MD, van der Lugt A, Hofman A, Krestin GP, Stricker BH, et al. Use of antithrombotic drugs and the presence of cerebral microbleeds: the Rotterdam Scan Study. Arch Neurol. Jun/2009. 66(6):714-20. [Medline].
Biffi A, Anderson CD, Battey TW, Ayres AM, Greenberg SM, Viswanathan A, et al. Association Between Blood Pressure Control and Risk of Recurrent Intracerebral Hemorrhage. JAMA. 2015 Sep 1. 314 (9):904-12. [Medline].
Yamashita T, Ando Y, Ueda M, Nakamura M, Okamoto S, Zeledon ME. Effect of liver transplantation on transthyretin Tyr114Cys-related cerebral amyloid angiopathy. Neurology. 2008 Jan 8. 70(2):123-8. [Medline].

Media Gallery

MRI Brain GRE 3.0 TeslaTop: Multiple scattered microbleeds in multiple vascular territories in patient with hyperhomocysteinemia and methylene-tetrahydrofolate reductase mutation. Middle: Acute parenchymal hematoma with typical appearance of right occipital microbleed and left parietal chronic microhemorrhage.Bottom: Microbleeds involving multiple lobes. Chronic hemorrhage in the left parietal lobe with typical slit-like appearance.

of 1

Author

Ravi S Menon, MD Assistant Professor of Neurology, Georgetown University School of Medicine

Ravi S Menon, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Society of Neuroimaging, American Stroke Association

Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2; Physician Advisory Board for Coherex Medical; National Leader and Steering Committee Clinical Trial, Bristol Myers Squibb; Consultant, Abbott Vascular, Inc. .

Additional Contributors

Jose G Merino, MD Vascular Neurologist, Johns Hopkins Community Physicians

Jose G Merino, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Stroke Association, Asociacion Mexicana de Enfermedad Vascular Cerebral

Disclosure: Nothing to disclose.

Vladimir Hachinski, MD, MSc, DSc, FRCPC Distinguished University Professor, Departments of Clinical Neurological Sciences, Epidemiology and Biostatistics, University of Western Ontario Faculty of Medicine and Dentistry, London Health Sciences Centre, Canada

Vladimir Hachinski, MD, MSc, DSc, FRCPC is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Neurological Association, Ontario Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

Thomas A Kent, MD Professor and Director of Stroke Research and Education, Department of Neurology, Baylor College of Medicine; Chief of Neurology, Michael E DeBakey Veterans Affairs Medical Center

Thomas A Kent, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, New York Academy of Sciences, Royal Society of Medicine, Sigma Xi, and Stroke Council of the American Heart Association

Disclosure: Nothing to disclose.

Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association

Disclosure: BMS/Sanofi Honoraria Speaking and teaching

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

How is hemorrhage prevented in cerebral amyloid angiopathy (CAA)?

Answer

Related Questions:

References

Tables

Contributor Information and Disclosures