The association between cerebral amyloid angiopathy and intracerebral haemorrhage: systematic review and meta-analysis
- Division of Clinical Neurosciences, Centre for Clinical Brain Sciences, University of Edinburgh, Bramwell Dott Building, Western General Hospital, Edinburgh, UK
- Correspondence to Dr R Al-Shahi Salman, Bramwell Dott Building, Division of Clinical Neurosciences, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK;
Contributors Agree with the manuscript results and conclusions: NS, CS, RASS. Designed the experiments/study: RASS. Analyzed the data: NS, RASS. Collected data/did experiments for the study: NS, CS, RASS. Wrote the first draft of the paper: NS, RASS. Contributed to the writing of the paper: NS, CS, RASS.
- Received 21 April 2011
- Revised 13 July 2011
- Accepted 3 October 2011
- Published Online First 5 November 2011
Background The aim of this study was to determine the strength of the association between intracerebral haemorrhage (ICH) and cerebral amyloid angiopathy (CAA) in a systematic review of published neuropathological studies.
Methods In April 2011, Ovid Medline (from 1950) and Embase (from 1980) were searched for neuropathological studies that quantified the prevalence of CAA in patients with ICH and in a control group without ICH. Two authors extracted data from each study and meta-analysed their results using a random effects model.
Results 10 neuropathological cross sectional or case control studies were identified, involving 481 cases with ICH and 3219 controls. There was no association between CAA and ICH in any location (OR 1.21, 95% CI 0.87 to 1.68; 10 studies, I2 29%), deep ICH (OR 0.81, 95% CI 0.30 to 2.19; five studies, I2 58%) or cerebellar ICH (OR 2.05, 95% CI 0.55 to 7.63; four studies, I2 0%). CAA was significantly associated with lobar ICH, both overall (OR 2.21, 95% CI 1.09 to 4.45; six studies, I2 40%) and in the three studies where average ages for cases and controls were comparable (OR 3.24, 95% CI 1.02 to 10.26).
Conclusions There is an association between CAA and lobar ICH, although the association might be stronger if potential confounding factors, distinctive clinical and imaging features of ICH due to CAA and CAA neuropathological severity are taken into account.
Funding NS was funded by a clinical research training fellowship from the UK Medical Research Council and The Stroke Association. RASS was funded by a clinician scientist fellowship from the UK Medical Research Council.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.