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Risk Factors for Lobar and Non-Lobar Intracerebral Hemorrhage in Patients with Vascular Disease
Authors:Philip H C Kremer  Wilmar M T Jolink  L Jaap Kappelle  Ale Algra  Catharina J M Klijn  SMART and ESPRIT Study Groups
Institution:1. Department of Neurology and Neurosurgery, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands.; 2. Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, The Netherlands.; 3. Department of Neurology, Donders Institute for Brain, Cognition and Behavior, Centre for Neuroscience, Radboud University Medical Center, Nijmegen, The Netherlands.; University of Kansas, UNITED STATES,
Abstract:

Introduction

Lobar and non-lobar non-traumatic intracerebral hemorrhage (ICH) are presumably caused by different types of small vessel diseases. The aim of this study was to assess risk factors for ICH according to location.

Methods

In two large prospective studies, SMART (n = 9088) and ESPRIT (n = 2625), including patients with manifest cardiovascular, cerebrovascular or peripheral artery disease or with vascular risk factors, we investigated potential risk factors for ICH during follow-up according to lobar or non-lobar location by Cox proportional hazards analyses.

Results

During 65,156 patient years of follow up 19 patients had lobar ICH (incidence rate 29, 95% CI 19–42 per 100,000 person-years) and 24 non-lobar ICH (incidence rate 37, 95% CI 26–51 per 100,000 person-years). Age significantly increased the risk of lobar ICH (HR per 10 years increase 1.90; 95% CI 1.17–3.10) in the multivariable analysis, but not of non-lobar hemorrhage. Anticoagulant medication (HR 3.49; 95% CI 1.20–10.2) and male sex (HR 3.79; 95% CI 1.13–12.8) increased the risk of non-lobar but not lobar ICH.

Conclusion

This study shows an elevated risk of future ICH in patients with manifestations of, or risk factors for, cardiovascular, cerebrovascular or peripheral artery disease. Our data suggest that risk factors for ICH vary according to location, supporting the hypothesis of a differential pathophysiology of lobar and non-lobar ICH.
Keywords:
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