Background: Recurrent intracerebral hemorrhage (ICH) in patients with hypertension has been reported in Asia and is attributed to poor control of blood pressure, but there may be a genetic basis. This study evaluates the roles of apolipoprotein E (APOE) and α-1 antichymotrypsin (ACT) genes in patients with recurrent hypertensive ICH and compares patients with nonrecurring hypertensive ICH and normal controls.
Methods: Thirty-three recurrent and 101 nonrecurrent patients with hypertension and ICH were included. The demographic, stroke risk factors, and computed tomographic or magnetic resonance imaging findings were recorded. Magnetic resonance angiography or digital subtraction angiography and vasculitic profile were done in recurrent group to exclude secondary causes of ICH. APOE and ACT gene polymorphisms were assessed with polymerase chain reaction studies in patients with ICH and 188 healthy controls.
Results: The demographic and clinical variables were similar in patients with recurrent and nonrecurrent ICH, but patients with recurrent ICH were older (61.1 vs 57.2 years). In the recurrent ICH group, only 7 (10%) out of 69 episodes were lobar; the remaining were deep-seated hematomas. In the nonrecurrent group, 7 (6.9%) patients had lobar ICH. The E2 (odds ratio 4.32; 95% confidence interval 1.65-11.28; P = .003) and E4 alleles of APOE (odds ratio 11.33; 95% confidence interval 5.37-23.02; P < .0001) were significantly related to recurrent ICH compared to healthy controls. The E4 allele was also independently related to recurrent compared to nonrecurrent ICH, even after adjustment for stroke risk factors (odds ratio 25.99; 95% confidence interval 11.65-57.97; P < .0001). ACT gene polymorphism, however, was not related to recurrent ICH compared to controls and nonrecurrent ICH.
Conclusions: APOE polymorphism may contribute to the recurrence of hypertensive ICH.
Keywords: Antichymotrypsin; apolipoprotein E; gene; hypertension; intracerebral hemorrhage; recurrent; stroke.
Copyright © 2013 National Stroke Association. Published by Elsevier Inc. All rights reserved.