BACKGROUND AND PURPOSE: It would be essential to clinicians, familial aneurysm study groups, and aneurysm families to understand the genetic basis of subarachnoid hemorrhage (SAH), but there are no large population-based heritability estimates assessing the relative contribution of genetic and environmental factors to SAH. METHODS: We constructed the largest twin cohort to date, the population-based Nordic Twin Cohort, which comprised 79 644 complete twin pairs of Danish, Finnish, and Swedish origin. The Nordic Twin Cohort was followed up for 6.01 million person-years using nationwide cause-of-death and hospitalization registries. RESULTS: One hundred eighty-eight fatal and 321 nonfatal SAH cases were recorded in the Nordic Twin Cohort. Thus, SAH incidence was 8.47 cases per 100,000 follow-up years. Data for pairwise analyses were available for a total of 504 SAH cases, of which 6 were concordant (5 monozygotic and 1 opposite sex) and 492 discordant twin pairs for SAH. The concordance for SAH in monozygotic twins was 3.1% compared with 0.27% in dizygotic twins, suggesting at most a modest role for genetic factors in the etiology of SAH. The population-based probability estimate for SAH in dizygotic siblings of a patient with SAH is 0.54%, and only 1 of 185 full siblings experience familial SAH. The corresponding risk of SAH in monozygotic twins is 5.9%. Model-fitting, which was based on the comparison of the few monozygotic and dizygotic pairs, suggested that the estimated heritability of SAH is 41%. CONCLUSIONS: SAH appears to be mainly of nongenetic origin, and familial SAHs can mostly be attributed to environmental risk factors.
BACKGROUND AND PURPOSE: It would be essential to clinicians, familial aneurysm study groups, and aneurysm families to understand the genetic basis of subarachnoid hemorrhage (SAH), but there are no large population-based heritability estimates assessing the relative contribution of genetic and environmental factors to SAH. METHODS: We constructed the largest twin cohort to date, the population-based Nordic Twin Cohort, which comprised 79 644 complete twin pairs of Danish, Finnish, and Swedish origin. The Nordic Twin Cohort was followed up for 6.01 million person-years using nationwide cause-of-death and hospitalization registries. RESULTS: One hundred eighty-eight fatal and 321 nonfatal SAH cases were recorded in the Nordic Twin Cohort. Thus, SAH incidence was 8.47 cases per 100,000 follow-up years. Data for pairwise analyses were available for a total of 504 SAH cases, of which 6 were concordant (5 monozygotic and 1 opposite sex) and 492 discordant twin pairs for SAH. The concordance for SAH in monozygotic twins was 3.1% compared with 0.27% in dizygotic twins, suggesting at most a modest role for genetic factors in the etiology of SAH. The population-based probability estimate for SAH in dizygotic siblings of a patient with SAH is 0.54%, and only 1 of 185 full siblings experience familial SAH. The corresponding risk of SAH in monozygotic twins is 5.9%. Model-fitting, which was based on the comparison of the few monozygotic and dizygotic pairs, suggested that the estimated heritability of SAH is 41%. CONCLUSIONS:SAH appears to be mainly of nongenetic origin, and familial SAHs can mostly be attributed to environmental risk factors.
Authors: Teresa Santiago-Sim; Xiaoqian Fang; Morgan L Hennessy; Stephen V Nalbach; Steven R DePalma; Ming Sum Lee; Steven C Greenway; Barbara McDonough; Georgene W Hergenroeder; Kyla J Patek; Sarah M Colosimo; Krista J Qualmann; John P Hagan; Dianna M Milewicz; Calum A MacRae; Susan M Dymecki; Christine E Seidman; J G Seidman; Dong H Kim Journal: Stroke Date: 2016-11-15 Impact factor: 7.914
Authors: Miikka Korja; Karri Silventoinen; Tiina Laatikainen; Pekka Jousilahti; Veikko Salomaa; Jaakko Kaprio Journal: Neurology Date: 2013-01-09 Impact factor: 9.910