OBJECTIVES: The aim of this study was to investigate the relationship between the apo E genotype with acute cerebral infarction and primary intracerebral haemorrhage and to examine the relationship of the apo E genotype with mortality following acute stroke. MATERIALS AND METHODS: We studied 592 cases of acute stroke and 289 healthy control subjects clinically free of cerebrovascular disease. Pathological type of stroke was determined by cranial computed tomography and the subtype of cerebral infarction classified according to the Oxfordshire Community Stroke Project Classification (OCSP). Apo E genotype was determined using polymerase chain reaction. RESULTS: There was no difference in apo E genotype frequency between cases and controls (chi2 = 3.58, 5 d.f., P = 0.60). Apo E genotypes were not related to the pathological type of stroke (cerebral infarction, CI, n = 532 and primary intracranial haemorrhage, PICH, n = 60, (chi2 =3.738, 4 d.f., P=0.44) nor with the Oxfordshire Community Stroke Project Classification subtypes of cerebral infarction, lacunar infarction, LACI (n = 169), total anterior circulation infarction, TACI (n = 117), partial anterior circulation infarction, PACI (n = 173), posterior circulation infarction, POCS (n = 54) and including those cerebral infarcts which could not be classified (n= 19), chi2 =31.1, 20 d.f., P=0.153). At the time of the analysis, 243 cases (41.0%) had died. The median follow-up (including death) was 851 days. There was no relationship between time to death and apo E genotype in cases of either CI or PICH. CONCLUSION: In this population, there was no relationship between the apolipoprotein E polymorphism and the pathogenesis of cerebral infarction or primary intracerebral haemorrhage. Apo E genotype was not related to all-cause mortality following stroke.
OBJECTIVES: The aim of this study was to investigate the relationship between the apo E genotype with acute cerebral infarction and primary intracerebral haemorrhage and to examine the relationship of the apo E genotype with mortality following acute stroke. MATERIALS AND METHODS: We studied 592 cases of acute stroke and 289 healthy control subjects clinically free of cerebrovascular disease. Pathological type of stroke was determined by cranial computed tomography and the subtype of cerebral infarction classified according to the Oxfordshire Community Stroke Project Classification (OCSP). Apo E genotype was determined using polymerase chain reaction. RESULTS: There was no difference in apo E genotype frequency between cases and controls (chi2 = 3.58, 5 d.f., P = 0.60). Apo E genotypes were not related to the pathological type of stroke (cerebral infarction, CI, n = 532 and primary intracranial haemorrhage, PICH, n = 60, (chi2 =3.738, 4 d.f., P=0.44) nor with the Oxfordshire Community Stroke Project Classification subtypes of cerebral infarction, lacunar infarction, LACI (n = 169), total anterior circulation infarction, TACI (n = 117), partial anterior circulation infarction, PACI (n = 173), posterior circulation infarction, POCS (n = 54) and including those cerebral infarcts which could not be classified (n= 19), chi2 =31.1, 20 d.f., P=0.153). At the time of the analysis, 243 cases (41.0%) had died. The median follow-up (including death) was 851 days. There was no relationship between time to death and apo E genotype in cases of either CI or PICH. CONCLUSION: In this population, there was no relationship between the apolipoprotein E polymorphism and the pathogenesis of cerebral infarction or primary intracerebral haemorrhage. Apo E genotype was not related to all-cause mortality following stroke.
Authors: Alessandro Biffi; Akshata Sonni; Christopher D Anderson; Brett Kissela; Jeremiasz M Jagiella; Helena Schmidt; Jordi Jimenez-Conde; Björn M Hansen; Israel Fernandez-Cadenas; Lynelle Cortellini; Alison Ayres; Kristin Schwab; Karol Juchniewicz; Andrzej Urbanik; Natalia S Rost; Anand Viswanathan; Thomas Seifert-Held; Eva-Maria Stoegerer; Marta Tomás; Raquel Rabionet; Xavier Estivill; Devin L Brown; Scott L Silliman; Magdy Selim; Bradford B Worrall; James F Meschia; Joan Montaner; Arne Lindgren; Jaume Roquer; Reinhold Schmidt; Steven M Greenberg; Agnieszka Slowik; Joseph P Broderick; Daniel Woo; Jonathan Rosand Journal: Ann Neurol Date: 2010-12 Impact factor: 10.422
Authors: Alessandro Biffi; Christopher D Anderson; Jeremiasz M Jagiella; Helena Schmidt; Brett Kissela; Björn M Hansen; Jordi Jimenez-Conde; Caroline R Pires; Alison M Ayres; Kristin Schwab; Lynelle Cortellini; Joanna Pera; Andrzej Urbanik; Javier M Romero; Natalia S Rost; Joshua N Goldstein; Anand Viswanathan; Alexander Pichler; Christian Enzinger; Raquel Rabionet; Bo Norrving; David L Tirschwell; Magdy Selim; Devin L Brown; Scott L Silliman; Bradford B Worrall; James F Meschia; Chelsea S Kidwell; Joseph P Broderick; Steven M Greenberg; Jaume Roquer; Arne Lindgren; Agnieszka Slowik; Reinhold Schmidt; Daniel Woo; Jonathan Rosand Journal: Lancet Neurol Date: 2011-07-06 Impact factor: 44.182
Authors: James F Meschia; Thomas G Brott; Robert D Brown; Richard J P Crook; Michael Frankel; John Hardy; José G Merino; Stephen S Rich; Scott Silliman; Bradford Burke Worrall Journal: BMC Neurol Date: 2003-07-08 Impact factor: 2.474
Authors: George Peck; Liam Smeeth; John Whittaker; Juan Pablo Casas; Aroon Hingorani; Pankaj Sharma Journal: PLoS One Date: 2008-11-14 Impact factor: 3.240