Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2005
Angiotensin converting enzyme insertion/deletion polymorphisms in vasovagal syncope.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Newton Julia L, Donaldson Peter, Parry Steve, Kenny Rose Anne, Smith Jennifer, Gibson Alison M, Morris Christopher
Аннотация
UNLABELLED: Recent studies suggest vasovagal syncope (VVS) has a significant heritable component (crude estimate sibling relative risk (lambda(s)): 1080) indicating that at least some forms of VVS may have a genetic cause. Here we present the first study examining a potential genetic abnormality in VVS.
METHODS: DNA was collected from consecutive patients attending our unit with head up tilt confirmed VVS (n=165). One hundred and fourteen affected and unaffected first-degree relatives of those with a definitive diagnosis of VVS and positive family history also provided DNA.
RESULTS: DNA from 165 VVS index cases was genotyped for the ACE insertion/deletion polymorphism. Mean+/-SD age of cases was 56+/-19 years (103 (62%) females). There was no significant difference in distribution of ACE insertion or deletion gene frequencies in cases compared with a large (>6000 subjects) national control population. No preferential transmission of alleles in families was identified using tests of association (P=0.1789)
CONCLUSION: We have shown using both a case control and a small family based association study that polymorphisms of ACE alone are not associated with increased risk of VVS. Further studies are planned to clarify the genotype/phenotype relationship in VVS and examine other candidate genes.
METHODS: DNA was collected from consecutive patients attending our unit with head up tilt confirmed VVS (n=165). One hundred and fourteen affected and unaffected first-degree relatives of those with a definitive diagnosis of VVS and positive family history also provided DNA.
RESULTS: DNA from 165 VVS index cases was genotyped for the ACE insertion/deletion polymorphism. Mean+/-SD age of cases was 56+/-19 years (103 (62%) females). There was no significant difference in distribution of ACE insertion or deletion gene frequencies in cases compared with a large (>6000 subjects) national control population. No preferential transmission of alleles in families was identified using tests of association (P=0.1789)
CONCLUSION: We have shown using both a case control and a small family based association study that polymorphisms of ACE alone are not associated with increased risk of VVS. Further studies are planned to clarify the genotype/phenotype relationship in VVS and examine other candidate genes.