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Genetic polymorphism of angiotensin-converting enzyme and hypertrophic cardiomyopathy risk: A systematic review and meta-analysis
BACKGROUND: Genetic factors in the pathogenesis of cardiomyopathies have received a lot of attention during the past 2 decades. Some studies have reported that angiotensin-converting enzyme (ACE) gene has been associated with hypertrophic cardiomyopathy (HCM). However, there have been inconsonant re...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer Health
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5728739/ https://www.ncbi.nlm.nih.gov/pubmed/29310338 http://dx.doi.org/10.1097/MD.0000000000008639 |
Sumario: | BACKGROUND: Genetic factors in the pathogenesis of cardiomyopathies have received a lot of attention during the past 2 decades. Some studies have reported that angiotensin-converting enzyme (ACE) gene has been associated with hypertrophic cardiomyopathy (HCM). However, there have been inconsonant results among different studies. To clarify the influence of ACE on HCM, a systemic review and meta-analysis of case–control studies were performed. METHODS: The following databases were searched to indentify related studies: PubMed database, the Embase database, the Cochrane Central Register of Controlled Trials database, China National Knowledge Information database, and Chinese Scientific and Technological Journal database. Search terms included “hypertrophic cardiomyopathy,” “angiotensin converting enzyme” or “ACE,” and “polymorphism or mutation.” RESULTS: Fifteen separate studies were suitable for the inclusion criterion. The selected studies contained 2972 participants, including 1047 in HCM group and 1925 controls. Pooled odds ratios (ORs) were calculated to assess the association between ACE insertion/deletion (I/D) polymorphism and HCM. Our case–control data indicated that D allele carrier is a risk allele in all genetic models: allele contrast (D vs I: OR = 1.35, 95% confidence interval [CI]: 1.10–1.65, P = .004), homozygous comparison (DD vs II: OR = 1.69; 95% CI: 1.12–2.54; P = .01), dominant model (DD + ID vs II: OR = 1.52, 95% CI: 1.15–2.02, P = .003), and recessive model (DD vs ID + II: OR = 1.34, 95% CI: 0.99–1.81, P = .03). CONCLUSION: In summary, the current meta-analysis provided solid evidence suggesting that ACE gene I/D polymorphism was probably a genetic risk factor for HCM. |
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