BACKGROUND: Findings on the association between the insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene and cardiovascular morbidity and mortality have been inconsistent. Considering the possible interaction between this polymorphism and smoking, we evaluated the association between ACE I/D polymorphism and myocardial infarction (MI), mortality due to coronary heart disease (CHD), and cardiovascular disease (CVD). METHODS: The study was performed within the Rotterdam Study, a population based cohort study. The ACE I/D polymorphism was determined for 6714 participants and smoking status recorded at baseline. Fatal and non-fatal MIs and mortality events were regularly recorded. Cox proportional hazard analysis was performed separately for current smokers and non-smokers. We used age as the follow up time, presenting age specific survivals. RESULTS: During follow up, 248 MIs and 301 and 482 deaths, respectively, due to CHD and CVD occurred. There were no significant differences between the genotypes as regards MI incidence. Among smokers, there was an increased risk of CHD and CVD mortality in carriers of the DD genotype compared to the II genotype, which diminished at later ages (p<0.01 for gene-age interaction). Subgroup analysis in a younger and older group (based on the median age of 68.2 years) showed a significantly increased risk of CVD mortality in the younger group (hazard ratio = 5.19; 95% confidence interval: 1.15 to 23.42). CONCLUSIONS: This study showed that the ACE I/D polymorphism is not a strong risk factor for MI but its interaction with smoking might play a role in cardiovascular mortality especially at younger ages.
BACKGROUND: Findings on the association between the insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene and cardiovascular morbidity and mortality have been inconsistent. Considering the possible interaction between this polymorphism and smoking, we evaluated the association between ACE I/D polymorphism and myocardial infarction (MI), mortality due to coronary heart disease (CHD), and cardiovascular disease (CVD). METHODS: The study was performed within the Rotterdam Study, a population based cohort study. The ACE I/D polymorphism was determined for 6714 participants and smoking status recorded at baseline. Fatal and non-fatal MIs and mortality events were regularly recorded. Cox proportional hazard analysis was performed separately for current smokers and non-smokers. We used age as the follow up time, presenting age specific survivals. RESULTS: During follow up, 248 MIs and 301 and 482 deaths, respectively, due to CHD and CVD occurred. There were no significant differences between the genotypes as regards MI incidence. Among smokers, there was an increased risk of CHD and CVD mortality in carriers of the DD genotype compared to the II genotype, which diminished at later ages (p<0.01 for gene-age interaction). Subgroup analysis in a younger and older group (based on the median age of 68.2 years) showed a significantly increased risk of CVD mortality in the younger group (hazard ratio = 5.19; 95% confidence interval: 1.15 to 23.42). CONCLUSIONS: This study showed that the ACE I/D polymorphism is not a strong risk factor for MI but its interaction with smoking might play a role in cardiovascular mortality especially at younger ages.
Authors: Anna F C Schut; Fakhredin A Sayed-Tabatabaei; Jacqueline C M Witteman; Aida M Bertoli Avella; Jeannette M Vergeer; Huibert A P Pols; Albert Hofman; Jaap Deinum; Cornelia M van Duijn Journal: J Hypertens Date: 2004-02 Impact factor: 4.844
Authors: E Ilveskoski; M Perola; T Lehtimäki; P Laippala; V Savolainen; J Pajarinen; A Penttilä; K H Lalu; A Männikkö; K K Liesto; T Koivula; P J Karhunen Journal: Circulation Date: 1999-08-10 Impact factor: 29.690
Authors: Francesco U S Mattace-Raso; Tischa J M van der Cammen; Fakhredin A Sayed-Tabatabaei; Nicole M van Popele; Roland Asmar; Maarten A D H Schalekamp; Albert Hofman; Cornelia M van Duijn; Jacqueline C M Witteman Journal: Atherosclerosis Date: 2004-05 Impact factor: 5.162
Authors: F A Sayed-Tabatabaei; A F C Schut; A Hofman; A M Bertoli-Avella; J Vergeer; J C M Witteman; C M van Duijn Journal: J Med Genet Date: 2004-02 Impact factor: 6.318
Authors: John W Cole; Huichun Xu; Kathleen Ryan; Thomas Jaworek; Nicole Dueker; Patrick McArdle; Brady Gaynor; Yu-Ching Cheng; Jeffrey O'Connell; Steve Bevan; Rainer Malik; Naveed Uddin Ahmed; Philippe Amouyel; Sheraz Anjum; Joshua C Bis; David Crosslin; John Danesh; Stefan T Engelter; Myriam Fornage; Philippe Frossard; Christian Gieger; Anne-Katrin Giese; Caspar Grond-Ginsbach; Weang Kee Ho; Elizabeth Holliday; Jemma Hopewell; M Hussain; W Iqbal; S Jabeen; Jim Jannes; Ayeesha Kamal; Yoichiro Kamatani; Sandip Kanse; Manja Kloss; Mark Lathrop; Didier Leys; Arne Lindgren; W T Longstreth; Khalid Mahmood; Christa Meisinger; Tiina M Metso; Thomas Mosley; Martina Müller-Nurasyid; Bo Norrving; Eugenio Parati; Annette Peters; Alessandro Pezzini; I Quereshi; Asif Rasheed; A Rauf; T Salam; Jess Shen; Agnieszka Słowik; Tara Stanne; Konstantin Strauch; Turgut Tatlisumak; Vincent N Thijs; Steffen Tiedt; Matthew Traylor; Melanie Waldenberger; Matthew Walters; Wei Zhao; Giorgio Boncoraglio; Stéphanie Debette; Christina Jern; Christopher Levi; Hugh Markus; James Meschia; Arndt Rolfs; Peter Rothwell; Danish Saleheen; Sudha Seshadri; Pankaj Sharma; Cathie Sudlow; Bradford Worrall; O Colin Stine; Steven J Kittner; Braxton D Mitchell Journal: PLoS One Date: 2018-11-01 Impact factor: 3.240