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https://hdl.handle.net/11499/4381
Title: | Early sign of atherosclerosis in slow coronary flow and relationship with angiotensin-converting enzyme I/D polymorphism | Authors: | Tanrıverdi, Halil Evrengul, H. Mergen, H. Acar, C. Seleci, D. Kuru, O. Tanriverdi, S. |
Keywords: | ACEI/D polymorphism AT1R A/C1166 polymorphism Carotid atherosclerosis Intima-media thickness Renin-angiotensin gene system Slow coronary flow angiotensin 1 receptor dipeptidyl carboxypeptidase adult aged allele angiocardiography artery intima artery media artery wall article atherosclerosis cardiovascular disease carotid artery clinical article common carotid artery controlled study coronary artery blood flow coronary artery disease correlation analysis disease association echography enzyme polymorphism female gene deletion gene insertion genotype human image display inheritance male pathogenesis priority journal regulatory mechanism renin angiotensin aldosterone system risk factor statistical significance thickness transducer vascular disease Adult Aged Alleles Carotid Artery Diseases Coronary Angiography Coronary Vessels Female Humans Male Middle Aged Peptidyl-Dipeptidase A Polymorphism, Genetic Regional Blood Flow Renin-Angiotensin System Tunica Intima Tunica Media |
Abstract: | Increase in carotid artery intima-media thickness (IMT) is an early sign of atherosclerosis. Slow coronary flow (SCF) is characterized by delay of opacification of coronary arteries in coronary angiography in the absence of any evident obstructive lesion, but its etiopathogenesis remains unclear. Genes that regulate the renin angiotensin system also play a role in developing cardiovascular system disorders. The presence of deletion (D) allele in angiotensin converting enzyme (ACE) gene polymorphism is associated with coronary artery disease. The aim of this study was to investigate the carotid artery IMT measurement, as an early sign of atherosclerosis, in patients with SCF and without SCF and also to assess the effect of the renin-angiotensin gene system on carotid IMT. Forty-four patients with angiographically proven SCF and 44 cases with normal coronary flow (NCF) pattern with similar risk profile were enrolled in the study. Coronary flow patterns of the cases were determined by thrombolysis in myocardial infarction (TIMI) frame count method. Intima-media thickness was measured by recording ultrasonographic images of both the left and right common carotid artery with a 12-MHz linear array transducer. ACE I/D polymorphism and Angiotensin II tip 1 receptor (AT1R) A/C gene polymorphism were determined by polymerase chain reaction (PCR) amplification. Demographic characteristics and coronary artery disease risk factors of SCF and NCF groups were similar. Mean TIMI frame count and carotid IMT (mm) were significantly higher in the SCF group than controls (45.9 ± 12 vs 23.3 ± 3.7, P = 0.0001; 0.75 ± 0.08 vs 0.69 ± 0.06, P = 0.0001, respectively). Mean TIMI frame count was positively correlated with IMT of carotid artery in correlation analysis (r = 0.45, P = 0.0001). When analyzed in regard to ACE genotype in all subjects, IMT values were statistically different (0.78 ± 0.06 for DD genotype, 0.72 ± 0.05 for ID genotype, and 0.64 ± 0.06 for II genotype, P = 0.0001). This difference remained significant in subgroup analyses for each genotype. No association could be observed between the AT1R A/C1166 polymorphism and IMT of carotid artery measurement (P > 0.05). Lack of association was still observed with analysis carried out when genotype effect was assumed to be inherited as additive (CC versus AA versus AC) or dominant (AA versus AC+CC). Increased IMT in patients with SCF shows that subclinical atherosclerosis may play role in this phenomenon. This increase was most marked in the presence of D allele of ACE genotype, which is associated with vascular hypertrophy. © Springer-Verlag Tokyo 2007. | URI: | https://hdl.handle.net/11499/4381 https://doi.org/10.1007/s00380-006-0925-1 |
ISSN: | 0910-8327 |
Appears in Collections: | PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection Tıp Fakültesi Koleksiyonu WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection |
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