Please use this identifier to cite or link to this item: 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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