Document Detail


Early sign of atherosclerosis in slow coronary flow and relationship with angiotensin-converting enzyme I/D polymorphism.
MedLine Citation:
PMID:  17285438     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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/C(1166) 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.
Authors:
Halil Tanriverdi; Harun Evrengul; Hatice Mergen; Ceren Acar; Deniz Seleci; Omur Kuru; Seyhan Tanriverdi; Asuman Kaftan
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Publication Detail:
Type:  Comparative Study; Journal Article     Date:  2007-01-26
Journal Detail:
Title:  Heart and vessels     Volume:  22     ISSN:  0910-8327     ISO Abbreviation:  Heart Vessels     Publication Date:  2007 Jan 
Date Detail:
Created Date:  2007-02-07     Completed Date:  2007-10-09     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8511258     Medline TA:  Heart Vessels     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  1-8     Citation Subset:  IM    
Affiliation:
Department of Cardiology, Pamukkale University School of Medicine, Denizli, Turkey. drhaliltanriverdi@yahoo.com.tr
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Alleles
Carotid Artery Diseases / genetics*,  physiopathology*
Coronary Angiography
Coronary Vessels / physiopathology*
Female
Humans
Male
Middle Aged
Peptidyl-Dipeptidase A / genetics*
Polymorphism, Genetic / physiology*
Regional Blood Flow
Renin-Angiotensin System
Tunica Intima / pathology
Tunica Media / pathology
Chemical
Reg. No./Substance:
EC 3.4.15.1/Peptidyl-Dipeptidase A

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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