Early sign of atherosclerosis in slow coronary flo

Authors: Halil Tanriverdi Harun Evrengul Hatice Mergen Ceren Acar Deniz Seleci Omur Kuru Seyhan Tanriverdi Asuman Kaftan

Publish Date: 2007/01/26

Volume: 22, Issue: 1, Pages: 1-8

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Abstract

Increase in carotid artery intimamedia 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 reninangiotensin gene system on carotid IMT Fortyfour 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 Intimamedia thickness was measured by recording ultrasonographic images of both the left and right common carotid artery with a 12MHz 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 459 ± 12 vs 233 ± 37 P = 00001 075 ± 008 vs 069 ± 006 P = 00001 respectively Mean TIMI frame count was positively correlated with IMT of carotid artery in correlation analysis r = 045 P = 00001 When analyzed in regard to ACE genotype in all subjects IMT values were statistically different 078 ± 006 for DD genotype 072 ± 005 for ID genotype and 064 ± 006 for II genotype P = 00001 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 005 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

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