Abstract

SummaryBackgroundWe examined the effects of ACE, PAI-1 and eNOS gene polymorphisms on endothelial function. The genes are related to atherosclerosis and endothelial dysfunction in coronary slow flow (CSF).MethodsThirty-three patients with angiographically proven CSF and 48 subjects with normal coronary flow were enrolled in this study. Coronary flow patterns were determined by the thrombolysis in myocardial infarction (TIMI) frame count method. Endothelial function was assessed in the brachial artery by endothelium-dependent flow-mediated dilatation (FMD). PAI-1 4G/5G, eNOS T-786C and ACE I/D polymorphisms were determined by polymerase chain reaction (PCR) amplification.ResultsNo difference was found between the groups regarding age, heart rate and blood pressure. Males were more prevalent among patients with CSF than control subjects (58.8 vs 29.8%, p = 0.009). Mean TIMI frame counts were significantly higher in CSF patients (24.2 ± 4.0 vs 13.1 ± 2.5 fpm, p = 0.001). FMD was significantly lower in CSF patients than in the controls (4.9 ± 6.6 vs 7.9 ± 5.6%, p = 0.029). TIMI frame count and FMD were found to be negatively correlated in a correlation analysis (r = –0.269, p = 0.015). PAI-1 4G/5G, eNOS T-786C and ACE I/D polymorphisms were similar in the two groups.ConclusionsThis study showed that endothelial function was impaired in patients with CSF. PAI-1, ACE and eNOS polymorphisms were not related to CSF in our study population.

Highlights

  • We examined the effects of angiotensin converting enzyme (ACE), plasminogen activator inhibitor 1 (PAI-1) and endothelial Nitric oxide (NO) synthase (eNOS) gene polymorphisms on endothelial function

  • flow-mediated dilatation (FMD) was significantly lower in coronary slow flow (CSF) patients than controls (4.9 ± 6.6 vs 7.9 ± 5.6%, p = 0.029)

  • This study showed that ACE, PAI and eNOS gene polymorphisms were not related to CSF in our population

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Summary

Introduction

We examined the effects of ACE, PAI-1 and eNOS gene polymorphisms on endothelial function. The genes are related to atherosclerosis and endothelial dysfunction in coronary slow flow (CSF). Methods: Thirty-three patients with angiographically proven CSF and 48 subjects with normal coronary flow were enrolled in this study. Coronary flow patterns were determined by the thrombolysis in myocardial infarction (TIMI) frame count method. PAI-1 4G/5G, eNOS T-786C and ACE I/D polymorphisms were determined by polymerase chain reaction (PCR) amplification. Mean TIMI frame counts were significantly higher in CSF patients (24.2 ± 4.0 vs 13.1 ± 2.5 fpm, p = 0.001). PAI-1 4G/5G, eNOS T-786C and ACE I/D polymorphisms were similar in the two groups. PAI-1, ACE and eNOS polymorphisms were not related to CSF in our study population

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