{'fraction_non_alphanumeric': 0.052107728337236536, 'fraction_numerical': 0.0351288056206089, 'mean_word_length': 5.103571428571429, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Carotid-femoral pulse wave velocity in patients with isolated coronary artery ectasia: an observational study.

OBJECTIVE
Carotid-femoral pulse wave velocity (PWV), the current "gold-standard" measure of arterial stiffness, has emerged as an important independent predictor of cardiovascular events. The increased PWV is recognized as an indicator of atherosclerosis. The relationship between isolated coronary artery ectasia (CAE) and carotid-femoral PWV has not been well-described. The aim of our study was to assess this relation.


METHODS
Thirty-four patients with isolated CAE without any visible coronary stenosis and 24 control subjects with angiographically normal coronary arteries were enrolled to this cross-sectional observational study. Applanation tonometry was applied to assess the carotid-femoral PWV. Statistical analyses were performed by Mann-Whitney U and Chi-square tests. Multiple linear regression analysis was used for the evaluation of the relations of parameters.


RESULTS
The baseline clinical and laboratory parameters of the both groups were similar. Patients with isolated CAE had significantly higher carotid-femoral PWV compared to control subjects (10.5±2.4 vs 9.2±1.7 m/s, p=0.02). In multiple regression analysis, age (beta=0.23, 95% CI=0.001-0.094, p=0.04), number of ectatic vessels (beta=0.24, 95% CI=0.044-1.07, p=0.03), and systolic blood pressure (beta=0.52, 95% CI=0.028-0.1, p=0.001) were found independently related to PWV.


CONCLUSION
We have shown an association between increased carotid-femoral PWV and isolated CAE, suggesting that atherosclerosis may be involved in the pathogenesis of isolated CAE without any coronary stenosis in the adult population.