{'fraction_non_alphanumeric': 0.014828544949026877, 'fraction_numerical': 0.0037071362372567192, 'mean_word_length': 5.789308176100629, '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}}
Noninvasive evaluation of endothelial function.

Endothelial dysfunction is generally believed to be the inciting event in atherosclerosis, and is probably important in ischemic manifestations as well. The release of endothelium-derived vasoactive substances is not only triggered by acetylcholine, but also controlled by a host of neuromediators and by shear forces exerted by the blood flowing through the blood vessel. However, this balance is altered in disease states such as atherosclerosis, diabetes, chronic heart failure, coronary artery disease, or hypertension. The most important mechanism in the decrease in endothelium-dependent relaxation appears to be a reduced release of nitric oxide. In healthy people, the predominant effect of stimulation of the endothelium is vasodilation. It is tempting to hypothesize that endothelial dysfunction is one of the initial steps involved in the development of atherosclerosis, but also in peripheral artery atherosclerosis. Impairment of endothelium-dependent vasodilation in the coronary arteries has been demonstrated not only in patients with documented atherosclerosis and/or established cardiovascular risk factors. Noninvasive evaluation of brachial artery vasoactivity using high resolution B-mode ultrasound is currently being established to evaluate endothelial function. We studied the endothelial function in 50 normal volunteers, 28 hypertensive subjects, and 31 hypercholesterolemia subjects. The diameter of the target artery was measured from two-dimensional ultrasound images with 10 MHz linear transducer. The results suggested that antihypertensive therapy with a certain calcium antagonist did not have a favorable effect on endothelial function and after cessation of cholesterol lowering therapy, the endothelial dysfunction developed again. The endothelial function can now be readily measured in humans and is very useful research tool to assess the effect of risk factors and their treatment on vascular function. Endothelial function testing will assume a prominent role in the evaluation and treatment of patients at risk of developing coronary atherosclerosis and its sequelae.