{'fraction_non_alphanumeric': 0.01639344262295082, 'fraction_numerical': 0.004553734061930784, 'mean_word_length': 5.701219512195122, '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}}
Coronary artery spasm. Mechanisms and clinical relevance.

DURING the first half of this century, studies based on postmortem examinations of the hearts of patients who had experienced angina pectoris and myocardial infarction implicated fixed coronary artery stenoses secondary to arteriosclerosis as the cause of myocardial ischemia. Interest in the causal role of coronary artery spasm was stimulated by Prinzmetal et al1in 1959 who described a group of patients with angina at rest associated with ST-segment elevations. They postulated that this clinical syndrome, which they termed "variant angina," is due to spasm of a large, proximal, coronary artery. Subsequently, coronary arteriography provided unequivocal evidence of coronary artery spasm, thus establishing firmly the validity of the hypothesis by Prinzmetal et al. These important clinical observations were followed by studies on experimental animals that showed that coronary vascular resistance can be influenced notably by stimulation or blockade of the α-adrenergic nerves innervating the coronary vascular bed, indicating that