This paper deals with 2 female cases, aged 21 and 17, diagnosed as the Romano-Ward syndrome. They belonged to different families. Both showed autosomal dominant inheritant traits. From their traits one case (Case 1) was suspected as being in the heterozygous state, while the other (Case 2) in the homozygous. The severity in clinical symptoms did not differ from each other. By studying our cases and the literature so far published, the combined use of propranolol, diphenylhydantoin, and phenobarbital was inferred to act effectively for the prevention of arrhythmias seen in the present syndrome.
SUMMARYFour cases of variant angina pectoris with normal findings on coronary arteriogram were experienced.The facts may show that the existence of serious arteriosclerotic lesions in a major branch of coronary artery as pointed out by Prinzmetal is at least not essential for the occurrence of anginal attack in the present disease.But the finding that age and sex distribution of variant angina was nearly the same as that of effort angina seems to still indicate the possibility that arteriosclerotic lesion somehow participates in the mechanism of occurrence of the present disease.
AdditionalIndexing Words: Four case reports Coronary arteriogram Spasm Arteriosclerotic lesion N 1959, Prinzmetal and his coworkers first reported of variant angina. Autopsy findings of their 3 cases all disclosed arteriosclerotic narrowing of over 80% each in a major branch of the coronary arteries. Prinzmetal and others therefore considered that the occurrence of attacks in variant angina was due to a temporary occlusion induced by accelerating the tonus of coronary artery at rest with a marked arteriosclerotic narrowing.1),2) Some recent papers on variant angina pectoris have been found to be based on coronary arteriographic examinations, successively reporting no detection of serious arteriosclerotic narrowing as described by Prinzmetal. The present-day studies have attached importance to the spasm of coronary arteries as a possible etiological role in onset of variant anginal attacks. This article deals with 4 cases of variant angina lacking abnormality on coronary arteriogram, with some speculations on the coronary arteriosclerotic disease as a possible cause on onset of the present disease.
SUMMARYIn view of the apparent contrast in clinical symptoms between the variant form of angina pectoris and conventional effort angina and of tendency towards the decrease of heart rate at the beginning of the former attack, an entirely different mechanism was assumed between these 2 diseases. Based on this assumption, 3 patients with this disease were studied from the viewpoint of catecholamines in blood.As the result, the decrease of catecholamines in blood, especially adrenaline, immediately before and at the beginning of attack, was established.Based on this fact, the mechanism of the development of the attack of the variant form of angina pectoris was explained by the temporary state of obstruction of the large branch of the coronary artery with advanced stenosis due to the increased tonus, following the weakening of the dilation effect of the coronary artery due to decrease of blood adrenaline at rest. The mechanism of development of specific clinical symptoms might be explained too by fluctuations of catecholamines in blood due to stress such as cardiac ischemia or anginal pain.
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