ArticleTanaka N, Tanaka H, Toyama Y, Kashima T, Niimura T.
Am Heart J. 1975 Sep;90(3):369-75.
Three patients with aortitis syndrome ehibited paroxysmal hypertension which seemed to result from baroreceptor dysfunction. All of the patients had signs of active inflammation of aortitis syndrome and stenotic carotid and subclavian arteries. During the attacks, the blood pressure rose to at least 230 mm. Hg systolic and the heart rate exceeded 100. However, with prolonged administration of steroid hormones, the attacks ceased. In two patients with dilated thoracic aortas and aortic regurgitation, the attacks of paroxysmal hypertension occurred without apparent precipitating factors and were followed by anginal pain with marked ST depression. The sympathicotonic state resulting from the disturbance of the baroreceptors was considered to be responsible for the attacks. In another patient, the attacks occurred in the course of treatment with a steroid hormone and were provoked only by voluntary micturition. This post-micturition hypertension was presumed to be an expression of abnormal overshooting following a fall in blood pressure after voiding.