Suppression of exercise-induced angina by magnesium sulfate in patients with variant angina.
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In 19 patients with variant angina, handgrip test as an isometric exercise was performed in 3 conditions on different successive days in the early morning: in the control, after administration of phentolamine (0.3 mg/kg) and after administration of atropine sulfate (0.04 mg/kg). Angina associated with ST-segment elevation on the electrocardiogram was induced in 5 patients (26%) in the control condition, in 14 (74%) after phentolamine and in 5 of 16 (31%) after atropine. All anginal events but 1 occurred after the cessation of the exercise and were not associated with the significant increase of rate-pressure products. These attacks were considered to be due to coronary spasm. The frequency of the induction of angina was significantly higher after phentolamine than in the other 2 conditions (p less than 0.01). It is concluded that the attack can be induced by the handgrip exercise in a sizable number of patients with variant angina, and that the administration of phentolamine increases the incidence of angina induced by handgrip exercise. The mechanism or mechanisms by which coronary spasm is induced by handgrip exercise remains to be elucidated.
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Platelet aggregation was studied in patients with angina pectoris in whom coronary sclerosis was found by arteriography. The subjects consisted of 20 patients with stable angina pectoris, 12 with unstable angina pectoris and 4 with variant form of angina pectoris. Fifteen healthy subjects served as controls. ADP- and collagen-induced platelet aggregations were estimated during resting conditions before and immediately after an exercise test. In patients with unstable angina pectoris, ADP-induced as well as collagen-induced platelet aggregations during resting conditions were significantly less than those in normal subjects. After exercise, however, they significantly increased. In stable angina pectoris, they did not differ from those in the control group and their responses to exercise were also not significant. In general, platelet aggregation during resting conditions was accelerated in relation to an increase in the number of coronary arteries involved. The results demonstrate that examination of platelet aggregation during resting conditions and following exercise aids in a more accurate evaluation of the types and the stages of patients with angina pectoris.
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Thyrotoxicosis may exacerbate angina pectoris in patients with coronary artery disease but angina also occurs in thyrotoxic patients with normal coronary arteries. Four female severely thyrotoxic patients presented with apparent angina pectoris as a manifestation of their thyrotoxicosis. Two of them had transiently abnormal ECGs during pain. Treatment for thyrotoxicosis immediately stopped the chest pain, which did not recur. All patients had negative exercise ECGs, and one had a normal coronary angiogram. The possible mechanisms to explain this phenomenon are discussed. Coronary artery spasm has been demonstrated in thyrotoxic patients previously and may explain the features in these patients. An alternative hypothesis is that myocardial metabolism is fundamentally changed by thyrotoxicosis. We would recommend that thyroid function assessment should be considered in young female patients with atypical angina.
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