Why the study?
Does autonomic nervous system activity differ in patients with vasospastic angina compared to controls, and does pilocarpine induce anginal attacks associated with these changes?
Does autonomic nervous system activity differ in patients with vasospastic angina compared to controls, and does pilocarpine induce anginal attacks associated with these changes?
The study demonstrates that increased sympathetic nervous system activity and responsiveness, potentially on the basis of parasympathetic hyperactivity, contribute to the development of vasospastic angina.
Answers are grounded in this paper and cite their sources.
May implicate autonomic imbalance in vasospastic angina; hypothesis-generating and should not yet change practice.
To evaluate the role of the autonomic nervous system in vasospastic angina, plasma catecholamine and cyclic nucleotide levels were measured and the pilocarpine test was performed in 19 patients with vasospastic angina, 14 patients with nonvasospastic angina and 7 control subjects who were hospitalized patients without heart disease. Diurnal and nocturnal levels of plasma catecholamines were significantly higher in patients with angina pectoris, especially in patients with vasospastic angina, as compared with those of controls. In addition, an increase in plasma catecholamines preceded the onset of spontaneous and pilocarpine induced anginal attacks associated with significant increases in plasma catecholamines in patients with vasospastic angina. On the other hand, while nifedipine significantly suppressed both spontaneous and pilocarpine induced anginal attacks, the increase in plasma catecholamines remained. These results indicate that increased activity and responsiveness of the sympathetic nervous system may possibly contribute to the development of vasospastic angina on the basis of parasympathetic hyperactivity.
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TAMADA et al. (1985) studied this question.
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