Abstract

BACKGROUND: The clinical features of vasospastic angina are well known, but pathogenesis remains a subject of discussion. Changes in the autonomic regulation of coronary artery tone and endothelial function that contribute to the development of vasospasm are not well understood. The data on the subject from the published studies are contradictory.
 AIM: To evaluate features of endothelial function and autonomic regulation of heart rhythm in patients with vasospastic angina.
 MATERIALS AND METHODS: The study included 16 patients with proven vasospastic angina. All the patients have been evaluated for the heart rate variability at rest and vegetative tests (deep breathing, and active standing tests). Endothelial function has been assessed in terms of reactive hyperemia index by peripheral arterial tonometry using an Endo-PAT 2000 device.
 RESULTS: The baseline of the total heart rate variability was borderline with the normal parameters SDNN 50 (32.5; 50) ms in the patients with vasospastic angina. There were 14 patients who have demonstrated an imbalance of the autonomic nervous system at rest, mainly due to an increase of parasympathetic influences. The appropriate reaction of the autonomic nervous system, characterized by an increase of vagal influences, has been determined in 13 patients in the deep-breathing test. A paradoxical reaction, characterized by an increase of vagal influences on the heart rhythm, has been registered in 13 patients in the active standing tests. Endothelial dysfunction has been observed in half of the studied patients. Furthermore, a combination of both pathophysiological mechanisms, i.e., endothelial and autonomic dysfunctions have been observed in all the patients with a reduced reactive hyperemia index.
 CONCLUSIONS: According to the results of our study, the parasympathetic influences of the autonomic nervous system on the heart rhythm were predominant in the patients with vasospastic angina, which is not typical for coronary heart disease. All the patients had autonomic or endothelial dysfunction. A combination of both pathophysiological mechanisms has been observed in half of the examined patients.

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