Direct evidence of sympathetic hyperactivity in patients with vasospastic angina

The autonomic nervous system is reported to be involved in the pathogenesis of vasospastic angina (VSA). Studies based on heart rate variability analysis have shown conflicting results with both a reduction and an enhancement of sympathetic nervous system (SNS) activity in patients with Prinzmetal's variant angina, but direct assessment has never been performed. The aim of our study was to evaluate the SNS activity using microneurography in patients with VSA.

The SNS was evaluated by measuring the muscle sympathetic nerve activity (MSNA) with microneurography in 15 patients with VSA confirmed by positive ergonovine provocation test and 15 controls subjects negative for the provocation test. Over the baseline period, SNS activity was higher in patients with VSA compared with control patients (56.8 ± 5 vs. 49.3 ± 6.3 burst/min, p < 0.001, respectively). During mental stress, SNS activity increased significantly only in patients with VSA, which still presented a higher SNS activity than control patients (66.1 ± 7.2 vs. 53.6 ± 8.7 burst/min; p < 0.001, respectively). Furthermore only VSA patients showed significant hemodynamic modifications with an increase in mean arterial blood pressure (96.2 ± 13.4 vs. 86.6 ± 9.6 mmHg in VSA patients and control subjects, respectively; p < 0.05).

Our results provide the first direct evidence of lasting increased sympathetic activity that is worsened by mental stress in patients with VSA. These results suggest that SNS participate to the pathogenesis of VSA by enhancing coronary vascular tone.