OBJECTIVE: The sympathetic nervous system is a key modulator of prognosis and outcome in cardiac ischaemia and infarction. The effects of acute cardiac ischaemia on sympathetic neural traffic in humans are unknown. We tested the hypothesis that angioplasty, and associated transient myocardial ischaemia, elicits changes in neural circulatory control, including direct intraneural measures of sympathetic traffic. METHODS: We measured muscle sympathetic nerve activity (MSNA), blood pressure and heart rate in 12 patients (11 men, one woman) undergoing clinically indicated elective coronary angioplasty of the left anterior descending (n = 7) or circumflex (n = 5) coronary artery. Baseline data were obtained for 2 min before occlusion. Each balloon inflation was designed to last up to 120 s. RESULTS: Coronary occlusion had no significant effect on blood pressure or heart rate. In contrast, occlusion resulted in a significant increase in MSNA, in 10 of the 12 patients, and in all seven of those patients undergoing angioplasty of the left anterior descending artery. The group mean increase in MSNA during occlusion was 36 ± 11% (P = 0.008 versus preocclusion). MSNA increased within 60 s of occlusion (129 ± 12% of baseline; n = 12; P = 0.04), and increased further during the next 60 s to 141 ± 12% of baseline levels (n = 10; P < 0.001). Increases in MSNA were similar in patients with and without significant chest pain (39 ± 9% versus 34 ± 13%, respectively; P = 0.84). CONCLUSION: Acute coronary occlusion during angioplasty increases central sympathetic outflow, but there is no systematic change in heart rate. The increase in sympathetic nerve traffic cannot be explained by blood pressure changes or occlusion-related chest pain.
- Coronary artery disease
- Nervous system
ASJC Scopus subject areas
- Internal Medicine
- Cardiology and Cardiovascular Medicine