Ankylosing spondylitis and muscle sympathetic nerve activity: a case study.

Inflammatory diseases are associated with elevated cardiovascular (CV) risk, and heightened muscle sympathetic nerve activity (MSNA) is a potential contributor. This case study characterized MSNA in two patients with ankylosing spondylitis (AS) and evaluated the effect of tumor necrosis factor-α (TNF-α) blockade therapy. Two males diagnosed with AS (case 1: 34 yr, 26 kg/m2; case 2: 22 yr, 31 kg/m2) participated. In case 1, 10-min of continuous beat-to-beat blood pressure, heart rate (HR), and MSNA were recorded on two occasions 3-mo apart. Case 2 similarly underwent 10-min of autonomic monitoring before and after 6-mo of routine-care TNF-α blockade. In case 1, systolic blood pressure (SBP: 120 vs. 121 mmHg) and diastolic blood pressure (DBP: 64 vs. 70 mmHg), HR (58 vs. 59 beats/min), and MSNA (32 vs. 37 bursts/min) were similar across the two visits, suggesting reliable MSNA in our patient with AS. Case 2 also demonstrated higher-than-expected resting MSNA (45 bursts/min) when considering age and body mass index, and further demonstrated marked reductions in SBP (146 vs. 124 mmHg), DBP (84 vs. 70 mmHg), HR (76 vs. 69 beats/min), and MSNA (45 vs. 26 bursts/min) following 6-mo of TNF-α blockade. The present case study indicates that heightened sympathetic activity is a potential physiological mechanism contributing to increased CV disease in populations with AS. Furthermore, suppression of inflammation or symptom amelioration may help attenuate the increased sympathetic activity and potentially lower cardiovascular risk over time within this unique rheumatic population. Although caution is necessary given the case study approach, future work examining neural cardiovascular control in patients with AS appears warranted.NEW & NOTEWORTHY Ankylosing spondylitis (AS) is associated with cardiovascular risk, but the role of sympathetic hyperactivity in this association remains uncharacterized. This case study demonstrated that 1) muscle sympathetic nerve activity was elevated in two individuals with AS and 2) routine clinical care with TNF-α blockade in one participant substantially reduced resting sympathetic outflow. These findings offer preliminary evidence and rationale for future work on the role of inflammation, sympathetic hyperactivity, and cardiovascular risk in AS.