Key result
TNF-α blockade linked to ~42% lower MSNA and reduced systolic BP in ankylosing spondylitis.
Why the study?
Inflammatory diseases are associated with elevated cardiovascular risk, and heightened muscle sympathetic nerve activity is a potential contributor.
Does TNF-α blockade therapy reduce muscle sympathetic nerve activity and blood pressure in patients with ankylosing spondylitis?
Case Report (n=2)
Does TNF-α blockade therapy reduce muscle sympathetic nerve activity and blood pressure in patients with ankylosing spondylitis?
TNF-α blockade may attenuate heightened sympathetic activity and lower cardiovascular risk in patients with ankylosing spondylitis.
Answers are grounded in this paper and cite their sources.
MSNA in AS may link inflammation to CV risk; leaves open TNF-α blockade effects on sympathetic activity.
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 TNF-α blockade therapy. Two males diagnosed with AS (Case 1: 34 years, 26kg/m 2 ; Case 2: 22 years, 31kg/m 2 ) participated. In Case 1, 10-minutes of continuous beat-to-beat blood pressure, heart rate (HR), and MSNA were recorded on two occasions 3-months apart. Case 2 similarly underwent 10-minutes of autonomic monitoring before and after 6-months of routine-care TNF-α blockade. In Case 1, systolic (SBP: 120 vs. 121 mmHg) and diastolic (DBP: 64 vs. 70 mmHg) blood pressure, HR (58 vs. 59 beats/min), and MSNA (32 vs. 37 bursts/min) were similar across the two visits, suggesting reliable MSNA in our AS patient. Case 2 also demonstrated higher-than-expected resting MSNA (45 bursts/min) when considering age and BMI, 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. While caution is necessary given the case study approach, future work examining neural cardiovascular control in AS patients appears warranted.
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Murvich et al. (2026) conducted a case report in Ankylosing spondylitis (n=2). TNF-α blockade vs. Baseline (pre-treatment) was evaluated on Muscle sympathetic nerve activity (MSNA). In a patient with ankylosing spondylitis, 6 months of TNF-α blockade therapy reduced muscle sympathetic nerve activity from 45 to 26 bursts/min and lowered systolic blood pressure from 146 to 124 mmHg.
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