Resting Sympathetic Nervous System Activity and Transduction in Females with a History of Spontaneous Coronary Artery Dissection Compared to Healthy Females

Introduction: Spontaneous coronary artery dissection (SCAD) is one of the most common causes of myocardial infarction in females under the age of 50 and peripartum females. Furthermore, approximately 10% of patients with a history of SCAD have recurrent SCAD within 5 years. In a subset of patients, SCAD events are preceded by sympathoexcitatory stimuli, such as emotional or physical stress. This implicates the sympathetic nervous system in the pathophysiology of SCAD. Thus, we aimed to investigate this relationship through measuring muscle sympathetic nerve activity (MSNA) and quantifying MSNA transduction into diastolic blood pressure (BP) in females with a history of SCAD compared to healthy female controls. We hypothesized that females with a history of SCAD would have both augmented MSNA and MSNA transduction at rest compared to their healthy counterparts. Methods: Females with a history of SCAD and healthy controls (HC) were recruited for the study. MSNA was continuously recorded using microneurography at the peroneal nerve during 10-minute supine rest. Heart rate (HR, 3-lead electrocardiography) and BP (finger photoplethysmography) were continuously recorded during this period. We plotted binned MSNA burst areas against diastolic BP, using linear regression analysis in MATLAB R2023a to quantify the transduction slope. We compared peak bins of transduction slopes between the two groups. Data are presented as mean±SD. Independent samples t-tests were performed for statistical analyses. Results: Seven females with a history of SCAD (49±11 years; BMI: 28.5±7 kg/m 2 ) and six controls (51±8 years; BMI: 26.2±6.3 kg/m 2 ) participated in the study (both p>0.05). Resting systolic BP (SCAD: 121±8 vs. HC: 122±15 mmHg), diastolic BP (SCAD: 78±9 vs. HC: 75±7 mmHg) and HR (SCAD: 59±13 vs. HC: 67±18 bpm) were not different between groups (all p >0.05). MSNA burst frequency (SCAD: 25±12 vs. HC: 27±7 bursts/minute), burst incidence (SCAD: 42±18 vs. HC: 46±15 bursts/100 heartbeats), and total MSNA (SCAD: 820±286 vs. HC: 1050±119 au/minute) did not differ between groups (all p >0.05). MSNA transduction at rest was not different between females with a history of SCAD and healthy controls (0.02±0.03 vs. 0.05±0.05 mmHg(%·s) -1 , p>0.05). Conclusions: These preliminary data suggest that resting MSNA and transduction do not differ between females with a history of SCAD and healthy controls, contrary to our hypothesis. Further investigation is needed to determine if this observation is preserved with exposure to sympathoexcitatory stimuli. Funding: NIH K23 HL155506, T32 DK07352, K01 HL148144, UL1 TR0022377, and AHA 898649 This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.