Oana Dickinson1, Baris Akdemir1, Venkata Krishna Puppala1, Balaji Krishnan1, Barry L S Detloff1, Scott Sakaguchi1, Wayne O Adkisson1, David G Benditt2. 1. Department of Medicine, Cardiovascular Division, Cardiac Arrhythmia and Syncope Center, University of Minnesota Medical School, Minneapolis, Minnesota. 2. Department of Medicine, Cardiovascular Division, Cardiac Arrhythmia and Syncope Center, University of Minnesota Medical School, Minneapolis, Minnesota; Centracare Heart and Vascular Center, St. Cloud, Minnesota. Electronic address: Bendi001@umn.edu.
Abstract
OBJECTIVES: This study compared hemodynamic and chronotropic responses to cough in cough syncope (CS) patients to those in control subjects. BACKGROUND: Cough syncope is an uncommon form of situational fainting variously attributed to both reflex and mechanical causes. We hypothesized that if baroreflex responses contribute to CS, post-cough hypotension should be associated with cardioinhibition comparable to that observed in other reflex faints. METHODS: The study population consisted of 8 CS patients (group 1), 21 patients with vasovagal syncope (group 2), and 6 patients with nonvertiginous "lightheadedness" (group 3). Testing with patients seated included volitional coughing that achieved a transient blood pressure (BP) of ≥200 mm Hg. Beat-to-beat blood pressure (systolic blood pressure [SBP]) before cough, minimum cough-induced SBP and heart rate (HR) (beats/min) after cough, and HR change during cough-induced hypotension were recorded, along with SBP recovery time from SBP nadir after cough. RESULTS: Compared to controls, cough-induced SBP drop was greater in CS patients (CS patients: -48 ± 13.1 mm Hg vs. -29 ± 11.2 mm Hg for group 2 controls; p = 0.005; or -25 ± 10 mm Hg in group 3 controls; p = 0.02), and recovery time was longer (CS: 46 ± 19 s vs. 11 ± 3.6 s in group 1 controls; p = 0.002; or 12 ± 5 s in group 3 controls; p = 0.01). Furthermore, despite greater induced hypotension, post-cough chronotropic response was less in CS patients (+15% above baseline rate) than in either group 2 (+31% above baseline rate; p < 0.001) or group 3 (+28%; p = 0.01) controls. CONCLUSIONS: In CS patients, post-cough chronotropic response is blunted compared to that in controls despite greater cough-induced hypotension favoring baroreflex cardioinhibition contribution to the pathophysiology of cough syncope.
OBJECTIVES: This study compared hemodynamic and chronotropic responses to cough in cough syncope (CS) patients to those in control subjects. BACKGROUND:Cough syncope is an uncommon form of situational fainting variously attributed to both reflex and mechanical causes. We hypothesized that if baroreflex responses contribute to CS, post-cough hypotension should be associated with cardioinhibition comparable to that observed in other reflex faints. METHODS: The study population consisted of 8 CS patients (group 1), 21 patients with vasovagal syncope (group 2), and 6 patients with nonvertiginous "lightheadedness" (group 3). Testing with patients seated included volitional coughing that achieved a transient blood pressure (BP) of ≥200 mm Hg. Beat-to-beat blood pressure (systolic blood pressure [SBP]) before cough, minimum cough-induced SBP and heart rate (HR) (beats/min) after cough, and HR change during cough-induced hypotension were recorded, along with SBP recovery time from SBP nadir after cough. RESULTS: Compared to controls, cough-induced SBP drop was greater in CS patients (CS patients: -48 ± 13.1 mm Hg vs. -29 ± 11.2 mm Hg for group 2 controls; p = 0.005; or -25 ± 10 mm Hg in group 3 controls; p = 0.02), and recovery time was longer (CS: 46 ± 19 s vs. 11 ± 3.6 s in group 1 controls; p = 0.002; or 12 ± 5 s in group 3 controls; p = 0.01). Furthermore, despite greater induced hypotension, post-cough chronotropic response was less in CS patients (+15% above baseline rate) than in either group 2 (+31% above baseline rate; p < 0.001) or group 3 (+28%; p = 0.01) controls. CONCLUSIONS: In CS patients, post-cough chronotropic response is blunted compared to that in controls despite greater cough-induced hypotension favoring baroreflex cardioinhibition contribution to the pathophysiology of cough syncope.