Author + information
- Received January 19, 2016
- Revision received February 16, 2016
- Accepted February 25, 2016
- Published online December 1, 2016.
- Oana Dickinson, MDa,
- Baris Akdemir, MDa,
- Venkata Krishna Puppala, MDa,
- Balaji Krishnan, MDa,
- Barry L.S. Detloff, BSa,
- Scott Sakaguchi, MDa,
- Wayne O. Adkisson, MDa and
- David G. Benditt, MDa,b,∗ ()
- aDepartment of Medicine, Cardiovascular Division, Cardiac Arrhythmia and Syncope Center, University of Minnesota Medical School, Minneapolis, Minnesota
- bCentracare Heart and Vascular Center, St. Cloud, Minnesota
- ↵∗Reprint requests and correspondence:
Dr. David G. Benditt, Cardiac Arrhythmia Center, Department of Medicine, University of Minnesota Medical School, 420 Delaware Street, SE, MMC 508, Minneapolis, Minnesota 55455.
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.
This work was supported in part by a grant from the Dr. Earl E. Bakken Family in support of Heart-Brain research. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received January 19, 2016.
- Revision received February 16, 2016.
- Accepted February 25, 2016.
- American College of Cardiology Foundation