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Cerebral hemodynamics in carotid sinus syndrome and atrioventricular block
G Lefthériotis1, J M Dupuis, J Victor
1Department of Cardiology, Medical School and Teaching Hospital of Angers, France. explovasc@chu-angers.fr
Insights
Carotid sinus syndrome (CSS) impairs cerebral blood flow regulation during syncope. Patients with CSS show reduced cerebral autoregulation compared to those with atrioventricular block (AVB), indicating altered hemodynamic responses.
Area of Science:
- Neurology
- Cardiology
- Physiology
Background:
- Carotid sinus syndrome (CSS) causes syncope via exaggerated baroreceptor reflexes.
- Understanding cerebral hemodynamic regulation in CSS is crucial for managing syncope.
Purpose of the Study:
- To compare cerebral hemodynamics and regulation in CSS patients versus those with atrioventricular block (AVB).
- To investigate alterations in cerebrovascular resistance and dynamic cerebral autoregulation during induced cardioinhibition or asystole.
Main Methods:
- Translingual Doppler sonography and Finapres were used to record cerebral blood flow velocity and mean arterial blood pressure.
- Carotid massage (CSS) and temporary pacemaker inhibition (AVB) induced transient hemodynamic challenges.
- Cerebrovascular resistance, rate of regulation, and autoregulatory index were calculated.
Main Results:
- Both CSS and AVB groups experienced decreased arterial pressure and cerebral flow velocity.
- CSS patients exhibited a lower rate of regulation and autoregulatory index compared to AVB patients.
- Cerebral hypoperfusion in CSS was compensated by autoregulation, but with a slower response.
Conclusions:
- Cerebral autoregulation is less efficient in CSS patients during syncope-inducing events.
- Persistent peripheral vasodepression from carotid massage may explain the reduced autoregulatory response in CSS.
- These findings highlight distinct cerebral hemodynamic regulatory mechanisms in different syncope etiologies.
Abstract:
Carotid sinus syndrome (CSS) is a cause of syncope due to exaggerated baroreceptor-mediated cardioinhibitory/vasodepressive reflexes. We sought to determine if cerebral hemodynamics and regulation were specifically altered in these patients by comparison with pure asystole without vasodepression in patients with atrioventricular block (AVB). Mean blood flow velocity (transcranial Doppler sonography) and mean arterial blood pressure (Finapres) were recorded during cardioinhibition induced by carotid massage in patients with CSS (n = 14, 75 +/- SD 8 years) and asystole induced by temporary pacemaker inhibition in patients with complete AVB (n = 10, 69 +/- 11 years). Cerebrovascular resistance was estimated by the arterial pressure/cerebral flow velocity ratio, and dynamic cerebral autoregulatory responses were determined by the rate of regulation and autoregulatory index. Asystole and cardioinhibition each induced a decrease in arterial pressure (CSS 55 +/- 9% vs AVB 40 +/- 14%, p <0.05) and cerebral flow velocity (CSS 66 +/- 19% vs AVB 69 +/- 14%, p = NS), with an initial transient increase in cerebrovascular resistance (CSS 102 +/- 136% vs AVB 128 +/- 92%, p = NS) followed by a decrease (CSS 38 +/- 12%, AVB 29 +/- 13%, p = NS). The rate of regulation and autoregulatory index were higher with AVB (0.43 +/- 0.20 and 8.5 +/- 1.1 second(-1)) than CSS (0.20 +/- 0.12 and 4.8 +/- 1.3 second(-1), respectively, p <0.01 and p <0.001 vs AVB). During asystole and vasodepression, cerebral hypoperfusion in CSS is normally compensated for by cerebral autoregulation. The lower rate of regulation in CSS compared with AVB likely results from persistent peripheral vasodepression triggered by carotid massage.