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Predictors of Heart Rate Depression During Carotid Artery Stenting in Presumed Low-Risk Patients: A Retrospective
Itamar Gothelf1, Farouq Alguayn2, Galia Karp1,3
1Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva 8410501, Israel.
Insights
Carotid artery stenting (CAS) can cause hemodynamic depression. Lesion proximity to the carotid bifurcation predicts this complication, even in low-risk patients, suggesting a need for tailored management.
Area of Science:
- Cardiovascular Medicine
- Interventional Neurology
- Vascular Surgery
Background:
- Hemodynamic depression (bradycardia, hypotension) is a common carotid artery stenting (CAS) complication, often due to carotid sinus baroreceptor stimulation.
- Prophylactic atropine is used for high-risk patients, but predictors of unexpected hemodynamic depression in low-risk individuals are not well-defined.
Purpose of the Study:
- To identify clinical, anatomical, and procedural predictors of hemodynamic depression during CAS in patients not receiving prophylactic atropine.
Main Methods:
- Retrospective, single-center observational study of 125 patients undergoing CAS without prophylactic atropine.
- Hemodynamic depression defined as >20% heart rate reduction; bradycardia (<50 bpm) and hypotension (>40% SBP reduction) also recorded.
- Multivariable analysis to identify independent predictors.
Main Results:
- Nearly half (49.6%) of included patients experienced significant heart rate reduction during CAS.
- Shorter lesion distance to the carotid bifurcation was independently associated with hemodynamic depression (OR 0.90 per mm; p=0.023).
- Greater intraprocedural blood pressure reductions also correlated with heart rate depression; traditional risk factors were not predictive.
Conclusions:
- Hemodynamic depression is frequent during CAS, even in low-risk patients.
- Lesion proximity to the carotid bifurcation is a key anatomical predictor of autonomic instability.
- This finding underscores limitations of standard risk stratification and supports a lesion-specific approach to hemodynamic management.
Abstract:
Background: Hemodynamic depression, characterized by bradycardia and hypotension, is a common complication of carotid artery stenting (CAS) and is primarily attributed to carotid sinus baroreceptor stimulation. While prophylactic atropine is often used in high-risk patients, predictors of unexpected hemodynamic depression among patients initially deemed low-risk remain incompletely defined. Objective: To identify clinical, anatomical, and procedural predictors of hemodynamic depression in patients undergoing CAS without prophylactic atropine. Methods: We performed a retrospective, single-center observational study of consecutive patients undergoing CAS between January 2015 and May 2024. Patients who received prophylactic atropine for low baseline heart rate (HR) were excluded. Hemodynamic depression was defined as a >20% reduction in HR from baseline. Absolute bradycardia (HR <50 bpm) and hypotension (>40% reduction in systolic blood pressure) were recorded descriptively. Results: A total of 158 patients underwent CAS, of whom 33 (20.9%) were excluded due to prophylactic atropine administration for low pre-procedural heart rates (<60 bpm). Among 125 included patients, 62 (49.6%) experienced significant HR reduction during CAS. In multivariable analysis, a shorter distance between the stenotic lesion and the carotid bifurcation was independently associated with hemodynamic depression (OR 0.90 per mm increase; 95% CI 0.82-0.99; p = 0.023). Greater intraprocedural reductions in systolic and mean arterial pressure were also associated with HR depression. Traditional clinical risk factors, including age, sex, comorbidities, degree of stenosis, calcification severity, anesthesia type, and procedure urgency, were not independently predictive. Conclusions: Hemodynamic depression remains frequent during CAS even among patients classified as low risk. Lesion proximity to the carotid bifurcation is a key anatomical predictor of autonomic instability, highlighting the limitations of standard risk stratification and supporting a lesion-specific approach to periprocedural hemodynamic management.
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