Abstract Title

Exaggerated Pressor Response to Voluntary Apneas in Patients with a History of Anxiety

RAD Assignment Number

411

Presenter Name

Brandon Griffin

Abstract

Background and Hypothesis: Patients with anxiety disorders tend to have an increased risk of cardiovascular complications including heart failure,cardiovascular mortality, and coronary heart disease. Knowing that an increase in sympathetic activity is detrimental to cardiovascular health this study was conducted to test the hypothesis that anxiety patients would demonstrate increased sympathetic responses to a voluntary apnea, a recognized physiologic stress that simulates the typical stress response.

Methods: Previously, our laboratory has shown that systolic arterial pressure (SAP) changes are a reliable index of sympathetic responses during voluntary apneas. Therefore, we studied the SAP responses to voluntary apneas in 10 patients diagnosed with generalized anxiety disorder and 37 healthy control subjects. Room air voluntary apneas were performed by each subject six times while SAP (Finometer and auscultatory) and heart rate (ECG) responses were measured continuously during each apneic episode. Peak changes in arterial pressure from baseline to end of apnea were quantified.

Results: The pressor responses to voluntary apneas in the anxiety patients exhibited a marked increase in SAP (16.962 ± 8.002, P<0.001), whereas the control group did not show a significant change in SAP (1.730 ± 7.441, P=0.166). Furthermore, when compared to the control subjects, the increase in SAP of the anxiety subjects was also significantly elevated (P<0.01).

Conclusions: These data demonstrate that anxiety subjects have enhanced sympathetic neural activity responses (as measured by the pressor response) to a mild physiologic stressor that does not provoke a response in non-anxious individuals. These data may explain, in part, the increased cardiovascular complications seen is this population, and suggest that the pressor response to apnea may be a simple tool for assessing altered physiologic function and cardiovascular risk in these patient populations.

Research Area

Cardiovascular

Presentation Type

Poster

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Exaggerated Pressor Response to Voluntary Apneas in Patients with a History of Anxiety

Background and Hypothesis: Patients with anxiety disorders tend to have an increased risk of cardiovascular complications including heart failure,cardiovascular mortality, and coronary heart disease. Knowing that an increase in sympathetic activity is detrimental to cardiovascular health this study was conducted to test the hypothesis that anxiety patients would demonstrate increased sympathetic responses to a voluntary apnea, a recognized physiologic stress that simulates the typical stress response.

Methods: Previously, our laboratory has shown that systolic arterial pressure (SAP) changes are a reliable index of sympathetic responses during voluntary apneas. Therefore, we studied the SAP responses to voluntary apneas in 10 patients diagnosed with generalized anxiety disorder and 37 healthy control subjects. Room air voluntary apneas were performed by each subject six times while SAP (Finometer and auscultatory) and heart rate (ECG) responses were measured continuously during each apneic episode. Peak changes in arterial pressure from baseline to end of apnea were quantified.

Results: The pressor responses to voluntary apneas in the anxiety patients exhibited a marked increase in SAP (16.962 ± 8.002, P<0.001), whereas the control group did not show a significant change in SAP (1.730 ± 7.441, P=0.166). Furthermore, when compared to the control subjects, the increase in SAP of the anxiety subjects was also significantly elevated (P<0.01).

Conclusions: These data demonstrate that anxiety subjects have enhanced sympathetic neural activity responses (as measured by the pressor response) to a mild physiologic stressor that does not provoke a response in non-anxious individuals. These data may explain, in part, the increased cardiovascular complications seen is this population, and suggest that the pressor response to apnea may be a simple tool for assessing altered physiologic function and cardiovascular risk in these patient populations.