Sympathetic and cardiac baroreflex function in panic disorder

Lambert, Elisabeth; Thompson, Jocelyn S.; Schlaich, Markus P.; Laude, Dominique; Elghozi, Jean‐Luc; Esler, Murray; Lambert, Gavin

doi:10.1097/00004872-200212000-00025

Cited by 57 publications

(36 citation statements)

References 48 publications

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“…However, the mechanism for the reduced blood-pressure reactivity to mental stress was not explored. Individuals with panic disorder have elevated anxiety levels and are reported to be at an increased risk for cardiovascular complications, but Lambert et al (15) found that patients with panic disorder have improved sympathetic BRS. This provided mechanistic insight for reduced blood-pressure responses to stress in individuals with high trait anxiety and raises the possibility that improved baroreflex function can result from chronic stress.…”

Section: Discussionmentioning

confidence: 99%

Attenuation of sympathetic baroreflex sensitivity during the onset of acute mental stress in humans

Durocher

Klein

Carter

2011

American Journal of Physiology-Heart and Circulatory Physiology

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Durocher JJ, Klein JC, Carter JR. Attenuation of sympathetic baroreflex sensitivity during the onset of acute mental stress in humans. Am J Physiol Heart Circ Physiol 300: H1788-H1793, 2011. First published February 25, 2011 doi:10.1152/ajpheart.00942.2010.-Mental stress consistently induces a pressor response that is often accompanied by a paradoxical increase of muscle sympathetic nerve activity (MSNA). The purpose of the present study was to evaluate sympathetic baroreflex sensitivity (BRS) by examining the relations between spontaneous fluctuations of diastolic arterial pressure (DAP) and MSNA. We hypothesized that sympathetic BRS would be attenuated during mental stress. DAP and MSNA were recorded during 5 min of supine baseline, 5 min of mental stress, and 5 min of recovery in 32 young healthy adults. Burst incidence and area were determined for each cardiac cycle and placed into 3-mmHg DAP bins; the slopes between DAP and MSNA provided an index of sympathetic BRS. Correlations between DAP and MSNA were strong (Ͼ0.5) during baseline in 31 of 32 subjects, but we evaluated the change in slope only for those subjects maintaining a strong correlation during mental stress (16 subjects). During baseline, the relation between DAP and MSNA was negative when expressed as either burst incidence [slope ϭ Ϫ1.95 Ϯ 0.18 bursts·(100 beats) Ϫ1 ·mmHg Ϫ1 ; r ϭ Ϫ0.86 Ϯ 0.03] or total MSNA [slope ϭ Ϫ438 Ϯ 91 units·(beat) Ϫ1 mmHg Ϫ1

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Section: Discussionmentioning

confidence: 99%

Attenuation of sympathetic baroreflex sensitivity during the onset of acute mental stress in humans

Durocher

Klein

Carter

2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…12 Muscle sympathetic bursts were advanced by 1.3 seconds to compensate for baroreflex delay. The sensitivity or reflex gain was defined as the slope of the regression line.…”

Section: Assessment Of Spontaneous Arterial Baroreflex Control Of Msnamentioning

confidence: 99%

Sympathetic Augmentation in Hypertension

et al. 2004

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Abstract-There is growing evidence that essential hypertension is commonly neurogenic and is initiated and sustained by sympathetic nervous system overactivity. Potential mechanisms include increased central sympathetic outflow, altered norepinephrine (NE) neuronal reuptake, diminished arterial baroreflex dampening of sympathetic nerve traffic, and sympathetic neuromodulation by angiotensin II. To address this issue, we used microneurography and radiotracer dilution methodology to measure regional sympathetic activity in 22 hypertensive patients and 11 normotensive control subjects. The NE transport inhibitor desipramine was infused to directly assess the potential role of impaired neuronal NE reuptake. To evaluate possible angiotensin sympathetic neuromodulation, the relation of arterial and coronary sinus plasma concentrations of angiotensin II to sympathetic activity was investigated. Hypertensive patients displayed increased muscle sympathetic nerve activity and elevated total systemic, cardiac, and renal NE spillover. Cardiac neuronal NE reuptake was decreased in hypertensive subjects. In response to desipramine, both the reduction of fractional transcardiac 3[H]NE extraction and the increase in cardiac NE spillover were less pronounced in hypertensive patients. DNA sequencing analysis of the NE transporter gene revealed no mutations that could account for reduced transporter activity. Arterial baroreflex control of sympathetic nerve traffic was not diminished in hypertensive subjects. Angiotensin II plasma concentrations were similar in both groups and were not related to indexes of sympathetic activation. Increased rates of sympathetic nerve firing and reduced neuronal NE reuptake both contribute to sympathetic activation in hypertension, whereas a role for dampened arterial baroreflex restraint on sympathetic nerve traffic and a peripheral neuromodulating influence of angiotensin II appear to be excluded. Key Words: hypertension, essential Ⅲ catecholamines Ⅲ sympathetic nervous system Ⅲ norepinephrine Ⅲ angiotensin II A lthough there is growing evidence that essential hypertension is commonly neurogenic 1,2 and is initiated and sustained by overactivity of the sympathetic nervous system, the precise causal mechanisms leading to sympathetic augmentation in hypertensive subjects are still poorly understood. Among others, possible mechanisms include increased sympathetic nerve firing rates, 1,2 altered neuronal norepinephrine (NE) reuptake, 3,4 diminished arterial baroreflex buffering of sympathetic nerve traffic, 5 and facilitation of NE release by neurohumoral factors such as angiotensin II. 6 These possibilities, however, have not yet been conclusively tested for in humans.To further address some of these issues, we combined microneurography, to measure sympathetic nerve firing rates, with relevant radiotracer methodology to comprehensively study systemic and regional kinetics of NE and its intraneuronal and extraneuronal metabolites. To directly assess whether decreased neuronal NE reuptake contributes ...

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“…18 Panic attacks usually are accompanied by high sympathetic tone and resulting increased heart rate and blood pressure, decreased heart rate variability, and even cardiac arrhythmia, all of which may indicate risk of CVD, including stroke. [3][4][5][6] The results linking PD with stoke provide further evidence of the sympathetic hyperactivity hypothesis. 19,20 Third, psychological distress may cause deleterious effects on cardiovascular conditions and consequently trigger CVD events.…”

Section: Discussionmentioning

confidence: 99%

“…Panic attacks usually are accompanied by sympathetic nervous system arousal, and the resulting effects on cardiovascular regulation, such as increased heart rate and blood pressure, imply risk for CVD, including stroke. [3][4][5][6] Compelling evidence shows that PD is commonly present with CVD, especially cardiovascular death. Higher than expected risk of cardiovascular-cerebrovascular mortality has been observed among patients with PD or paniclike anxiety both in retrospective [7][8][9] and prospective studies.…”

mentioning

confidence: 99%

An Increased Risk of Stroke among Panic Disorder Patients: A 3-Year Follow-up Study

Chen

Lee

et al. 2010

Can J Psychiatry

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Objective: To explore whether panic disorder (PD) increases the risk for stroke, using a nationwide, population-based dataset. Methods:Our study used data from Taiwan's National Health Insurance Research Database. The study cohort included patients who received ambulatory psychiatric care for PD between 2002 and 2003, inclusive (n = 3891). We selected our comparison cohort by randomly recruiting enrollees (n = 19 455) matched with the study group by sex and age. Each patient was tracked for 3 years, from their index ambulatory care visit until the end of 2006, to identify whether or not a patient had a stroke during the follow-up period. Cox proportional hazard regressions were performed as a means of computing the 3-year survival rate, adjusting for potential confounding factors.Results: Among the total sample, 2029 patients (8.7%) experienced a stroke during the 3-year follow-up period, including 647 from the study cohort (16.6% of the PD patients) and 1382 (7.1%) from the comparison cohort. After adjusting for the patients' sex, age, monthly income, level of urbanization, and comorbid medical disorders, the hazard of stroke occurring during the 3-year follow-up period was 2.37 (P < 0.001) times greater for patients with PD than for patients in the comparison cohort. In further analyses, stratified by medical diseases and age, the significant risk of PD on subsequent stroke persisted. Conclusions:We conclude that PD is an independent risk factor for stroke. For patients with PD, aggressive treatment of PD may be considered as part of stroke prevention.Can J Psychiatry. 2010;55(1):43-49. Clinical Implications· We found that about 1 in 6 PD patients (16.6%) experienced a stroke within 3 years, stressing the significant need for possible intervention. · After adjusting for potential confounders, the hazard of stroke occurring during the 3-year follow-up period was 2.37 (95% CI 2.12 to 2.67, P < 0.001) times greater for PD patients than for patients in the comparison cohort. Limitations· PD diagnoses, which rely on administrative claims data reported by hospitals, may be less accurate than diagnoses made according to a standardized procedure.

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Sympathetic and cardiac baroreflex function in panic disorder

Cited by 57 publications

References 48 publications

Attenuation of sympathetic baroreflex sensitivity during the onset of acute mental stress in humans

Attenuation of sympathetic baroreflex sensitivity during the onset of acute mental stress in humans

Sympathetic Augmentation in Hypertension

An Increased Risk of Stroke among Panic Disorder Patients: A 3-Year Follow-up Study

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