A brief cognitive-behavioral intervention for treating depression and panic disorder in patients with noncardiac chest pain: a 24-week randomized controlled trial.

BACKGROUND: Most patients with noncardiac chest pain experience anxiety and depressive symptoms. Commonly they are reassured and referred back to primary care, leaving them undiagnosed and untreated. Some small studies have suggested efficacy of 12 cognitive behavioral therapy (CBT) sessions. Our aim was to examine efficacy of brief CBT in reducing anxiety and depressive symptoms in patients with noncardiac chest pain and comorbid panic and/or depressive disorders. METHODS: In this 24-week randomized controlled trial comparing CBT (n = 60) versus treatment as usual (TAU, n = 53), we included all adults who presented at the cardiac emergency unit of a university hospital with noncardiac chest pain, scored ≥8 on the hospital anxiety and depression scale (HADS) and were diagnosed with a comorbid panic and/or depressive disorder with the Mini International Neuropsychiatric Interview. CBT consisted of six individual sessions. Main outcome was disease severity assessed with the clinical global inventory (CGI) by a blinded independent rater. RESULTS: ANCOVA in the intention-to-treat and completer sample showed that CBT was superior to TAU after 24 weeks in reducing disease severity assessed with CGI (P < .001). Secondary outcomes on anxiety (HADS-anxiety, state trait anxiety inventory (STAI)-trait) and depressive symptoms (Hamilton depression rating scale) were in line with these results except for HADS-depression (P = .10), fear questionnaire (P = .13), and STAI-state (P = .11). CONCLUSIONS: Brief CBT significantly reduces anxiety and depressive symptoms in patients with noncardiac chest pain who are diagnosed with panic and/or depressive disorders. Patients presenting with noncardiac chest pain should be screened for psychopathology and if positive, CBT should be considered.

Predictability, controllability, and fear of symptoms of anxiety in epinephrine-induced panic.

BACKGROUND: Psychological manipulations (supplied information, safety cues) may influence panic rates during pharmacologic challenge tests in subjects with panic disorder (PD). Psychological panic models assume that fear of stress-related bodily sensations is central to the etiology of PD. METHODS: Prior to infusion of epinephrine, 50 subjects with PD were randomly assigned to one out of four experimental conditions: with or without extensive information and with or without external control, according to a 2 x 2 design. The panic rate was hypothesized to be lower in subgroups possessing extensive information and/or control. Fear of bodily sensations was used as a predictor. RESULTS: Thirty-four out of 50 patients (68%) panicked during the infusion. Subjects who received extensive information were marginally less likely to panic, but manipulation of control did not influence panic rates. Panickers did not differ from nonpanickers in measures of fear of fear. Anxiety sensitivity best predicted baseline anxiety and cognitive symptom scores, but was not associated with other outcome measures in panickers. Only baseline partial pressure of CO2 discriminated between panickers and nonpanickers. CONCLUSIONS: Manipulating external safety cues appears to be of limited value in modulating responses to epinephrine challenge. Together with our finding that fear of anxiety symptoms does not predict panic rates, these data argue against "fear of fear" as a key mechanism in epinephrine-induced panic.

Epinephrine-induced panic attacks and hyperventilation.

To assess the effects of epinephrine on ventilation in patients with panic disorder and in social phobics, analyses were performed on pooled data from two previous infusion studies. Throughout the infusion, changes in transcutaneous PCO2 (tcPCO2), subjective anxiety, heart rate and blood pressure were recorded continuously. Twenty-nine patients received epinephrine, ten patients received placebo. Thirteen patients (45%) had a panic attack during epinephrine. The fall in tcPCO2 and the cardiovascular response was greater in panicking patients than patients who did not panic. Although the fall in tcPCO2 associated with panic was not substantial and did not indicate clinically significant acute hyperventilation, it appears to be a sensitive index for epinephrine-induced panic. The fall in tcPCO2 was predicted rather by the frequency of occurrence of anxiety-related somatic symptoms than by the fear of these symptoms. These findings further reduce a role for fear of bodily sensations in epinephrine-induced panic attacks and favor a biological sensitivity to sympathetic stimulation.

Epinephrine infusions in panic disorder: a double-blind placebo-controlled study.

Twenty-four subjects with Panic Disorder were infused with epinephrine in physiological doses or placebo according to a double-blind design. The panic rate in the epinephrine group (67%) was higher than in the placebo group (25%). Placebo panic occurred early during the procedure and was apparently associated with anticipation anxiety and stress-provoking situational factors. Panickers were characterized by a greater increase in heart rate as well as a drop in pCO2. Fear of bodily sensations was only weakly associated with state anxiety levels at point of panic. It is concluded that cognitive factors may not be important in epinephrine-induced panic.

Adrenaline and the relationship between neurosomatism, aerobic fitness and mental task performance.

The influence of neurotic instability as manifested by functional somatic complaints (neurosomatism) and aerobic fitness on responses to mental stress and to intravenous adrenaline infusions were investigated in 44 university students. Adrenaline-induced changes from resting levels in state anxiety and somatic anxiety were significantly more pronounced in high than in low neurosomatic subjects and all anxiety ratings were generally negatively related to aerobic fitness. Cardiovascular reactivity was induced by mental stress and by adrenaline infusions, but was not altered by neurosomatism. In individuals assumed to be characterized by a susceptibility to adrenergic effects, interference of adrenaline-induced arousal with cognitive performance may not occur. In contrast, a further increase in performance may occur when adrenaline is infused. Performance measures correlated negatively with anxiety during the baseline task and the placebo task, but this negative relation was absent during the adrenaline infusion and was replaced by positive relations between performance and aerobic power. The complex relations between bodily symptoms of anxiety, aerobic fitness and mental stress are discussed.