PANIC DISORDER IN PATIENTS REFERRING FOR AMBULATORY HEART-RATE RECORDING

The relationship of anxiety with cardiovascular function and symptoms has been of long historic interest, culminating in the recent emphasis given to the modulation of cardiovascular response in panic patients. Cognitive approaches postulate an interaction of physiological and psychological factors in the maintenance of panic disorder. Pharmacological approaches postulate a dysfunction of central alpha-adrenoceptors in panic and also in some cardio-vascular diseases. Ambulatory heart rate recordings confirm the presence of major cardiovascular changes during panic attacks in several studies. We have carried out a study in an unselected population being explored in an outpatient cardiology unit with 24 hours ambulatory heart rate recordings. Hundred and ninety-seven consecutive referrals for an ambulatory heart rate examination were assessed with the seven anxiety items of the Hospital Anxiety and Depression Scale (HAD-A). Fifty patients (26 males and 24 females), with an higher score than 8, were interviewed with the SADS-La. Sixty-two per cent of them fit DSM III-R criteria for panic disorder. Among these 50 interviewed patients, 19 (11 males and 8 females) were referred for organic heart disease and 31 (15 males and 16 females) were investigated only for functional symptomatology The proportion of panickers was similar in patients referred either for functional or organic heart disease (63.2 vs 61.3 ; chi2 = .02 ; p = .89). Nineteen patients (11 males and 8 females) had pathological ECG ambulatory recording results and 31 patients (15 males and 16 females) were classified as Holter (-). The proportion of panickers was found similar in these two subgroups of patients (63.2 vs 61.3; chi2 = .02; p = .89). PD patients had higher maximal HR (128.8 +/- 17.1 vs 106.2 +/- 21.9 bpm ; p < 10(-4)) and lower PR interval (0.14 +/- 0.0.3 vs 0.16 +/- 0.02 s; p < .02) than non-panickers. In PD patients, there was no correlation between maximal HR and minimal PR interval. These findings could be attributed to a hypersensitivity of beta-adrenergic receptors in panic disorder.