The Development of a Cognitive-behavior Group Intervention Program to Reduce the Hostility Levels of Coronary Heart Disease Patients and Its Effect on Autonomic Nervous System Function

Objective: To develop a cognitive-behavior group intervention program to reduce the hostility levels of coronary artery heart disease (CHD) patients and examine its effect on autonomic nervous system (ANS) function. Method: Forty three documented CHD patients (mean age = 58.42±7.54, male 69.8%) recruited from the cardiology clinics of a general hospital participated in the study. All the participants attended one of the five cognitivebehavior therapy groups for two hours weekly during two months. The intervention program included psychoeducation, biofeedback-assistant relaxation training, stress management, and cognitive flexibility training . All the participants completed the Chinese Hostility Inventory Short-Form, Beck Depression Inventory-II, State- Trait Anxiety Inventory, and Perceived stress Inventory as well as the autonomic nervous system examinations before and after the intervention. Low frequency (LF) power (0.04-0.15Hz) reflects as both sympathetic nervous system (SNS) and parasympathetic nervous system (PNS) influences. High frequency (HF) power (0.15-0.4Hz) as the index of PNS activation. LF/HF ratio reflects SNS activity. Results: After intervention, there were significant reductions in hostility (t = 6.79, p < .001), depression (t = 3.79, p < .001), anxiety (t = 6.03, p < .001), and perceived stress (t = 3.39, p < .01) level. Furthermore, there was a significant reduction in respiration rate (F = 16.80, p < .0001) and a significant increase in blood volume pulse (F = 4.43, p < .05). Moreover, for heart rate variability, there was a significant increase in SNS activity (F = 8.93, p < .01) and a marginal significant decrease in PNS activity (F = 4.09, p = .051) among the CAD participants. Conclusion: The cognitive-behavior group intervention program not only has an effect to reduce psychological distress, but also has an effect to increase the ANS regulation function, thus may reduce the recurrent risk of CHD.