The correlation between the clinical characteristics and psychological status in syndrome X patients

Patients with anginal symptoms and normal coronary arteries have been found to present with high levels of neuroticism i.e. anxiety, depression and somatic concerns. Whether neuroticism plays a role in precipitating coronary hypoperfusion and symptoms is still a matter of investigation. The present study was undertaken to assess the relation between psychological status and clinical symptoms in 22 patients with syndrome X (angina and ST depression with angiographically normal coronary arteries and reversible myocardial perfusion abnormalities). Neuroticism was evaluated by Beck Depression Inventory, Hamilton Anxiety Rating Scale (HAM-A), State-Trait Anxiety Inventory, Sheehan Patient Rated Anxiety Scale, State-Trait Anger Expression Inventory (STAXI), Brief Psychiatric Rating Scale and Clinical Global Impression. Data were compared with those obtained in 30 patients with stable angina as well as coronary artery disease. All patients underwent an exercise stress testing and a 24-hour ambulatory Holter monitoring. Patients with syndrome X scored significantly higher than stable angina (p 28 in HAM-A (Group 1, with frank psychiatric abnormalities). The remaining 10 patients were labelled as Group 2. No significant differences between Group 1 and Group 2 were found in exercise capacity (time to 0.1 m V ST depression: 397 +/- 73 and 419 +/- 137 s, respectively; NS) or in the number of anginal episodes per day (0.9 +/- 1.3/24 hours and 0.6 +/- 0.8/24 hours respectively; NS). In contrast, Holter monitoring showed a significantly higher number of ischemic episodes in Group 1 than in Group 2 (1.6 +/- 1.7 vs 0.1 +/- 0.3/24 hours; p < 0.02) and a greater duration of ischemia (23.8 +/- 32 vs 0.3 +/- 1 min/24 hours; p < 0.03). We conclude that: patients with syndrome X evidence elevated neuroticism scores; a high degree of anxiety correlates with increased transient myocardial ischemia during daily life; neuroticism may itself cause changes in coronary microvascular function in syndrome X. Alternatively it may simply modulate the threshold for ischemia in the presence of underlying dysfunction.