Significance of hyperventilation-induced st segment depression in patients with coronary artery disease

To investigate the significance of hyperventilation-induced ST segment depression, 329 consecutive patients with angina and documented coronary artery disease who underwent hyperventilation and exercise tests during pharmacologic washout were studied. The hyperventilation test induced ST segment depression in 79 patients. In 36 of these 79 patients; the electrocardiographic changes occurred early during overbreathing (Group I), whereas in 26 they occurred late during recovery (Group II). Seventeen patients developed ST segment depression both during overbreathing and during recovery (Group III). Group I patients had a higher frequency of history of angina during exercise, multivessel disease and lower tolerance to exercise as compared with patients in Group II. In Group I, the rate-pressure product at the time to onset of ST depression during overbreathing was similar to that during exercise (152 ± 24 versus 148 ± 42; p = NS), whereas in Group II the rate-pressure product at the time to onset of ST depression during recovery was comparable with that under control conditions (104 ± 30 versus 98 ± 27; p = NS) and far less than that required to produce ischemia during exercise (104 ± 30 versus 201 ± 56; p <0.001). In nine Group III patients, the acute administration of propranolol prevented the early hyperventilation-induced ST segment depression, whereas nifedipine abolished the delayed hyperventilation-induced ST segment depression. These findings suggest that early hyperventilation-induced ST segment depression is due to increased oxygen demand in patients with poor coronary reserve and may be prevented by beta-adrenergic blockers, which are useful for lowering oxygen consumption. Delayed hyperventilation-induced ST segment depression, occurring in patients with a high incidence of angina at rest and longer exercise duration, is probably related to a primary reduction in coronary blood flow and may be prevented by calcium antagonists that abolish abnormal coronary vasoconstriction.