Circadian variation of ischemic threshold in syndrome X

To evaluate whether the ischemic threshold has a circadian rhythm in patients with syndrome X, we analyzed 90 episodes of ST depression detected on 24-hour Holter recordings of 12 such patients. Ischemic threshold was considered as heart rate (HR) at 1 mm ST depression. To correct for differences in basal HR among patients, however, the ischemic threshold was also calculated as a normalized index of HR at 1 mm ST depression: [(HR at 1 mm ST-24-hour modal HR)/ 24-hour modal HR].100. Mean hourly values of both absolute and normalized HRs at 1 mm ST depression were obtained by grouping and averaging respective values of all episodes detected in every hour of she day in all patients. Chronobiologic analysis was performed by single cosinor method. A significant circadian rhythm was found for HR (mesor 76 beats/min, amplitude 10 beats/min, acrophase at 2:16 P.M., p <0.001), number of episodes of ST depression (mesor 3.75, amplitude 2.9, ocrophase at 2:45 P.M., p <0.001) and cumulative lime of ischemia, with a high correlation of distributions. Episodes of ST depression showed a double peak initially in the morning, and again in the afternoon. Both raw and normalized values of HR at 1 mm ST depression also had a significant arcadian variation in ischemic threshold, which was lower in the night and early morning hours, progressively increased until the first afternoon hours, and subsequently decreased in the evening. Normalized HR had a mesor of +20.5%, amplitude 14.5%, and acrophase at 2:55 P.M. (p<0.01).Thus, our data demonstrate that ischemic episodes and ischemic threshold follow a significant circadian variation in patients with syndrome X The similarity between the circadian rhythms of the episodes of ST depression and HR suggests a significant role of the increase in myocordial oxygen demand in the induction of ischemia. The significant circadian rhythm in ischemic threshold, however, indicates that variations in vasomotor tone have a remarkable role in the pathophysiologic mechanisms of transient ST-segment depression in these patients.