Abstract

The relation between heart rate and ischemic ST-segment depression was studied in 70 patients with documented obstructive coronary artery disease (CAD) and reproducible effort angina. Symptom-limited treadmill exercise testing was performed before and after a 2-week placebo period and 24-hour FM ambulatory electrocardiographic monitoring at the end of the placebo period. The means (± standard deviation) of the basal and placebo values for exercise time, heart rate and maximal ST-segment depression were: 6.4 ± 2.6 minutes vs 6.9 ± 2.8 minutes (difference not significant [NS]), 125 ± 17 beats/min vs 125 ± 19 beats/min (NS) and 2.3 ± 0.8 mm vs 2.1 ± 0.8 (NS), respectively. Ambulatory monitoring revealed 205 episodes of significant ST-segment depression (J + 80 ms; 49 episodes with more than 1 mm, 83 with more than 2 mm, 39 with more than 3 mm and 34 with more than 4 mm). Of all episodes of ST-segment depression, 130 (64%) were asymptomatic. The episodes lasted for 3 to 110 minutes. The maximal 24-hour ambulatory heart rate and ST-segment depression during ischemic episodes were expressed as a percentage of those seen during exercise-induced ischemia. When all ambulatory ischemic episodes (both symptomatic and asymptomatic) were compared with exercise-induced ischemic changes in the individual patient, there was little difference in heart rate (91 ± 15% vs 90 ± 18%, NS) but there was a greater magnitude of ST-segment depression (122 ± 57% vs 104 ± 52%, p < 0.05). When the symptomatic and asymptomatic ambulatory episodes were compared, the variables of heart rate, duration of the episodes and diurnal variation were not significantly different. The magnitude of ST-segment depression was greater during the symptomatic episodes than during the asymptomatic episodes (p < 0.05). Since heart rate reflects myocardial oxygen demand, the variation in magnitude of ST depression between these 2 types of episode suggests different mechanisms of ischemia. Changes in myocardial perfusion secondary to transient impairment in coronary flow cannot be ruled out in the genesis of silent myocardial ischemia during daily life in patients with chronic stable angina.

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