Ambulatory heart rate and ST-segment depression during painful and silent myocardial ischemia in chronic stable angina pectoris.
Ambulatory heart rate and ST-segment depression during painful and silent myocardial ischemia in chronic stable angina pectoris.
复制标题
慢性稳定性心绞痛疼痛和无症状心肌缺血期间的动态心率和 ST 段压低。
DOI：
10.1016/0002-9149(87)90843-5
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
E. Raftery
中科院分区：
文献类型：
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作者：
G.Piero Carboni;Avijit Lahiri;Peter Cashman;E. Raftery
本文对70例有明确诊断的阻塞性冠状动脉疾病（CAD）和反复发作的劳力型心绞痛患者的心率与缺血性ST段压低的关系进行了研究。在2周安慰剂治疗前后进行症状限制性平板运动试验，并在安慰剂治疗结束时进行24小时FM动态心电图监测。运动时间、心率和最大ST段压低的基础值和安慰剂值的平均值（±标准差）分别为：6.4 ± 2.6分钟vs 6.9 ± 2.8分钟（差异不显著[NS]）、125 ± 17次/分钟vs 125 ± 19次/分钟（NS）和2.3 ± 0.8 mm vs 2.1 ± 0.8 mm（NS）。动态监测显示205次ST段显著压低（J + 80 ms; 49次ST段压低大于1 mm，83次ST段压低大于2 mm，39次ST段压低大于3 mm，34次ST段压低大于4 mm）。在所有ST段压低事件中，130例（64%）无症状。发作持续3至110分钟。缺血发作期间的最大24小时动态心率和ST段压低表示为运动诱导缺血期间观察到的百分比。将所有动态缺血发作（包括症状性和无症状性）与个体患者运动诱发的缺血性变化进行比较，心率差异很小（91 ± 15% vs 90 ± 18%，NS），但ST段压低幅度更大（122 ± 57% vs 104 ± 52%，p < 0.05）。当比较有症状和无症状的非卧床发作时，心率、发作持续时间和昼夜变化的变量无显著差异。ST段压低的幅度在有症状发作期间大于无症状发作期间（p < 0.05）。由于心率反映了心肌需氧量，这两种类型发作之间ST段压低幅度的变化表明缺血的机制不同。在慢性稳定型心绞痛患者日常生活中，不能排除继发于冠状动脉血流短暂性受损的心肌灌注改变是无症状心肌缺血的原因。
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.