Koike A, Hiroe M, Adachi H, Yajima T, Itoh H, Takamoto T, Taniguchi K, Marumo F
Second Department of Internal Medicine, Tokyo Medical and Dental University, Japan.
Circulation. 1992 May;85(5):1713-9. doi: 10.1161/01.cir.85.5.1713.
The cardiac output-O2 uptake (VO2) relation, which is thought to be linear and predictable in normal humans, has not been clarified in cardiac patients. We evaluated the relation between cardiac output and VO2 during the incremental exercise test in patients with previous myocardial infarction.
Twenty-two patients (age, 58.1 +/- 8.0 years) with previous myocardial infarction performed a symptom-limited exercise test on a cycle ergometer. VO2 was calculated from the expired gas analysis, and cardiac output was measured by a computerized cadmium telluride detector every 10 seconds during exercise. The ratio of increase in VO2 to the increase in work rate (delta VO2/delta WR) below and above the anaerobic threshold (AT) was 11.1 +/- 3.6 and 11.1 +/- 2.9 ml/min/W, respectively, showing no significant difference. However, the ratio of increase in cardiac output to increase in work rate (delta CO/delta WR) below the AT was 50.1 +/- 26.6 ml/min/W and was significantly decreased to 11.8 +/- 25.3 ml/min/W above the AT (p = 0.0002). The decreased delta CO/delta WR above the AT primarily would be due to silent myocardial ischemia produced by exercise, as there was the presence of 201Tl redistribution in 15 of 16 patients in whom myocardial 201Tl scintigraphy with dipyridamole or exercise stress testing was evaluated. delta CO/delta VO2, which has been reported to be approximately 5.5 in normal subjects, was only 4.4 +/- 2.6 at work rates below the AT and was decreased to 1.1 +/- 2.3 at work rates above the AT.
The relation between cardiac output and VO2 during exercise in patients with previous myocardial infarction differs profoundly from that reported in normal subjects. These findings must be considered when we noninvasively estimate the change in cardiac output during exercise by obtaining VO2 in patients with coronary artery disease.
心输出量与摄氧量(VO₂)的关系在正常人中被认为是线性且可预测的,但在心脏病患者中尚未明确。我们评估了既往心肌梗死患者在递增运动试验中心输出量与VO₂之间的关系。
22例(年龄58.1±8.0岁)既往有心肌梗死的患者在自行车测力计上进行了症状限制性运动试验。VO₂通过呼出气体分析计算得出,运动期间每10秒用计算机化碲化镉探测器测量一次心输出量。无氧阈(AT)以下和以上VO₂增加量与工作率增加量的比值(δVO₂/δWR)分别为11.1±3.6和11.1±2.9 ml/min/W,无显著差异。然而,AT以下心输出量增加量与工作率增加量的比值(δCO/δWR)为50.1±26.6 ml/min/W,而在AT以上显著降至11.8±25.3 ml/min/W(p = 0.0002)。AT以上δCO/δWR的降低主要是由于运动诱发的无症状性心肌缺血,因为在16例接受双嘧达莫或运动负荷试验的心肌201Tl闪烁显像患者中,有15例存在201Tl再分布。据报道,正常受试者的δCO/δVO₂约为5.5,在低于AT的工作率下仅为4.4±2.6,在高于AT的工作率下降至1.1±2.3。
既往心肌梗死患者运动期间心输出量与VO₂的关系与正常受试者报道的情况有很大不同。当我们通过获取冠状动脉疾病患者的VO₂来无创估计运动期间心输出量的变化时,必须考虑这些发现。