心脏输出-O2吸收关系在以前心肌梗塞患者的增量运动期间
1Second Department of Internal Medicine, Tokyo Medical and Dental University, Japan.
Circulation
|May 1, 1992
概括
在患有心肌梗塞的患者中,运动期间的心脏输出和氧气吸收的关系与健康人不同. 这种差异,特别是在厌氧值以上,与运动诱导的无声缺血有关.
科学领域:
- 心脏病学 心脏病学
- 运动生理学 运动生理学
背景情况:
- 心脏输出和氧气吸收 (VO2) 之间的关系在健康人群中是线性的,但在心脏病患者中不太清楚.
- 以前的心肌梗塞 (MI) 可以改变运动期间的心血管反应.
研究的目的:
- 为了评估心脏输出和VO2之间的关系,在以前的MI患者在增量运动期间.
- 调查这种关系与无氧值 (AT) 相对如何变化.
主要方法:
- 22名先前患有心脏病发作的患者接受了限症状循环人体力计运动测试.
- 心脏输出量 (CO) 通过使用 telluride 探测器进行非侵入性测量.
- 氧气吸收 (VO2) 通过过期气体分析来确定.
- 碳排放和工作率 (delta CO/delta WR) 和VO2和工作率 (delta VO2/delta WR) 的变化之间的关系被评估在AT以下和以上.
主要成果:
- VO2随着AT以下和AT以上的工作率线性增加 (delta VO2/delta WR是相似的).
- 心脏输出显著增加,工作率低于AT (三角形CO/三角形WR=50.1毫升/分钟/W).
- 然而,心脏输出增加在AT以上显著下降 (delta CO/delta WR = 11.8 ml/min/W,p=0.0002).
- 心脏输出与VO2 (delta CO/delta VO2) 的比率低于正常,并且在AT (1.1 +/- 2.3) 以上大幅下降.
- 静态心肌缺血症,以201Tl再分配为标志,在15/16名评估患者中存在.
结论:
- 在心脏病发作后的患者中,运动期间心脏输出-VO2的关系与正常人之间的关系明显不同.
- 沉默的心肌缺血可能有助于这些患者在AT以上的心脏输出响应.
- 在冠状动脉疾病患者中,从VO2中对心脏输出变化的非侵入性估计需要仔细考虑这些发现.
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