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腺苷诱发的无症状和有症状心肌缺血患者胸痛:提示痛觉刺激普遍感知缺陷作为无症状缺血病因的重要性的又一线索。

Adenosine-induced chest pain in patients with silent and painful myocardial ischaemia: another clue to the importance of generalized defective perception of painful stimuli as a cause of silent ischaemia.

作者信息

Crea F, el-Tamimi H, Vejar M, Kaski J C, Davies G, Maseri A

机构信息

Cardiovascular Unit, RPMS-Hammersmith Hospital, London, U.K.

出版信息

Eur Heart J. 1988 Dec;9 Suppl N:34-9. doi: 10.1093/eurheartj/9.suppl_n.34.

DOI:10.1093/eurheartj/9.suppl_n.34
PMID:3246254
Abstract

Adenosine is formed from adenosine triphosphate within the ischaemic cells from where it is released into the coronary circulation. Adenosine exhibits several cardiovascular effects which tend to protect the ischaemic myocardium. Based on the observation that in healthy volunteers the intravenous infusion of adenosine produces angina-like chest pain, it has been recently proposed that another cardioprotective action of this substance could be provocation of angina. If this is the case adenosine should not produce chest pain in patients with silent ischaemia. To test this hypothesis we infused this substance intravenously at increasing doses of 50, 100, 150, 200, 250 and 300 micrograms kg-1 min-1 in eight patients with silent ischaemia (group A). All of them developed ST depression (1.8 +/- 0.2 mm) during exercise testing and seven also during adenosine infusion (1.1 +/- 0.8 mm). However, none of the patients had chest pain during exercise while seven had chest pain during adenosine. We then infused adenosine in eight other patients (Group B) who had painful ischaemia and an exercise tolerance similar to that of Group A patients (time to 1 mm ST depression 8.6 +/- 2.7 min and 8.4 +/- 3 min, respectively, P = NS). Adenosine induced chest pain in all Group B patients. The time to pain onset during adenosine was similar in the two groups (9.3 +/- 2.3 min in Group B and 12.4 +/- 4.9 min in Group A).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

腺苷由缺血细胞内的三磷酸腺苷生成,然后释放到冠脉循环中。腺苷具有多种心血管效应,往往能保护缺血心肌。基于在健康志愿者中静脉输注腺苷会引发心绞痛样胸痛这一观察结果,最近有人提出该物质的另一心脏保护作用可能是诱发心绞痛。如果是这样,腺苷在无症状性缺血患者中不应引发胸痛。为验证这一假设,我们对8例无症状性缺血患者(A组)静脉输注腺苷,剂量递增,分别为50、100、150、200、250和300微克/千克·分钟。所有患者在运动试验时均出现ST段压低(1.8±0.2毫米),7例在输注腺苷时也出现ST段压低(1.1±0.8毫米)。然而,所有患者在运动时均无胸痛,而7例在输注腺苷时出现胸痛。然后我们对另外8例有疼痛性缺血且运动耐量与A组患者相似的患者(B组)输注腺苷(运动至ST段压低1毫米的时间分别为8.6±2.7分钟和8.4±3分钟,P=无显著性差异)。腺苷在所有B组患者中均诱发了胸痛。两组患者输注腺苷后疼痛发作时间相似(B组为9.3±2.3分钟,A组为12.4±4.9分钟)。(摘要截短于250词)

相似文献

1
Adenosine-induced chest pain in patients with silent and painful myocardial ischaemia: another clue to the importance of generalized defective perception of painful stimuli as a cause of silent ischaemia.腺苷诱发的无症状和有症状心肌缺血患者胸痛:提示痛觉刺激普遍感知缺陷作为无症状缺血病因的重要性的又一线索。
Eur Heart J. 1988 Dec;9 Suppl N:34-9. doi: 10.1093/eurheartj/9.suppl_n.34.
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Provocation of chest pain in patients with coronary insufficiency using the vasodilator adenosine.使用血管扩张剂腺苷诱发冠状动脉供血不足患者的胸痛
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Adenosine provokes myocardial ischaemia in patients with ischaemic heart disease without increasing cardiac work.腺苷可诱发缺血性心脏病患者的心肌缺血,而不增加心脏负荷。
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Role of adenosine in pathogenesis of anginal pain.腺苷在心绞痛发病机制中的作用。
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Silent myocardial ischaemia in patients referred for coronary bypass surgery because of angina: a comparison with patients whose symptoms were well controlled on medical treatment.因心绞痛而接受冠状动脉搭桥手术的患者中的无症状心肌缺血:与药物治疗症状得到良好控制的患者的比较。
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Br Heart J. 1993 Nov;70(5):438-42. doi: 10.1136/hrt.70.5.438.

引用本文的文献

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J Clin Med. 2020 May 6;9(5):1366. doi: 10.3390/jcm9051366.
2
Arrhythmias in vasodilator stress testing.血管扩张剂负荷试验中的心律失常
J Nucl Cardiol. 2017 Apr;24(2):410-412. doi: 10.1007/s12350-016-0407-5. Epub 2016 Feb 2.
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Differential cardioprotection with selective inhibitors of adenosine metabolism and transport: role of purine release in ischemic and reperfusion injury.腺苷代谢与转运选择性抑制剂的差异性心脏保护作用:嘌呤释放在缺血及再灌注损伤中的作用
Mol Cell Biochem. 1998 Mar;180(1-2):179-91.