Droste C
Rehabilitationszentrum für Herz- und Kreislaufkranke, Bad Krozingen, FRG.
Z Kardiol. 1990;79 Suppl 3:31-43.
The situation of absent pain with silent myocardial ischemia is highly difficult to define. There are probably several reasons for the lack of pain. Partly, nerve ways may be destroyed, partly, myocardial ischemia as peripheral pain stimulus may be to weak and beyond threshold, however, additionally, there are a lot of clues for the participation of endogenous pain modification systems therein. A certain amount of myocardial ischemia is a necessary, but not sufficient precondition for anginal pain. Myocardial ischemia is only felt painfully if the peripheral nociceptive impulse rate is high enough to pass the actual inhibitory pain threshold, and if the nerve ways are intact. It is generally accepted that the endogenous opiate system, to some extent, takes part in the endogenous analgesia system. A range of examinations in recent years hinted at the fact that endorphins are in relation to the absence of pain in silent ischemia. Patients with symptomatic and asymptomatic myocardial ischemia are significantly different in plasma beta-endorphin levels at rest and during physical exercise. A relation between peripheral endogenous opiates and suffering behavior can, at present, only be indicated correlatively. It is likely that the intensive overlaying of the cardiovascular and pain regulating systems is related to the absence of pain in silent myocardial ischemia.
无症状性心肌缺血时无痛的情况极难界定。疼痛缺失可能有多种原因。部分原因可能是神经通路遭到破坏,部分原因可能是作为外周疼痛刺激的心肌缺血过于微弱,未达到阈值,然而,除此之外,还有许多线索表明内源性疼痛调节系统也参与其中。一定程度的心肌缺血是心绞痛发作的必要但不充分前提条件。只有当外周伤害性冲动频率足够高,能够超过实际的抑制性疼痛阈值,并且神经通路完整时,心肌缺血才会被感知为疼痛。人们普遍认为,内源性阿片系统在一定程度上参与了内源性镇痛系统。近年来的一系列检查暗示了内啡肽与无症状性缺血时疼痛缺失之间的关系。有症状和无症状心肌缺血患者在静息和运动时血浆β-内啡肽水平存在显著差异。目前,外周内源性阿片与痛苦行为之间的关系只能通过相关性来表明。心血管系统和疼痛调节系统的强烈重叠很可能与无症状性心肌缺血时的疼痛缺失有关。