• C Droste.
• Rehabilitationszentrum für Herz- und Kreislaufkranke, Bad Krozingen.
• Z Kardiol. 1988 Jan 1; 77 Suppl 5: 15-33.

AbstractCardiac nociceptive afferences are mainly transmitted by sympathetic nervous tracts. After passing the ganglion stellatum and neighbouring ganglia, the nerves enter the dorsal horn of the spinal cord at C8-Th9 (especially Th2-Th6). Here the nerve synapses for the first time, mainly to neurons which run up to the thalamus contralaterally by the tractus spinothalamicus. Apart from atypically localised pain (jaw, head, neck), the nervus vagus is rarely involved in transmitting angina pectoris pain. There is no close relation between peripheral pain localisation and localisation of coronary stenosis or myocardial ischemia areas. The localisation of angina pectoris is decided by viscero-somatic summation (convergence-projection-theory). Almost all the ascending tracts of the tractus spinothalamicus with visceral inflow also receive inflow from somatic afferences, from skin areas of the dermatome from the same segment level, and especially from deep somatic structures such as muscle and ligaments (Head's zones). Additional reflex mechanisms, where the efferent part is probably sympathetic, explain transferred effects in the matching dermatome such as hypothermic skin zones, cutaneous hyperalgesia, higher pressure sensitivity of the muscles and occasionally even dystrophic changes. The amount of spinal visceral afferences is relatively small (only 1.5-2.5% of all somatic spinal afferences). The low amount, the pronounced divergence and, compared to converging somatic afferences, the larger receptive fields in the organ explain the diffuse, barely localisable character of angina pectoris pain. Cardiac afferences are tonically and phasically inhibited at spinal and supraspinal levels, especially by descending tracts. This explains why angina pectoris can be missing in spite of pronounced peripheral nociceptive impulse rates. Patients with silent myocardial ischemia have a higher central pain threshold than patients with symptomatic myocardial ischemia. Endogenous opioids are involved in the body's own analgesia system. The beta-endorphin level in the serum rises significantly in many patients during exercise diagnostic tests. Patients with silent myocardial ischemia have higher beta-endorphin levels compared to symptomatic patients at the same exercise level. This can be interpreted as expressing quantitative differences in a superior pain regulation system. Myocardial ischemia is experienced as angina pectoris pain when the peripheral nociceptive impulse rate is so pronounced that the prevailing inhibitory pain threshold can be overcome and when the pain pathways are intact.

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