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Visceral chest pain in unstable angina pectoris and effects of transcutaneous electrical nerve stimulation (TENS)

Viszerale brustschmerzen bei instabiler angina pectoris und wirkung der transkutanen elektrischen nervenstimulation (TNS). Eine Übersicht

A review

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Abstract

A substantial proportion of patients with chest pain referred to hospital, show signs of coronary artery disease. Anginal pain could be conceptualized as a warning signal for coronary artery disease and impending death. But, for many reasons this theory is partly disputed. Firstly, not all ischemic episodes are accompanied by anginal pain (silent ischemia). Secondly, chest pain indistinguishable from true angina pectoris may be the result of other abnormalities of thoracic viscera.

Nevertheless acute severe cardiac ischemia often gives rise to anginal chest pain. Unstable angina pectoris is carrying a higher risk for future events in spite of intensive medical treatment. A special problem are patients awaiting coronary intervention because of severe ischemia and maximum medical treatment, who experience ischemic pain. New treatment regimens are needed for these patients.

This review discusses the symptom of visceral pain from the heart, angina pectoris, its relation to ischemia and unstable angina pectoris. It also addresses the role of afferent nerve stimulation (transcutaneous electrical nerve stimulation, TENS) in the treatment of severe angina pectoris as well as recent findings of TENS applicability in unstable angina.

Zusammenfassung

Eine große Zahl von Patienten, die zur Klinikaufnahme kommen, klagt über Brustschmerzen, die typisch für eine koronare Herzerkrankung sind. Die Angina pectoris ist ein Warnsignal für die koronare Herzerkrankung und geht als Präinfarktangina dem Herzinfarkt und plötzlichen Herztod voraus. Problematisch ist, daß nicht alle ischämischen Herzattacken von einer Angina pectoris begleitet werden (stumme Ischämie) und Brustschmerzen, die von der wahren Angina pectoris nicht getrennt werden, auch von anderen Organen des Thorax stammen können.

Die Angina pectoris zeigt die typischen Eigenschaften eines viszeralen Schmerzes. Er ist oft wenig genau lokalisiert, auf andere anatomische Regionen projiziert (linker Arm, Unterkiefer) aber auch von motorischen, autonomen Reflexen begleitet (Übelkeit, Schweißausbruch). Unspezifische Schmerzrezeptoren wurden im Bereich des Herzens lokalisiert. Der Stimulus, der über diese Rezeptoren Schmerzsensationen hervorruft, ist wahrscheinlich multifaktoriell. Viele verschiedene Stimuli sind diskutiert worden: chemische Stimulationen durch Lactate, Kalium und Adenosin, mechanische Stimulation durch das ischämische Herz wie auch durch Sensibilitätsstörungen und Entzündungen. Der Schmerz könnte aber durch eine Kombination verschiedener Stimuli ausgelöst sein, so daß eine genügend hohe Intensität erreicht wird, um die Nerven zu aktivieren.

Auf verschiedenen Ebenen kann die afferente Nervenbahn moduliert (verstärkt oder vermindert) werden durch afferente Aktivierung anderer viszeraler thorakaler Organe und somatischer Strukturen, wie lokaler Plexus, Ganglien und verschiedener segmentaler Ebenen des Rückenmarks. Verschiedene Schmerzmodulationsmechanismen, wie endogene Peptide, deszendierende inhibitorische und afferente Stimulatoren, konnten segmental aktiviert werden. Die sekundären Neuronen bewirken eine zentrale Weiterleitung, bevor der sensorische Kortex erreicht ist und die Empfindung wahrgenommen wird. Es wird verständlich, daß die Schmerzempfindung nicht automatisch zur Schwere der Ischämie in Bezug zu setzen ist. Die akute kardiale Ischämie führt häufig zur Angina pectoris. Die instabile Angina pectoris beinhaltet ein erhöhtes Risiko, im weiteren Verlauf Komplikationen zu entwickeln. Ein spezielles Problem haben die Patienten, die auf eine koronare Intervention warten, weil schwere Ischämien bestehen oder eine maximale medikamentöse Behandlung die Schmerzsymptomatik nicht beherrschen kann. Neue Behandlungsstrategien sind für diese Patienten notwendig. Die afferente Nervenstimulation hat eine gewisse Popularität erhalten, nachdem sie erstmalig durch Melzack u. Walls als “Gate Control Theory” 1965 veröffentlicht wurde. Der Effekt der transkutanen elektrischen Nervenstimulation (TENS) ist sowohl bei akuter als auch bei neuropathischer Schmerzsymptomatik hilfreich. Durch elektrische Stimulation können die afferenten Nervenfasern stimuliert werden. Der Schmerzverlust wird sekundär durch den segmentalen Mechanismus des Rückenmarks bewirkt.

TENS ist vermehrt bei ischämischem Schmerzstatus eingesetzt worden, so auch bei peripherer arterieller Verschlußkrankheit, primäre Dysmenorrhöen und seit 1970 bei myokardialer Ischämie. Die Methode scheint die Ischämie zu vermindern, wahrscheinlich weil der myokardiale Sauerstoffverbrauch gesenkt wird. Bei chronischer, schwerer Angina pectoris wird aus praktischen Gründen die TENS durch die spinale Rückenmarksstimulation (SCS) abgelöst. Kürzlich ist die Anwendung von TENS bei akutem Koronarsyndrom der instabilen Angina pectoris als Zusatzbehandlung eingeführt worden. TENS wurde als praktikable Methode erkannt, die nicht mit dem weiteren Standardmanagement für die Patienten interferiert und die Phasen der stummen Ischämie reduzieren kann.

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Correspondence to Mats Börjesson MD.

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Börjesson, M. Visceral chest pain in unstable angina pectoris and effects of transcutaneous electrical nerve stimulation (TENS). Herz 24, 114–125 (1999). https://doi.org/10.1007/BF03043850

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