Herz

, Volume 24, Issue 2, pp 114–125 | Cite as

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

A review
Article

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.

Key Words

Visceral pain Angina pectoris Unstable angina Transcutaneous electrical nerve stimulation (TENS) Afferent stimulation Spinal cord stimulation (SCS) 

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

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.

Schlüsselwörter

Viszeraler Schmerz Angina pectoris Instabile Angina pectoris Transkutane elektrische Nervenstimulation (TENS) Afferente Stimulation Spinale Rückenmarksstimulation (SCS) 

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References

  1. 1.
    Andrews TC, Raby K, Barry J, et al. Effect of cholesterol reduction on myocardial ischemia in patients with coronary disease. Circulation 1997; 95: 324–8.PubMedGoogle Scholar
  2. 2.
    Antman EM, Tanasijevic MJ, Thompson B, et al. Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes. N Engl J Med 1996; 335: 1342–9.PubMedGoogle Scholar
  3. 3.
    Areskog M, Tibbling L, Wranne B. Non-infarction coronary unit patients. Acta Med Scand 1981; 209: 51–7.PubMedGoogle Scholar
  4. 4.
    Augustinsson L, Linderoth B, Mannheimer C. Spinal cord stimulation in various ischemic conditions In: Illis L, ed. Spinal cord dysfunction, Vol III. Functional stimulation. Oxford University Press, Oxford, 1992: 272–95.Google Scholar
  5. 5.
    Baker DG, Coleridge HM, Coleridge JCG, et al. Search for a cardiac nociceptor: stimulation by bradykinin of sympathetic afferent nerve endings in the heart of the cat. J Physiol 1980; 306: 519–36.PubMedGoogle Scholar
  6. 6.
    Barish CF, Castell DO, Richter JE. Graded esophageal balloon distention-a new provocative test for non-cardiac chest pain. Dig Dis Sci 1986; 31: 1292–8.PubMedGoogle Scholar
  7. 7.
    Bates JAV, Nathan PW. Transcutaneous electrical nerve stimulation for chronic pain. Anaesthesia 1980; 35: 817–22.PubMedGoogle Scholar
  8. 8.
    Becker RC, Cannon CP, Bovill EG, et al. Prognostic value of plasma fibrinogen concentration in patients with unstable angina and non-Q wave myocardial infarction (TIMI IIIB trial). Am J Cardiol 1996; 78: 142–7.PubMedGoogle Scholar
  9. 9.
    Bennett JR, Atkinson M. The differentiation between oesophageal and cardiac pain. Lancet 1966; 2: 1123–7.PubMedGoogle Scholar
  10. 10.
    Bishop VS, Malliani A, Thorén P. Cardiac mechanoreceptors. In: Shepherd JT, Abboud FM. Geiger SR. Handbook of physiology, Vol. III. Washington. Am Physiological Soc 1983: 497–55.Google Scholar
  11. 11.
    Blackwell JN, Castell DO. Oesophageal chest pain: a point of view. Gut 1984; 25: 1–6.PubMedGoogle Scholar
  12. 12.
    Blair RW, Weber RN, Foreman RD. Responses of thoracic spinothalamic neurones to intracardiac injection of bradykinin in the monkey. Circ Res 1982; 51: 83–94.PubMedGoogle Scholar
  13. 13.
    Bortolotti M, Bacchelli S, Esposti SD, et al. Angina-like chest pain of esophageal origin: a possible side-effect of the chronic anti-anginal therapy. Gastroenterology 1990: A 24. abstract.Google Scholar
  14. 14.
    Bosch X, Theroux P, Waters D, et al. Early post-infarction ischemia: Clinical, angiographic, and prognostic significance. Circulation 1987; 75: 988–95.PubMedGoogle Scholar
  15. 15.
    Börjesson M, Eriksson P, Dellborg, et al. Transcutaneous electrical nerve stimulation in unstable angina pectoris. Coron Art Dis 1997; 8: 543–50.Google Scholar
  16. 16.
    Börjesson M, Pilhall M, Eliasson T, et al. Esophageal dysfunction in syndrome X. Am J Cardiol 1998; 82: 1187–91.PubMedGoogle Scholar
  17. 17.
    Caffrey JL, Gaugl JF, Jones CE. Local endogenous opiate activity in dog myocardium: Receptor blockade with naloxone. Am J Physiol 1985; 248: H382–8.PubMedGoogle Scholar
  18. 18.
    Campbell JA. A critical appraisal of the electrical output characteristics of ten transcutaneous nerve stimulators. Clin Phys Measurement 1982; 3: 141–50.Google Scholar
  19. 19.
    Campbell JN, Taub A. Local analgesia from percutaneous electrical stimulation. Arch of Neurol 1973;28:347–350.Google Scholar
  20. 20.
    Cannon CP, McCabe CH, Stone PH, et al. Circadian variation in the onset of unstable angina and non-Q wave acute myocardial infarction (the TIMI III registry and TIMI IIIB). Am J Cardiol 1997;79:253–8.PubMedGoogle Scholar
  21. 21.
    Cannon RO. The sensitive heart. A syndrome of abnormal cardiac pain perception. JAMA 1995;273:883–7.PubMedGoogle Scholar
  22. 22.
    Cervero F. Sensory innervation of the viscera: peripheral basis of visceral paint. Physiol Rev 1994;74:95–138.PubMedGoogle Scholar
  23. 23.
    Cervero F, Lumb BM. Bilateral inputs and supraspinal control of viscerosomatic neurones in the lower thoracic spinal cord of the cat. J Physiol 1988;403:221–37.PubMedGoogle Scholar
  24. 24.
    Cervero F, Tattersall JEH. Somatic and visceral sensory integration in the thoracic spinal cord. In: Cervero F, Morrison JFB. Visceral sensation. Progress in brain research, Vol 67 Amsterdam: Elsevier 1986:189–205.Google Scholar
  25. 25.
    Chandler MJ, Brennan TJ, Garrison DW et al. A mechanism of cardiac pain suppression by spinal cord stimulation: implications for patients with angina pectoris. Eur Heart J 1993;14:96–105.PubMedGoogle Scholar
  26. 26.
    Chauhan A, Mullins PA, Thuraisingham SI, et al. Effect of transcutaneous electrical nerve stimulation on coronary blood flow. Circulation 1994;89:694–702.PubMedGoogle Scholar
  27. 27.
    Chauhan A, Petch MC, Schofield PM. Effect of oesophageal acid instillation on coronary blood flow. Lancet 1993;341:1309–10.PubMedGoogle Scholar
  28. 28.
    Cherniack NS, Runold M, Prabhakar NR, et al. Effect of adenosine on vagal sensory pulmonary afferents. Fed Proc 1987;46:825.Google Scholar
  29. 29.
    Cohn PF. Silent myocardial ischemia in patients with a defective anginal warning system. Am J Cardiol 1980;45:697–702.PubMedGoogle Scholar
  30. 30.
    Cook AW, Oygar A, Baggenstos P. et al. Vascular disease of extremities-Electric stimulation of spinal cord and posterior roots. NY State J Med 1976;76:366–8.Google Scholar
  31. 31.
    Dawood MY, Ramos J. Transcutaneous electrical nerve stimulation (TENS) for the treatment of primary dysmenorrhea: a randomized crossover comparison with placebo TENS and ibuprofen. Obstet Gynecol 1990;75:656–60.PubMedGoogle Scholar
  32. 32.
    De Landsheere C, Mannheimer C, Habets A, et al. Effect of spinal cord stimulation on regional myocardial perfusion assessed by positron emission tomography. Am J Cardiol 1992;69:1143–9.PubMedGoogle Scholar
  33. 33.
    Deanfield JE, Shea M, Ribiero P, et al. Transient ST-segment depression as a marker of myocardial ischemia during daily life. Am J Cardiol 1984;54:1195–200.PubMedGoogle Scholar
  34. 34.
    Deedwania PC, Carbajal EV. Silent myocardial ischemia-a clinical perspective. Arch Intern Med 1991;151:2373–82.PubMedGoogle Scholar
  35. 35.
    Deedwania PC, Carbajal EV, Nelson JR, et al. Anti-ischemic effects of atenolol versus nifedipine in patients with coronary artery disease and ambulatory silent ischemia. J Am Coll Cardiol 1991;17:963–9.PubMedGoogle Scholar
  36. 36.
    DeJongste MJL, Haaksma J, Hautvast RWM, et al. Effects of spinal cord stimulation on myocardial ischemia during daily life in patients with severe coronary artery disease. Br Heart J 1993;71:413–8.Google Scholar
  37. 37.
    DeMeester TR, O’Sullivan GC, Bermudez G, et al. Esophageal function in patients with angina-type chest pain and normal coronary angiograms. Ann Surg 1982;196:488–98.PubMedGoogle Scholar
  38. 38.
    Diamond GA, Forrester JS. Analysis of probability as an aid in the clinical diagnosis of coronary-artery disease. N Engl J Med 1979;300:1350–8.PubMedGoogle Scholar
  39. 39.
    Droste C, Roskamm H. Experimental pain measurement in patients with asymptomatic myocardial ischemia. J Am Coll Cardiol 1983;1:940–5.PubMedGoogle Scholar
  40. 40.
    Edlund A, Fredholm BB, Patrignani P, et al. Release of two vasodilators — adenosine and prostacyclin — from isolated rabbit hearts during controlled hypoxia. J Physiol 1983;340:487–501.PubMedGoogle Scholar
  41. 41.
    Eliasson T, Jern S, Augustinsson L-E, et al. Safety aspects of spinal cord stimulation in severe angina pectoris. Coron Art Dis 1994;5:845–50.Google Scholar
  42. 42.
    Eliasson T, Mannheimer C, Waagstein F, et al. Myocardial turnover of endogenous opioids and calcitonin-gene-related peptide in the human heart and the effects of spinal cord stimulation on pacing induced angina pectoris. Cardiology 1998;89:170–7.PubMedGoogle Scholar
  43. 43.
    Epstein SE, Quyyumi AA, Bonow RO. Myocardial ischemia: Silent or symptomatic. N Engl J Med 1988;318:1038–43.PubMedGoogle Scholar
  44. 44.
    Eriksson MBE, Rosén I, Sjölund B. Thermal sensitivity in healthy subjects is decreased by a central mechanism after TNS. Pain 1985;22:235–42.PubMedGoogle Scholar
  45. 45.
    Fazzini PF, Prati PL, Rovelli F, et al. Epidemiology of silent myocardial ischemia in asymptomatic middle-aged men (the ECCIS Project). Am J Cardiol 1993;72:1383–8.PubMedGoogle Scholar
  46. 46.
    Foreman RD. Spinothalamic tract and cardiac afferents. In: Lown B, Malliani A, Prosdocimi M. Fidia research series, Vol. 5. Padova Liviana Press 1986;169–81.Google Scholar
  47. 47.
    Friedman M, Breall WS, Goodwin ML, et al. Effect of type A behavioral counseling on frequency of episodes of silent myocardial ischemia in coronary patients. Am Heart J, 1996;132:933–7.PubMedGoogle Scholar
  48. 48.
    Garcia-Pulido J, Patel PH, Hunter WC, et al. Esophageal contribution to chest pain in patients with coronary artery disease. Chest 1990;98:806–10.PubMedGoogle Scholar
  49. 49.
    Geft IL, Fishbein MC, Ninomiya K. Intermittent brief periods of ischemia have a cumulative effect and may cause myocardial necrosis. Circulation 1982;66:1150–3.PubMedGoogle Scholar
  50. 50.
    Gelford M, Rozen P, Gilat T. Isosorbide dinitrate and nifedipine treatment of achalasia: a clinical manometric and radionuclide evaluation. Gastroenterology 1982;83:963–9.Google Scholar
  51. 51.
    Gilbert NC, LeRoy GV, Fenn GK. The effect of distention of abdominal viscera on the blood flow in the circumflex branch of the left coronary artery of the dog. Am Heart J 1940;20:519–24.Google Scholar
  52. 52.
    Glazier JJ, Chierchia S, Brown MJ, et al. Importance of generalized defective perception of painful stimuli as a cause of silent myocardial ischemia in chronic stable angina pectoris. Am J Cardiol 1986;58:667–72.PubMedGoogle Scholar
  53. 53.
    Gottlieb S, Weisfeldt M, Ouyang P, et al. Effect of the addition of propranolol to therapy with nifedipine for unstable angina pectoris: a randomized, double-blind placebo-controlled trial. Circulation 1986;73:331–7.PubMedGoogle Scholar
  54. 54.
    Gottlieb SO, Gottlieb SH, Achuff SC, et al. Silent ischemia on Holter monitoring predicts mortality in high-risk postinfarction patients. JAMA 1988;259:1030–5.PubMedGoogle Scholar
  55. 55.
    Gottlieb SO, Weisfeldt ML, Ouyang P, et al. Silent ischemia as a marker for early unfavorable outcomes in patients with unstable angina. N Engl J Med 1986;314:1214–9.PubMedGoogle Scholar
  56. 56.
    Hautwast RWM, Blanksma PK, DeJongste MJL, et al. Effect of spinal cord stimulation on myocardial flow assessed by positron emission tomography in patients with refractory angina pectoris. Am J Cardiol 1996;77:462–7.Google Scholar
  57. 57.
    Held PH, Yusuf S, Furberg CD. Calcium channel blockers in acute myocardial infarction and unstable angina. An Overview. Br Med J 1989;299:1187–92.Google Scholar
  58. 58.
    Hoberg E. Symptomatic, versus asymptomatic ischemic episodes during Holter monitoring: patterns of high resolution trend recordings of ST segment and heart rate. In: von Arnim T: Maseri A. Silent ischemia. Darmstadt: Steinkopff 1987:125–30.Google Scholar
  59. 59.
    Jacobs MJMH, Jörning PJG, Beckers RCY, et al. Foot salavage and improvement of microvacular, blood flow as a result of epidural spinal cord electrical stimulation. J Vasc Surg 1990;12:354–60.PubMedGoogle Scholar
  60. 60.
    Janes RD, Brandys JC, Hopkins DA, et al. Anatomy of human extrinsic cardiac nerves and ganglia. Am J Cardiol 1986;57: 299–309.PubMedGoogle Scholar
  61. 61.
    Janssens J, Vantrappen G, Ghillebert G. 24-hour recording of esophageal pressure and pH in patients with noncardiac chest pain. Gastroenterology 1986;90:1978–84.PubMedGoogle Scholar
  62. 62.
    Jivegård LEH, Augustinsson L-E, Holm, J, et al. Effects of spinal cord stimulation (SCS) in patients with inoperable severe lower limb ischaemia: a prospective randomised controlled study. Eur J Vasc Endovasc Surg 1995;9:421–5.PubMedGoogle Scholar
  63. 63.
    Johnson MI, Ashton CH, Bousfield DR, et al. Analgesic effects of different, frequencies of transcutaneous electrical nerve stimulation on cold induced pain in normal subjects. Pain 1989;39:231–6.PubMedGoogle Scholar
  64. 64.
    Johnson MI, Ashton CH, Thompson JW. An in-depth study of long-term users of transcutaneous electrical nerve stimulation (TENS). Implications for clinical use of TENS. Pain 1991;44:221–9.PubMedGoogle Scholar
  65. 65.
    Kaada B Promoted healing of chronic ulceration by transcutaneous nerve stimulation (TNS). VASA 1983;12:262–9.PubMedGoogle Scholar
  66. 66.
    Kannel WB, Abbott RD. Incidence and prognosis of unrecognized myocardial infarction. N Engl J Med 1984;311:1144–7.PubMedGoogle Scholar
  67. 67.
    Kaplan B, Peled Y, Pardo J, et al. Transcutaneous electrical nerve stimulation (TENS) as a relief for dysmenorrhea Clin Exp Obstet Gynecol 1994;21:87–90.PubMedGoogle Scholar
  68. 68.
    Katon W, Vitaliano DD, Russo J, et al. Panic disorder: Epidemiology in primary care. J Fam Pract 1986;23:233–9.PubMedGoogle Scholar
  69. 69.
    Katz PO, Dalton CB, Richter JE, et al. Esophageal testing of patients with noncardiac chest pain or dysphagia-results of three years’ experience with 1161 patients. Ann Intern Med 1987;106: 593–7.PubMedGoogle Scholar
  70. 70.
    Keele CA, Armstrong D. Substances producing pain and itch. London: Arnold, 1964:329–37.Google Scholar
  71. 71.
    Kellermann JJ, Braunwald E. silent myocardial ischemia: a critical appraisal. Basel: Karger, 1990.Google Scholar
  72. 72.
    Knatterud GL, Bourassa MG, Pepine CJ, et al. Effects of treatment strategies to suppress ischemia in patients with coronary artery disease: 12-week results of the Asymptomatic Cardiac Ischemia Pilot (ACIP) study. J Am Coll Cardiol 1994;24:11–20.PubMedGoogle Scholar
  73. 73.
    Lam HGT, Dekker W, Kan G, et al. Acute noncardiac chest pain in a coronary care unit. Gastroenterology 1992;102:453–60.PubMedGoogle Scholar
  74. 74.
    Lindahl B, Andrén B, Ohlsson J, et al. Risk stratification in unstable coronary artery disease. Additive value of troponin T determination and pre-discharge exercise tests. Eur Heart J 1997;18: 762–70.PubMedGoogle Scholar
  75. 75.
    Lindahl B, Venge P, Wallentin L. Relation between troponin T and the risk of subsequent cardiac events in unstable coronary artery disease. Circulation 1996;93:1651–7PubMedGoogle Scholar
  76. 76.
    Linderoth B, Fedorcsak I, Meyerson BA. Peripheral vasodilatation after spinal cord stimulation animal studies of putative effector mechanisms Neurosurgery 1991;28:187–95.PubMedGoogle Scholar
  77. 77.
    Liuzzo G, Biasucci LM, Gallimore JR, et al. The prognostic value of C-reactive protein and serum amyloid A protein in severe unstable angina. N Engl J Med 1994;331:417–24.PubMedGoogle Scholar
  78. 78.
    Malliani A. The conceptualization of cardiac pain as a nonspecific and unreliable alarm system. In: Gebhart GF. Visceral pain, Vol. 5. Seattle: IASP Press, 1995;63–74.Google Scholar
  79. 79.
    Malliani A, Brown AM. Reflexes arising from coronary receptors. Brain Res 1970;24:352–5.PubMedGoogle Scholar
  80. 80.
    Malliani A, Lombardi F. Consideration of the fundamental mechanisms eliciting cardiac pain. Am Heart J 1982;103:575–8.PubMedGoogle Scholar
  81. 81.
    Malliani A, Pagani M, Lombardi F. Positive feedback reflexes. In: Zanchetti A, Tarazi RC, Handbook of hypertension. Vol. 8. Pathophysiology of hypertension. Amsterdam: Elsevier, 1986: 69–81.Google Scholar
  82. 82.
    Malliani A, Recordati G, Schwartz PJ. Nervous activity of afferent cardiac sympathetic fibres with atrial and ventricular endings. J Physiol 1973;229:457–69.PubMedGoogle Scholar
  83. 83.
    Mannheimer C, Carlsson C-A, Vedin A, et al. Transcutaneous electrical nerve stimulation (TENS) in angina pectoris. Pain 1986;26:291–300.PubMedGoogle Scholar
  84. 84.
    Mannheimer C, Carlsson CA, Emanuelsson H, et al. The effects of transcutaneous electrical nerve stimulation in patients with severe angina pectoris. Circulation 1985;71:308–16.PubMedGoogle Scholar
  85. 85.
    Mannheimer C, Carlsson CA, Ericson K, et al. Transcutaneous electrical nerve stimulation in severe angina pectoris. Eur Heart J 1982;3:297–302.PubMedGoogle Scholar
  86. 86.
    Mannheimer C, Eliasson T, Andersson B, et al. Effects of spinal cord stimulation in angina pectors induced by pacing and possible mechanisms of action. Br Med J 1993;307:477–80.Google Scholar
  87. 87.
    Marcassa C, Galli M, Baroffio C, et al. Ischemic burden in silent and painful myocardial ischemia: A quantitive exercise sestamibi tomographic study. J Am Coll Cardiol 1997;29:948–54.PubMedGoogle Scholar
  88. 88.
    Martin SJ, Gorham LW. Cardiac pain. An experimental study with reference to the tension factor. Arch Intern Med 1938;62: 840–52.Google Scholar
  89. 89.
    Maseri A, Crea F, Kaski JC, et al. Mechanisms and significance of cardiac ischemic pain. Prog Cardiovasc Dis 1992;35:1–18.PubMedGoogle Scholar
  90. 90.
    Mellow MH, Simpson AG, Watt L, et al. Esophageal acid perfusion in coronary artery disease. Induction of myocardial ischemia. Gastroenterology 1983;85:306–12.PubMedGoogle Scholar
  91. 91.
    Melzack R, Wall PD. Pain mechanisms: a new theory. Science 1965;150:971–9.PubMedGoogle Scholar
  92. 92.
    Milsom I, Hedner N, Mannheimer C. A comparative study of the effect of high-intensity transcutaneous nerve stimulation and oral naproxen on intrauterine pressure and menstrual pain in patients with primary dysmenorrhea. Am J Obstet Gynecol 1994;170:123–9.PubMedGoogle Scholar
  93. 93.
    Mulcahy D, Keegan J, Crean P, et al. Silent myocardial ischemia in chronic stable angina: a study of its frequency and characteristics in 150 patients. Br Heart J 1988;60:417–23.PubMedGoogle Scholar
  94. 94.
    Mulcahy R, Awadhi AH, de Bulleor M, et al. Natural history and prognosis of unstable angina. Am Heart J 1985;109:753–8.PubMedGoogle Scholar
  95. 95.
    Nesto RW, Kowalchuk GJ. The ischemic cascade: temporal sequence of hemodynamic, electrocardiographic and symptomatic expressions of ischemia. Am J Cardiol 1987;57:23C-30C.Google Scholar
  96. 96.
    Norrsell H, Eliasson T, Mannheimer C, et al. Effects of pacinginduced myocardial stress and spinal cord stimulation on whole body and cardiac norepinephrine spillover. Eur Heart J 1997; 18:1890–6.PubMedGoogle Scholar
  97. 97.
    Pepine CJ, Coha PF, Deedwania PC, et al. Effects of treatment on outcome in mildly symptomatic patients with ischemia during daily life. The atenolol silent ischemia study (ASIST). Circulation 1994;90:762–8.PubMedGoogle Scholar
  98. 98.
    Perl ER. Is pain a specific sensation? J Psychiat Res 1971;8: 273–87.PubMedGoogle Scholar
  99. 99.
    Perna G, Stanislao M, Salavatori MP, et al. Basal plasma betaendorphin and beta-lipotropin in patients, with symptomatic and asymptomatic myocardial ischemia. Cardiologia 1988;33:765–9.PubMedGoogle Scholar
  100. 100.
    Richter JE. Investigation and management of non-cardiac chest pain. Baillière’s Clin Gastroenterol 1991;5:281–306.Google Scholar
  101. 101.
    Richter JE. The esophagus and noncardiac chest pain. In: Castell DO. The esophagus, 2nd edn. Little Brown and Company. Boston 1995;699–724.Google Scholar
  102. 102.
    Richter JE, Barish CF, Castell DO. Abnormal sensory perception in patients with esophageal chest pain. Gastroenterology 1996;91: 845–52.Google Scholar
  103. 103.
    Ros E, Armengol X, Grande L, et al. Chest pain at rest in patients with coronary artery disease. Dig Dis Sci 1997;42:1344–53.PubMedGoogle Scholar
  104. 104.
    Ruch TC. Visceral sensation and referred pain. In: Howell’s textbook of physiology. Philadelphia. Saunders 1946:385–401.Google Scholar
  105. 105.
    Sanderson JE, Woo KS, Chung HK, et al. The effect, of transcutaneous electrical nerve stimulation on coronary and systemic haemodynamics in syndrome X. Coron Art Dis 1996;7:547–52.Google Scholar
  106. 106.
    Schuster EH, Bulkley BH. Early post-infarction angina: Ischemia at a distance and ischemia in the infarct zone. N Engl J Med 1981;305:1101–5.PubMedGoogle Scholar
  107. 107.
    Serneri GGN, Prisco D, Martini F, et al. Acute T-cell activation is detectable in unstable angina. Circulation 1997;95:1806–12.Google Scholar
  108. 108.
    Singh S, Richter JE, Hewson EG, et al. The contribution of gastroesophageal reflux to chest pain in patients with coronary artery disease. Ann Intern Med 1992;117:824–30.PubMedGoogle Scholar
  109. 109.
    Stone PH, Gibson RS, Glasser SP, et al. Comparison of propranolol, diltiazem and nifedipine in the treatment of ambulatory ischemia in patients with stable angina. Circulation 1990;82:1962–72.PubMedGoogle Scholar
  110. 110.
    Sylvén C. Angina pectoris. Clinical characteristics, neurophysiological and molecular mechanisms — a review. Pain 1989;36: 145–67.PubMedGoogle Scholar
  111. 111.
    Sylvén C, Beermann B, Jonzon B, et al. Angina pectoris-like pain provoked by intravenous adenosine in healthy volunteers. Br Med J 1986;293:227–30.Google Scholar
  112. 112.
    Sylvester K, Kendall GPN, Lennard-Jones JE. Treatment of functional abdominal pain by transcutaneous nerve stimulation. Br Med J 1986;293:481–2.Google Scholar
  113. 113.
    Taylor P, Hallett M, Flaherty L. Treatment of osteoarthritis of the knee with transcutaneous electrical nerve stimulation. Pain 1981;11:233–40.PubMedGoogle Scholar
  114. 114.
    Ten Vaarweerk IAM, Jessurun GAJ, Hautwast R, et al. Mortality and morbidity in patients treated with spinal cord stimulation for intractable angina pectoris. Heart (accepted for publication).Google Scholar
  115. 115.
    Thompson SG, Kienast J, Pyke SDM, et al. Homeostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. N Engl J Med 1995;332:635–41.PubMedGoogle Scholar
  116. 116.
    Thorsteinsson G, Stonnington HH Stillwell GK, et al. Transcutaneous electrical stimulation: a double-blind trial of its efficacy for pain. Arch Phys Med Rehab 1977;58:8–13.Google Scholar
  117. 117.
    Tijssen JG, Lubsen J. Early treatment of unstable angina with nifedipine and metoprolol — the HINT trial. J Cardiovasc Pharmacol 1988;12:Suppl 1:S71–7.Google Scholar
  118. 118.
    Toss H, Lindahl B, Siegbahn A, et al. Prognostic influence of increased fibrinogen and C-reactive protein level in unstable coronary artery disease. Circulation 1997;96:4201–10.Google Scholar
  119. 119.
    Traube M, Albibi R, McCallum RW. High-amplitude peristaltic esophageal contractions associated with chest pain. JAMA 1983;250:2655–9.PubMedGoogle Scholar
  120. 120.
    Tzivoni D, Gavish A, Zin D, et al. Prognostic significance of ischemic episodes in patients with previous myocardial infarction. Am J Cardiol 1988;62:661–4.PubMedGoogle Scholar
  121. 121.
    Vander Ark GD, McGrath KA. Transcutaneous electrical stimulation in treatment of postoperative pain. Am J Surg 1975; 130:338–40.Google Scholar
  122. 122.
    Vantrappen G, Janssens J. Angina and oesophageal pain — a gastroenterologist’s point of view. Eur Heart J 1986;7:828–34.PubMedGoogle Scholar
  123. 123.
    von Arnim T. Prognostic significance of transient ischemic episodes: Response to treatment shows improved prognosis. Results of the Total ischemic burden bisoprolol study (TIBBS). Follow up. J Am Coll Cardiol 1996;28:20–4.Google Scholar
  124. 124.
    Wall PD, Melzack R. Textbook of pain. 3rd edn. New York: Churchill Livingstone 1997.Google Scholar
  125. 125.
    Walsh DM. TENS Clinical applications and related theory. New York: Churchill Livingstone, 1997.Google Scholar
  126. 126.
    Walsh DM, Foster NF, Baxter GD, et al. Transcutaneous electrical nerve stimulation. Relevance of stimulation parameters to neurophysiological and hypoalgesic effects. Am J Phys Med Rehab 1995;74:199–206.Google Scholar
  127. 127.
    Webb SC, Poole-Wilson PA. Potassium exchange in the human heart during atrial pacing and myocardial ischaemia. Br Heart J 1986;55:554–9.PubMedGoogle Scholar
  128. 128.
    Weidinger F, Hammerle A, Sochor H, et al. Role of beta-endorphins in silent myocardial ischemia. Am J Cardiol 1986;58: 428–30.PubMedGoogle Scholar
  129. 129.
    White CW. Clinical applications of Doppler coronary flow reserve measurements. Am J Cardiol 1993;71:10D-6D.PubMedGoogle Scholar
  130. 130.
    Willerson JT, Golino P, Eidt J, et al. Specific platelet mediators and unstable coronary artery lesions. Circulation 1989;80: 198–205.PubMedGoogle Scholar

Copyright information

© Urban & Vogel 1999

Authors and Affiliations

  1. 1.Department of Medicine, Multidisciplinary Pain CenterSahlgrenska University Hospital/ÖstraGöteborgSweden

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