Increased Plasma Membrane Ion-Leakage: A New Hypothesis for Chest Pain and Normal Coronary Arteriograms

  • Anders Waldenström
  • Gunnar Ronquist
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 213)

Abstract

Approximately 10–15% of all patients in the US who are subjected to coronary angiography because of anginal chest pain do not show any obvious coronary artery disease. Approximately 15% of these patients have 201-thallium myocardial perfusion defects [1,2]. Despite the normal coronary angiogram most physicians still consider the patients symptoms being due to insufficient myocardial blood perfusion. This is not surprising given the fact that symptoms in this syndrome clearly suggest the presence of myocardial ischemia. Among these are: angina pectoris like chest pains, transient ECG changes suggestive of myocardial ischemia, and myocardial perfusion defects as assessed by 201-thallium scintigraphy. Interestingly, a sizeable proportion of patients with chest pain and normal coronary arteriograms have unexplained fatigue.

Keywords

Fatigue Hydrolysis Ischemia Lactate Adenosine 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Kemp HG: Left ventricular function in patients with the anginal syndrome and normal coronary angiograms. Am J Cardiol 1973; 32:375–376.PubMedCrossRefGoogle Scholar
  2. 2.
    Hutchison SJ, Poole-Wilson PA, Henderson AH: Angina with Normal Coronary Arteries: A review. Quart J Med 1988;72, No 268, pp.677–688.Google Scholar
  3. 3.
    Lagerqvist B, Sylvén Ch, Hedenström H & Waldenström A: Intravenous adenosine but not its first metabolite inosine provokes chest pain in healthy volunteers. J Cardiovasc Pharmacol 1990;16:173–176.PubMedCrossRefGoogle Scholar
  4. 4.
    Lagerqvist B, Sylvén C, Helmius G & Waldenström A: Effects of exogenous adenosine in a patient with transplanted heart. Evidence for adenosine as a messenger in angina. Upsala J Med Sci 1990;95:137–145.PubMedCrossRefGoogle Scholar
  5. 5.
    Lagerqvist B, Sylvén C, Beerman B, Helmius G, Waldenström A. Intracoronary adenosine causes angina pectoris like pain - an inquiry into the nature of visceral pain. Cardiovasc Res 1990; 24:609–13.PubMedCrossRefGoogle Scholar
  6. 6.
    Lagerqvist B, Sylvén C, Theodorsen E, Kaijser L, Helmius G, Waldenström A. Adenosine-induced chest pains - a comparison between intracoronary bolus injection and steady-state infusion. Cardiovasc Res 1992; 26:810–14.PubMedCrossRefGoogle Scholar
  7. 7.
    Lagerqvist B, Sylvén C, Waldenström A. Lower threshold for adenosine-induced chest pain in patients with angina and normal coronary angiograms. Br Heart J 1992; 68:282–285.PubMedCrossRefGoogle Scholar
  8. 8.
    Lagerqvist B, Bylund H, Götell P, Mannting F, Sandhagen B, Waldenström A. Coronary artery vaso-regulation and left ventricular function in patients with angina pectoris-like pain and normal coronary angiograms. J Int Med 1991; 230:55–65.CrossRefGoogle Scholar
  9. 9.
    Masahiro M, Masamichi K, Kensuke E, Hirofumi T, Toshihiro I, Hiroaki S, Akira T. Angina pectoris caused by coronary microvascular spasm. Lancet 1998; 351:1144–45.CrossRefGoogle Scholar
  10. 10.
    Kaski J C. Chest pain and normal coronary arteriograms: role of “microvascular spasm”. The Lancet 1998; 351:1165–69.CrossRefGoogle Scholar
  11. 11.
    Weiss JN, Lamp ST. Glycolysis preferentially inhibits ATP-sensitive K+ channels in isolated guinea pig cardiac myocytes. Science 1987; 283:67–69.CrossRefGoogle Scholar
  12. 12.
    Waldenström A, Ronquist G & Lagerqvist B. Angina pectoirs patients with normal coronary angiograms but abnormal thallium perfusion schan exhibit low myocardial and skeletal muscle energy charge. J Int Med 1992; 231: 327–31.CrossRefGoogle Scholar
  13. 13.
    Soussi B, Scherstén T, Waldenström A & Ronquist G. Phosphocreatine turnover and pH balance in forearm muscle of patients with syndrome X. Lancet 1993; 341: 829–830.PubMedCrossRefGoogle Scholar
  14. 14.
    Engström I, Waldenström A & Ronquist G. Ionophore A23187 reduces energy charge by enhanced ion pumping in suspended human erythrocytes. Scand J Clin Lab Invest 1993; 53: 239–246.PubMedCrossRefGoogle Scholar
  15. 15.
    Engstrom I, Waldenström A & Ronquist G. Effects of the ionophore gramicidin D on energy metabolism in human erythrocytes. Scand J Clin Lab Invest 1993; 53:247–252.PubMedCrossRefGoogle Scholar
  16. 16.
    Engström I, Waldenström A & Ronquist G. Dissipation of the calcium gradient in human erythrocytes results in increased heat production. Clin Chim Acta 1993; 219: 113–122.PubMedCrossRefGoogle Scholar
  17. 17.
    Martinussen HJ, Waldenström A & Ronquist G. Functional and biochemical effects of a K+-ionophore on the isolated perfused rat heart. Acta Physiol Scand 1993; 147: 221–225.PubMedCrossRefGoogle Scholar
  18. 18.
    Waldenström A, Fohlman J, Ilbäck N-G, Ronquist G, Häggren R & Gerdin B. Coxsacke B3 myocarditis induces a decrease in energy charge and accumulation of hyaluronan in the mouse heart. Eur J Clin Invest 1993; 23: 277–282.PubMedCrossRefGoogle Scholar
  19. 19.
    Ronquist G, Frithz G, Soussi B, Scherstén T & Waldenström A. Disturbed energy balance in skeletal muscle of patients with untreated primary hypertension. J Int Med 1995; 238: 167–174.CrossRefGoogle Scholar
  20. 20.
    Engström I, Ronquist G, Pettersson L & Waldenström A. Alzheimer amyloid B-peptides exhibit ionophore like properties in human erythrocytes. Eur J Clin Invest 1995; 25: 471–476.PubMedCrossRefGoogle Scholar
  21. 21.
    Sanderson KL, Butler L, Ingram VM. 1997. Aggregates of a ß-amyloid peptide are required to induce calcium currents in neuron-like human teratocarcinoma cells: relation to Alzheimer’s disease. Brain Res 744:7–14.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1999

Authors and Affiliations

  • Anders Waldenström
  • Gunnar Ronquist

There are no affiliations available

Personalised recommendations