Update 1988 pp 271-279 | Cite as

Coronary Vasomotor Tone: Implications in Ischemic Heart Disease

  • G. Berkenboom
  • P. Unger
Part of the Update in Intensive Care and Emergency Medicine book series (UICM, volume 5)


In the early 1950’s, the increase in myocardial oxygen demand was seen as the main mechanism responsible for episodes of angina pectoris [1]. The coronary stenosis was indeed considered as a fixed obstruction on the epicardial vessel, limiting the capacity of the coronary artery to augment coronary flow. Myocardial ischemia was assumed to occur for a given and very reproducible level of myocardial oxygen demands. However, this concept was progressively refuted by the development of coronary angiography. In 1959, Prinzmetal et al. [2] described a group of patients with typical angial pain which was provoked by large vessel coronary spasms, pointed out by coronary angiography. Moreover from angiographic studies [3], even severe atherosclerotic epicardial vessels appear to retain the capacity to dilate and to constrict. Pharmacological studies of isolated human coronary arteries [4] have also shown that severe atherosclerotic segments are not rigid structure.


Angina Pectoris Unstable Angina Myocardial Blood Flow Coronary Blood Flow Chronic Stable Angina 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Blumgart HL, Schlesinger MJ, Davis D (1940) Studies on the relation of the clinical manifestations of angina pectoris, coronary thrombosis and myocardial infarction to the pathologic findings. Am Heart J 19:1–91.CrossRefGoogle Scholar
  2. 2.
    Prinzmetal M, Kenamer R, Merliss R, et al (1959) Angina pectoris I. A variant form of angina pectoris. Am J Med 27:375–388.PubMedCrossRefGoogle Scholar
  3. 3.
    Brown GB, Bolson E, Dodge HT (1984) Dynamic mechanisms in human coronary stenosis. Circulation 70:917–922.PubMedCrossRefGoogle Scholar
  4. 4.
    Ginsburg R, Bristow M, Davis K, Dibiase A, Billingham ME (1984) Quantitative pharmacologic responses of normal and atherosclerotic isolated human epicardial coronary arteries. Circulation 69:430–440.PubMedCrossRefGoogle Scholar
  5. 5.
    Shepherd JT, Vanhoutte PM (1985) Spasm of the coronary arteries: causes and consequences. (The scientist’s viewpoint). Mayo Clin Proc 60:33–46.PubMedGoogle Scholar
  6. 6.
    Berkenboom G, Depierreux M, Fontaine J (1987) The influence of atherosclerosis on the mechanical responses of isolated human coronary arteries to substance P, isoprenaline and noradrenaline. Br J Pharmacol 92:113–120.PubMedGoogle Scholar
  7. 7.
    Kawachi Y, Tomoike H, Maruoka Y, et al (1984) Selective hypercontraction caused by ergonovine in the canine coronary artery under conditions of induced atherosclerosis. Circulation 69:441–450.PubMedCrossRefGoogle Scholar
  8. 8.
    Yasue H, Touyama M, Kato H, Tanaka S, Akiyama F (1976) Prinzmetal’s variant form of angina as a manifestation of alpha-adrenergic receptor mediated coronary artery spasm: documentation by coronary arteriography. Am Heart J 91:148–153.PubMedCrossRefGoogle Scholar
  9. 9.
    Ginsburg R, Bristow MR, Kantrowitz N, Bairn DS, Harrison DC (1981) Histamine provocation of clinical coronary artery spasm: implications concerning pathogenesis of variant angina pectoris. Am Heart J 109:819–822.CrossRefGoogle Scholar
  10. 10.
    Yasue H, Horio Y, Nakamura N, et al (1986) Induction of coronary artery spasm by acetylcholine in patients with variant angina: possible role of the parasympathetic nervous system in the pathogenesis of coronary artery spasm. Circulation 74:955–963.PubMedCrossRefGoogle Scholar
  11. 11.
    Hillis LD, Braunwald E (1978) Coronary artery spasm. N Engl J Med 299:695–701.PubMedCrossRefGoogle Scholar
  12. 12.
    Kaski JC, Crea F, Meran DO, et al (1986) Local coronary supersensitivity to diverse vasoconstrictor stimuli in patients with variant angina. Circulation 74:1255–1265.PubMedCrossRefGoogle Scholar
  13. 13.
    Mudge GH, Grossman W, Mills RM, Lesch M, Braunwald E (1976) Reflex increase in coronary vascular resistance in patients with ischemic heart disease. N Engl J Med 295:1333–1337.PubMedCrossRefGoogle Scholar
  14. 14.
    Brown BG, Lee AB, Bolson EL, Dodge HT (1984) Reflex constriction of significant coronary stenosis as a mechanism contributing to ischemic left ventricular dysfunction during isometric exercise. Circulation 70:18–24.PubMedCrossRefGoogle Scholar
  15. 15.
    Gage JE, Hess OM, Murakami T, Ritter M, Grimm J, Kreienbuehl HP (1986) Vasoconstriction of stenotic coronary arteries during dynamic exercise in patients with classic angina pectoris: reversibility by nitroglycerin. Circulation 73:865–876.PubMedCrossRefGoogle Scholar
  16. 16.
    Berkenboom G, Abramowicz M, Vandermoten P, Degre S (1986) Role of alpha-adrenergic coronary tone in exercise — induced angina pectoris. Am J Cardiol 57:195–198.PubMedCrossRefGoogle Scholar
  17. 17.
    Cohn PF (1987) Total ischemic burden: pathophysiology and prognosis. Am J Cardiol 59:3C–6C.PubMedCrossRefGoogle Scholar
  18. 18.
    Fox KM, Jonathan A, Selwyn AP (1982) Effects of platelet inhibition on myocardial ischemia. Lancet 2:727–730.PubMedCrossRefGoogle Scholar
  19. 19.
    Braunwald E, Cohn PF (1984) Unstable angina. In: Maseri A, Goodwin JF (eds) Hammersmith cardiology workshop series, vol 1. Raven Press, New York, pp 161–167.Google Scholar
  20. 20.
    Chierchia S, Brunelli C, Simonetti I, Lazzari M, Maseri A (1980) Sequence of events in angina at rest: primary reduction in coronary flow. Circulation 61:759–768.PubMedGoogle Scholar
  21. 21.
    Ambrose JA, Winters SL, Stern A, Eng A (1985) Angiographic morphology and the pathogenesis of unstable angina pectoris. J Am Coll Cardiol 5:609–614.PubMedCrossRefGoogle Scholar
  22. 22.
    Simoons ML, Balakumaran K (1981) The effects of drugs on the exercise electrocardiogram. Cardiology (suppl 2) 68:124–132.Google Scholar
  23. 23.
    Abrams J (1987) Tolerance to organic nitrates. Circulation 74:1185–1187.Google Scholar
  24. 24.
    May DC, Pupma JJ, Black WH, et al (1987) In vivo induction and reversal of nitroglycerin tolerance in human coronary arteries. N Engl J Med 317:805–809.PubMedCrossRefGoogle Scholar
  25. 25.
    Parker JO, Farrell B, Lahey KA, Rose BF (1987) Nitrate tolerance: the lack of effect of N-acetylcysteine. Circulation 76:572–576.PubMedCrossRefGoogle Scholar
  26. 26.
    Kukovetz WR, Holzmann S (1985) Mechanism of vasodilation by molsidomine. Am Heart J 109:637–640.PubMedCrossRefGoogle Scholar
  27. 27.
    Berkenboom G, Fontaine J, De Smet JM, Degre S (1987) Comparison of the effect of beta-adrenergic antagonists with different ancillary properties on isolated canine and human coronary arteries. Cardiovasc Res 21:299–304.PubMedCrossRefGoogle Scholar
  28. 28.
    Glazier J, Chierchia S, Gerosa S, Crean P, Berkenboom G, Maseri A (1986) Atenolol prevents silent and painful ischemia in patients with mixed angina. Circulation 74:11–45 (abst).Google Scholar
  29. 29.
    Stone PH, Antman EM, Muller JE, Braunwald E (1980) Calcium channel blocking agents in the treatment of cardiovascular disorders. Part II: Hemodynamic effects and clinical applications. Ann Int Med 93:886–891.PubMedGoogle Scholar
  30. 30.
    Hossak KF, Brown BG, Stewart DK, Dodge HT (1984) Diltiazem-induced blockade of sympathetically mediated constriction of normal and diseased coronary arteries: lack of epicardial coronary dilator effect in humans. Circulation 70:465–471.CrossRefGoogle Scholar
  31. 31.
    Specchia G, De Servi S, Falcone C, et al (1983) Effects of nifedipine on coronary hemodynamic findings which exercise in patients with stable exertional angina. Circulation 68:1035–1043.PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1988

Authors and Affiliations

  • G. Berkenboom
  • P. Unger

There are no affiliations available

Personalised recommendations