, Volume 43, Supplement 1, pp 9–14 | Cite as

Management of Angina Pectoris

Modern Concepts
  • Elieser Kaplinsky


While William Heberden gave us an excellent clinical description of angina pectoris more than 200 years ago, the understanding and management of this disorder have undergone major development since then, and especially so in recent years. The pathological basis for the disease was established shortly after Heberden’s account. The concept of the imbalance between supply and demand was postulated in the nineteenth century. Recent progress has been made in mainly three areas: the better definition of prognosis, new insights into pathophysiology, and newer management modalities and aims. Today, the combination of the patient’s functional state (exercise test), his heart (ventricular function) and coronary anatomy (angiography) enables us to accurately define the prognosis of the disease. Sophisticated studies have now demonstrated that during an exercise-induced angina attack there is a reduction in coronary blood flow and an increase in coronary resistance. Mechanisms associated with the angina attack involve the sclerotic epicardial arteries and the microcirculation. Further major advances in the medical management of angina pectoris now depend on our ability to improve prognosis and retard the development of the atherosclerotic process.


Verapamil Angina Pectoris Calcium Antagonist Coronary Blood Flow Gallopamil 
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. β-Blocker Heart Attack Research Group. A randomized trial of propranolol in patients with acute myocardial infarction. I. Mortality results. Journal of the American Medical Association 247: 1707–1714, 1982CrossRefGoogle Scholar
  2. Brocem BG, Lee AB, Bodson EL, Dodge HT. Reflex constriction of significant coronary stenosis as a mechanism contributing to ischemic left ventricular dysfunction during isometric exercise. Circulation 70: 18–24, 1984CrossRefGoogle Scholar
  3. Burns A. Observations on some of the most frequent and important diseases of the heart. Thomas Bryce, Edinburgh 1809Google Scholar
  4. S Principle Investigators and Their Associates: Coronary Artery Surgery Study (CASS): a randomized trial of coronary bypass surgery. Data Circulation 68: 939–950, 1983CrossRefGoogle Scholar
  5. Danish Study Group on Verapamil in Myocardial Infarction. Effect of verapamil on mortality and major events after acute myocardial infarction (The Danish Verapamil Infarction Trial II — DAVIT II). American Journal of Cardiology 66: 779–785, 1990CrossRefGoogle Scholar
  6. De Servi S, Mazzone A, Ricevuti G, Fioravanti A, Bramucci E, et al. Granulocyte activation after coronary angioplasty in humans. Circulation 82: 140–146, 1990PubMedCrossRefGoogle Scholar
  7. Epstein SE, Talbot TL. Dynamic coronary tone in precipitation, exacerbation, and relief of angina pectoris. American Journal of Cardiology 48: 797–803, 1981PubMedCrossRefGoogle Scholar
  8. Ernst E, Matai A. Haemorrhoealogical effects of gallopamil in angina pectoris. A controlled study. In Bender F, Meesmann W (Eds) Treatment with gallopamil, pp. 25–30, Steinkopff, Damstadt, 1989CrossRefGoogle Scholar
  9. Fleet WF, Johnson TA, Graebner LA, Engle CL, Gettes LS. Effects of verapamil in ischemia-induced changes in extracellular K+,p4 and local activation in the pig. Circulation 73: 837–846, 1986PubMedCrossRefGoogle Scholar
  10. Gallagher KP, Matsuzaki M, Koziol JA, Kemper WS, Ross Jr J. Regional myocardial perfusion and wall thickening during ischemia in conscious dogs. American Journal of Physiology 247: H727–H738, 1984PubMedGoogle Scholar
  11. Gallagher KP, Matsuzaki M, Osakada G, Kemper WS, Ross Jr J. Effect of exercise on the relationship between myocardial blood flow and systolic wall thickening in dogs with acute coronary stenosis. Circulation Research 52: 716–729, 1983PubMedCrossRefGoogle Scholar
  12. Gould KL, Lipscomb K. Effect of coronary stenosis on coronary flow reserve and resistance. American Journal of Cardiology 35: 48–55, 1974CrossRefGoogle Scholar
  13. Heberden W. Some account of disorder of the breast. Medical Transcript of the Royal College of Physicians 2: 59, 1772Google Scholar
  14. Heusch G, Deussen A. The effect of cardiac sympathetic nerve stimulation on perfusion of stenotic coronary arteries in the dog. Circulation Research 53: 8–15, 1983PubMedCrossRefGoogle Scholar
  15. Hurst JW, King III SB, Friesinger GC, Walter OF, Morris DC. Atherosclerotic coronary heart disease: recognition, prognosis and treatment. In Hurst JW (Ed.) The Heart, p. 884, McGraw Hill, New York, 1986Google Scholar
  16. Lichtlen PR, Hugenholtz PG, Rafflenbeul W, Hecker H, Jost S, et al. On behalf of the INTACT group investigators. Retardation of angiographic progression of coronary artery disease by nifedipine. Lancet 335: 1109–1113, 1990PubMedCrossRefGoogle Scholar
  17. Ludmer PL, Selwyn AP, Shook TL, Wayne RR, Mudge GH, et al. Paradoxical vasoconstriction induced by acetylcholine in atherosclerotic coronary arteries. New England Journal of Medicine 315: 1046–1051, 1986PubMedCrossRefGoogle Scholar
  18. Nayler WG, Ferrari R, Williams A. Protective effect of pretreatment with verapamil, nifedipine and propranolol on mitochondrial function in the ischemic and reperfused heart. American Journal of Cardiology 46: 242–248, 1980PubMedCrossRefGoogle Scholar
  19. Mork MB, Ringqvist I, Fisher LD, et al. Survival of medically treated patients in the Coronary Artery Surgery Study (CASS) registry. Circulation 66: 562–568, 1982CrossRefGoogle Scholar
  20. Multicenter Diltiazem Postinfarction Trial Research Group. The effect of diltiazem and mortality and reinfarction after myocardial infarction. New England Journal of Medicine 319: 385–392, 1988CrossRefGoogle Scholar
  21. Osakada G, Kumada T, Gallagher KP, Kemper WS, Ross Jr J. Reduction of exercise-induced ischemic regional myocardial dysfunction by verapamil in conscious dogs. American Heart Journal 101: 707–712, 1981PubMedCrossRefGoogle Scholar
  22. Parmley WW, Blumlein S, Sievers R. Modification of experimental atherosclerosis by calcium channel blockers. American Journal of Cardiology 55: 165B–171B, 1985PubMedCrossRefGoogle Scholar
  23. Perez JE, Sobel BE, Henry PD. Improved performance of ischemic canine myocardium in response to nifedipine and diltiazem. American Journal of Physiology 239: H658–H663, 1980PubMedGoogle Scholar
  24. Pupita G, Maseri A, Koski JC, Galassi AR, Gavrielides S, et al. Myocardial ischemia caused by distal coronary artery constriction in stable angina pectoris. New England Journal of Medicine 323: 514–519, 1990PubMedCrossRefGoogle Scholar
  25. Rauch B, Neumann J, Richardt G, Kranzhofen R, Barth R, et al. Effect of gallopamil on myocardial ischemia during percutaneous transluminal coronary angioplasty. Drugs 42(Suppl. 1): 31–36, 1991PubMedCrossRefGoogle Scholar
  26. Seitelberger R, Guth BD, Heusch G, Katayama K, Lee JD, et al. Intracoronary alpha-2 adrenergic receptor blockade attenuates ischemia in conscious dogs during exercise. Circulation Research 62: 436–442, 1988PubMedCrossRefGoogle Scholar
  27. Weiner DA, Ryan TJ, McCabe CH, Chaitman LT, Sheffield LT, et al. Prognostic importance of a clinical profile and exercise in medically treated patients with coronary artery disease. Journal of the American College of Cardiology 3: 772–779, 1984PubMedCrossRefGoogle Scholar
  28. Yusuf S, Peto R, Lewis J, Collins R, Sleight P. Beta blockade during and after myocardial infarction: an overview of the randomized trials. Progress in Cardiovascular Diseases 27: 335–371, 1985PubMedCrossRefGoogle Scholar

Copyright information

© Adis International Limited 1992

Authors and Affiliations

  • Elieser Kaplinsky
    • 1
    • 2
  1. 1.Sheba Medical CenterThe Heart InstituteTel-HashomerIsrael
  2. 2.Sackler School of MedicineTel-AvivIsrael

Personalised recommendations