Summary
The very first presentation of ischemic heart disease-acute infarction, sudden death, or unstable angina-most often occurs abruptly. The first approximation that it occurs as a random event only when a certain “threshold severity” of coronary atherosclerosis has gradually developed, although widely accepted, should perhaps be reconsidered and expanded on the basis of the following considerations. Acute coronary occlusion leading to myocardial infarction often occurs at the site of mild or noncritical coronary stenoses. Conversely, in patients with chronic angina severe coronary stenoses can remain unchanged for years with no detectable progression. When a coronary artery occludes, the size of infarction can vary greatly, and when ischemia and infarction occur, malignant arrhythmias occur in some patients but not in others.
Thus, in a second approximation, ischemic heart disease should be considered as the result of the variable combination of three major components: a) A very variable chronic atherosclerotic background, which can result from a variety of pathologic processes; b) A number of acute ischemic stimuli, which can unpredictably impair myocardial blood flow as a result of coronary thrombosis and/or vasoconstriction; c) A variable response of the heart to a sudden reduction of coronary blood flow in terms of collateral perfusion and malignant arrhythmias.
Therefore, at one extreme end of the spectrum in any individual, ischemic syndromes may present predominantly as a result of an extremely large chronic background component. At the other extreme, powerful acute ischemic stimuli can unexpectedly impair blood supply by coronary thrombosis, constriction, or their combination, in the presence of a mild chronic atherosclerotic background. A fatal outcome can result from an arrhythmia caused by acute myocardial ischemia, which might have been transient or which might have caused a small infarction. The consideration of the separate pathogenetic and etiologic causes of these three components should set the stage for more understanding of the causes of ischemic syndromes, their rational management, and specific prevention.
Similar content being viewed by others
Explore related subjects
Discover the latest articles and news from researchers in related subjects, suggested using machine learning.References
Solberg LA, Strong JP. Risk factors and atherosclerotic lesions. A review of autopsy studies. Arteriosclerosis 1983;3:187–198.
Fuster V. Badimon L, Cohen M, et al. Insights into the pathogenesis of acute ischemic syndromes. Circulation 1988;77:1213–1220.
Hackett D, Davies G, Maseri A. Pre-existing coronary stenoses in patients with first myocardial infarction are not necessarily severe. Eur Heart J 1988;9:1317–1323.
Little WC, Constantinescu M, Appelgate RJ, et al. Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild to moderate coronary artery disease? Circulation 1988;78:1157–1166.
Falk E. Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis: Characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi, Br Heart J 1983;50:127–134.
Davis MJ, Thomas AC. Plaque fissuring: The cause of acute myocardial infarction, sudden ischaemic death and crescendo angina. Br Heart J 1985;53:363–373.
Maseri A, Chierchia S, Davis GJ. Pathophysiology of coronary occlusion in acute infarction. Circulation 1986;73:233–239.
Willerson JT, Hillis LD, Winniford M, et al. Speculation regarding mechanisms responsible for acute ischemic heart disease syndromes. J Am Coll Cardiol 1986;8:245–250.
Maseri A, Davies G, Hackett D, et al. Coronary artery spasm and coronary vasoconstriction: The case for a distinction. Circulation 1990;81:1983–1991.
Maseri A, Chierchia S, Davies G, et al. Mechanisms of ischemic cardiac pain and silent myocardial ischemia. Am J Med 1985;79(Suppl 3A):7–11.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Maseri, A. Mechanisms of myocardial ischemia. Cardiovasc Drug Ther 4 (Suppl 4), 827–831 (1990). https://doi.org/10.1007/BF00051288
Issue Date:
DOI: https://doi.org/10.1007/BF00051288