Abstract
The traditional view that coronary stenoses cause myocardial ischemia by limiting increases in blood flow is now thought to be incomplete. Convincing evidence has accumulated that coronary narrowings play an active role in causing ischemia by intermittently interfering with coronary blood flow, not only among patients with the rare Prinzmetal’s variant angina, but also in nearly all patients with unstable and stable forms of angina pectoris (1, 2, 6, 7, 10, 13, 31). Studies of Chierchia and colleagues (2) in patients with unstable angina demonstrated a fall in coronary sinus oxygen saturation which could not be explained by a simultaneous increase in myocardial oxygen demand. Selwyn (1981) used radionuclides to monitor myocardial perfusion in patients with stable angina during rapid atrial pacing and found a net fall in myocardial blood flow in regions distal to coronary stenosis. More recently, positron emission tomography was used to assess changes in regional myocardial perfusion in patients with stable angina using rubidium-82. These studies also demonstrated decreases in regional blood flow which accompanied ischemia triggered by exercise, cold pressor stimulation or mental stress (6, 7). Ganz and colleagues (13) in patients with unstable angina directly measured coronary stenosis resistance by simultaneously determing pressure gradients and blood flow across moderately severe coronary narrowings, and they demonstrated increases in stenosis resistance both preceding and at the onset of episodes of ischemia.
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© 1991 Dr. Dietrich Steinkopff Verlag GmbH & Co. KG, Darmstadt
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Ganz, P. et al. (1991). Coronary vasospasm in humans: the role of atherosclerosis and of impaired endothelial vasodilator function. In: Drexler, H., Zeiher, A.M., Bassenge, E., Just, H. (eds) Endothelial Mechanisms of Vasomotor Control. Steinkopff. https://doi.org/10.1007/978-3-642-72461-9_21
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DOI: https://doi.org/10.1007/978-3-642-72461-9_21
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