C. Mechanism of Pain
When a coronary artery is severely obstructed with plaque, the heart muscle still receives an adequate amount of oxygen when the heart is at rest and beating slowly at about 72 beats per minute. During exertion or undue stress, however, the heart rate may increase from 72 to 90 or more beats per minute. A faster heart rate entails more work for the heart, which in turn requires more oxygen to accomplish the work. The obstruction to the artery does not allow sufficient oxygenated blood to reach the heart muscle. During those few moments, the lack of oxygen causes the heart muscle to become painful, and this sensation is perceived by the individual as pain or merely a mild but bothersome discomfort in the chest.
Myocardial ischemia is a dynamic process. Three deter¬minants play a major role in its pathogenesis:
1. Obstruction of a coronary artery by atheroma occludes the artery in a concentric process and is commonly observed in patients with stable angina, but in those with unstable angina the plaques are eccentric
2. Increased myocardial oxygen demand by the vigorously pumping heart muscle
3. A release of catecholamine occurs at the onset of angina and during the episode in most patients with stable angina; release of catecholamine may actually initiate ischemia, which stimulates further catecholamine release, and the vicious circle perpetuates the lack of oxygen by the myocardium, see Fig. 2

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