Pathophysiology of Anginal Pain

For a detailed discussion of the pathophysiology of ischemia, see Chap.,.4.7,. In brief, angina pectoris can be defined as any pain syndrome that is caused by lack of oxygen supply to the heart. Anginal symptoms are typically caused by obstructive coronary artery disease or coronary spasm, or both. Atherosclerotic plaques lining the walls of coronary arteries cause luminal stenosis in patients with coronary artery disease. During periods of low myocardial oxygen demand, blood flow through the stenosed vessels may be adequate to meet demand. However, during times of increased oxygen demand, flow through the fixed lesion is limited and the region of myocardium supplied by the affected vessel may become ischemic. Cardiac myocytes respond to oxygen deprivation by switching from aerobic to anaerobic metabolism, during which sufficient ATP cannot be produced to meet the metabolic demands of the cell. The lack of ATP causes dysfunction of all intracellular ATP-dependent processes, including ion channels in the sarcoplasmic and cell membranes, causing diminished contractility and cell integrity. Chemical mediators are subsequently released, stimulating visceral afferent nerve fibers in sympathetic nerves of coronary vessels. These nerves travel through deep and superficial cardiac plexuses and the sympathetic ganglia and enter the spinal cord through the lower cervical and upper five thoracic spinal nerve roots. Because of this wide spinal cord distribution of the cardiac pain fibers, the cerebral cortex often misinterprets the location and origin of the pain, therefore confusing myocardial ischemia with pain from any of the other structures in the chest.

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