Myocardial ischemia caused by distal coronary-artery constriction in stable angina pectoris

Article Abstract:

The coronary arteries are the vessels which bring oxygenated (oxygen-rich) blood to the heart muscle itself. When coronary vessels become blocked because of disease, the flow of blood to the areas which they serve is greatly reduced. This reduction in blood flow leads to decreased oxygen levels reaching the heart, a condition called cardiac ischemia. One sign of ischemia is the presence of stable angina pectoris, pain experienced in the chest, shoulder or (usually left) arm. When these patients are asked to exercise, the amount of exercise needed to trigger their angina (the threshold) is often extremely variable. The current theory attributes this variability to local changes in the diameter of the diseased coronary artery at the site of the disease, but other physiologic parameters including the diameter and resistance to flow of vessels deeper in the heart muscle could also be responsible for the variable response. In this experiment, patients in whom a single completely blocked artery was responsible for their stable angina were used. This group was subjected to exercise testing on at least two occasions when no drug therapy was administered. Nitroglycerine, a medication which causes dilation of heart blood vessels, was also used in some patients in an attempt to increase their tolerance of exercise. Nitroglycerine increased the amount of work that the heart could perform before reaching an ischemic condition by 19 percent, and a vasoconstrictor, ergonovine, decreased it by 18 percent. Patients were also studied with ambulatory electrocardiographic monitoring as they carried out their normal day's activities. Episodes of changes in blood flow were also recorded. These results indicate that cardiac ischemia can be caused by the distal arteries of the heart and also by changes in blood flow through the collateral arteries, arteries which have developed spontaneously to provide blood flow to the heart because the original arteries were blocked. Vascular spasms in these vessels can lead to periods of ischemia in patients with stable angina. (Consumer Summary produced by Reliance Medical Information, Inc.)

Causes of, Arterial occlusive diseases

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Effect of intracoronary serotonin on coronary vessels in patients with stable angina and patients with variant angina

Article Abstract:

Coronary atherosclerosis is a disorder in which the coronary arteries become narrowed by the deposition of fatty plaque, but the extent to which ischemia (insufficient blood for the heart's needs) develops is not related in a simple manner to the extent of the disease. It is possible that platelets (blood cells essential for clotting) collect at sites where plaques have formed, releasing their products, among which is serotonin. Little is known regarding the effects of serotonin on human coronary arteries. To learn more about this issue, three groups of patients were studied: eight with normal coronary arteries; nine with stable angina (severe chest pain developing with exercise); and five with variant angina (severe chest pain not associated with exercise, often during rest). The patients were studied by means of angiography (injection of a dye into a coronary artery followed by X-ray views of the vessel) to evaluate the diameters of their vessels before and after the injection of serotonin. Results showed that serotonin produced a different response in patients with healthy arteries and those with coronary disease. In normal arteries, low doses caused dilation, while higher doses caused constriction. For patients with stable angina, however, serotonin caused constriction at all doses, bringing on angina attacks in all nine subjects. Finally, patients with variant angina had constriction of already-narrowed segments of their vessels, perhaps due to hyperreactivity of these segments. For most patients in the latter two groups, myocardial ischemia occurred in response to serotonin. The results imply that release of serotonin plays a role in ischemia in cases where the coronary arteries have developed atherosclerosis. The effect was particularly pronounced in the smaller coronary arteries. (Consumer Summary produced by Reliance Medical Information, Inc.)

Measurement, Complications and side effects, Atherosclerosis, Serotonin

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Evidence of impaired endothelium-dependent coronary vasodilatation in patients with angina pectoris and normal coronary angiograms

Article Abstract:

Endothelium-dependent dilation of coronary arteries may be impaired in patients with angina pectoris (chest pain) and normal coronary arteries. The left coronary artery of 19 individuals was infused with the endothelium-dependent vasodilator acetylcholine and with the endothelium-independent vasodilators papaverine and isosorbide dinitrate. Nine individuals were patients with angina pectoris and 10 were healthy individuals. Treatment with acetylcholine caused an increase in coronary blood flow in individuals from both groups. The increase in coronary blood flow was significantly less in patients with angina pectoris than in the healthy individuals. Response to papaverine or isosorbide dinitrate was not significantly different in the two groups.

Endothelium-derived relaxing factors

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