Pathology of the coronary vasculature is the direct cause of death in about one third of the population in developed societies. Prior to death, most of these people have impaired cardiac function as a result of coronary artery disease, leading to heart failure with decreased quality of life. Progressive occlusion of coronary arteries by atherosclerotic plaques and acute occlusion as a result of the formation of blood clots in damaged coronary arteries are life-threatening because the metabolic needs of the cardiac muscle can no longer be met by the blood flow. Because the plaque or clot partially occludes the vessel lumen, vascular resistance is increased, and blood flow would decrease if smaller coronary vessels did not dilate to restore a relatively normal blood flow at rest. In doing so, the reserve for dilation of these vessels is compromised. While this usually has no effect at rest, when cardiac metabolism is increased, the decreased ability to increase blood flow can limit cardiac performance. In many cases, inadequate blood flow is first noticed as chest pain—known as angina pectoris—originating from the heart, and a feeling of shortness of breath during exercise or work. The vascular occlusion can cause conditions ranging from impaired contractile ability of the cardiac muscle, which limits cardiac output and tolerance to everyday work and exercise, to death of the muscle tissue, a cardiac infarct.
If the coronary occlusion is not severe, medication can be used to cause coronary vasodilation or decreased cardiac work, or both. If the arterial pressure is higher than normal, various approaches are used to lower the blood pressure, decreasing the heart's workload and oxygen needs. In addition to pharmacological treatment, mild to moderate exercise, depending on the status of the coronary disease, is often advised. Aerobic exercise stimulates the development of collateral vessels in the heart, improves the overall performance of the cardiovascular system, and increases the efficiency of the body during work and daily activities. This latter effect lowers the cardiac output needed for a given task, thereby decreasing the heart's metabolic energy requirement.
Significant changes in lifestyle—including strictly limiting dietary fat (especially saturated fat), strenuous and prolonged daily exercise, and reduced mental stress— have been shown to greatly slow and even slightly reverse coronary atherosclerosis. The goal is to lower blood levels of low-density lipoproteins (LDLs), which are known to accelerate the formation of cholesterol-containing arterial plaques. The LDL concentration should typically be lowered below 120 mg/dL, but some cardiologists favor lowering levels below 100 mg/dL. For most people, reductions in LDL below 120 mg/dL are not attainable with diet and exercise. In those persons, drugs, known as statins, which block the formation of cholesterol in the liver, appear to be highly effective in decreasing the risk and severity of coronary artery disease. Simultaneous o o treatment with an aerobic exercise program and large amounts of niacin, to increase high-density lipoproteins (HDLs), may help the body remove cholesterol for processing in the liver. (See Clinical Focus Box 17.1).
Was this article helpful?