Coronary Artery Disease

Coronary Atherosclerosis

The most common heart disorder in the United States coronary atherosclerosis. The pathologic condition of the coronary arteries is coronary arteries is characterized by an abnormal accumulation of lipid substances and fibrous tissue in the vessel wall that leads to change in arterial structure and function and reduction of blood flow to the myocardium. Causes of atherosclerotic heart disease probably involve alterations in lipid metabolism, blood coagulation, and the biophysical and biochemical properties of the arterial walls.

Although there is disagreement among authorities with regard to the origin of lesions, there is agreement that atherosclerosis is a progressive disease and that its progress can be curtailed and in some cases reversed.

Pathophysiology. The functional lesion of atherosclerosis is called the atheroma. Atherosclerosis begins when the waxy cholesterol atheroma, which looks like pearly gray mounds of tissue, becomes deposited on the intima of the major arteries. These deposits interfere with the absorption of nutrients by the endothelial cells that compose the vessel lining and obstruct blood flow by protruding into the lumen of the vessel (fig.1). The vascular endothelium in involved areas becomes necrotic and then scarred, further compromising the lumen and impeding the flow of blood.

Cardiovascular, Circulatory, and Hematologic Function

Figure 1. Cross-section of a normal and an atherosclerotic artery. (A) Cross-section of normal artery showing patent lumen. (B) Cross-section of artery showing atheroma and diminished patency of artery lume

At sites such as these where the lumen is narrowed and the wall rough, there is a great tendency for clots to form, which explains why intravascular coagulation, followed by thromboembolic disease, is among the most important complications of atherosclerosis.

Our knowledge of atherogenesis is limited. Several theories are proposed, but as yet none has been conclusively substantiated. Among suspected mechanisms are thrombus formation on the surface of the plaque, followed by fibrous cap of the plaque ruptures, the lipid debris is swept into the bloodstream and obstruction of the arteries and capillaries distal to the ruptured plaque results.

The anatomic structure of the coronary arteries makes them particularly susceptible to the mechanisms of atherosclerosis (fig. 2). They twist and turn as they supply the heart, thereby creating angles and nooks ripe for atheroma development.

Fig. 2

Clinical manifestations. Coronary atherosclerosis produces symptoms and complications as a result of the narrowing of the arterial lumen and obstruction of the blood flow to the myocardium. This impediment to blood flow is progressive, and the inadequate blood supply (ischemia) that results deprives the muscle cells of the blood components they need for their survival. Varying degrees of cell damage are produced by ischemia. The major manifestation of ischemia of the myocardium is chest pain. Angina pectoris refers to recurrent chest pain that is not accompanied by irreversible damage to myocardial cells. More severe ischemia with cell damage is termed myocardial infarction. Irreversibly damaged myocardium undergoes degeneration and is replaced by scar tissue. If the damage to myocardium is extensive, the heart may eventually fail, that is, it may be unable to support the bodys need for blood by providing an adequate cardiac output.

Other clinical manifestations of coronary artery disease may be ECG changes, ventricular aneurysms, dysrhythmias, and sudden death.

1.2 Risk Factors and Prevention of Coronary Heart Disease

Epidemiologic studies show that there are conditions that may precede or accompany the onset of coronary heart disease. These conditions are called risk factors because the presence of one or more is believed to increase on s risk of developing coronary heart disease. A risk factor may be modifiable or nonmodifiable. A modifiable risk factor is one over which an individual may exercise control by changing a life style or personal habit; a nonmodifiable risk factor is a consequence of genetics over which an individual has no control.

A major goal of risk factor identification and reduction is that of prevention of coronary heart disease. Prevention may be primary or secondary. Primary prevention involves measures taken before the development of symptoms of a diseases process; secondary prevention involves those measures that may be taken to reduce the progress of or prevent the reoccurrence of a disease process.

Five modifiable risk factors cigarette smoking, elevated blood pressure, hyperlipidemia, hyperglycemia, and certain behavior patterns have received popular attention. Two of these risk factors cited as major causes of coronary artery disease and its consequent complications are cigarette smoking and hypertension.

A.Cigarette Smoking contributes to the development and seventy of coronary artery disease in three way:

the inhalation of smoke increases the blood carbon monoxide level. Hemoglobin, the oxygen carrying component of blood, combines more readily with CO then with O₂. Thus, the oxygen being supplied to the heart is severely limited, which makes the heart work harder to produce the same amount of energy

nicotinic acid in tabacco products triggers the release of catecholamines, which cause arterial constriction. Blood flow and subsequent oxygenation are compromised.

cigarette smoking increases platelet adhesion, leading to higher probability of thrombus formation.

B. Elevated Blood Pressure is the most insidious of all risk factory because it is asymptomatic until hypertension is well advanced. An elevated blood pressure creates a very high pressure gradient against which the left ventricle must pump. The continued high pressure forces the myocardial oxygen demands to exceed the supply. The initiates the vicious cycle of pain associated with coronary artery disease.

Early detection of high blood pressure and compliance with a therapeutic regimen can prevent the serious consequences associated with untreated elevated blood pressure.

C. Hyperlipidemia . The association of elevated blood lipids with coronary artery disease has been established through epidemiologic studies. Lipids are mixed group biochemical substances that may be manufactured by the body or derived from metabolism of ingested substances. An endogenous lipid is one produced by the normal metabolic functions of the body; an example of an endogenous lipid is sterol. An exogenous lipid is one derived from a source external to the body, such as a food that is high in fat.

Lipids have the common property of being more soluble in fat or organic solvents than in water. In the blood, the principal lipids are cholesterol and triglycerides; an elevation of one or both is referred to as hyperlipidemia. To render them suitable for transport in the blood, the lipids are attached to a variety of proteins the resulting product is called a lipoprotein. The presence of lipoproteins in the blood is lipoproteinemia.

The lipoproteins are described clinically by their respective densities. Each lipoprotein has a distinct function in the metabolism of exogenous and endogenous lipids. Some, such as LDL (low-density lipoprotein), are belleved to play a role in the aggressiveness of the development of coronary heart disease. An excessive amount of lipoproteins in the blood is called hyperlipoproteinemia

Composition, Sources, and Functions of Lipoproteins Present in Plasma

There are five types of hyperlipidemia. The next table describes the five types the lipoprotein abnormality, and the potential clinical outcomes of elevated levels. Determining the underlying lipid abnormality by blood studies is essential before suggesting dietary control

Risk Factors for Atherosclerosis

Hyperlipidemia may be primary or secondary. Primary hyperlipidemia is generally a hereditary disorder and is the rarest of phenotypes. The secondary type occurs as manifestation of numerous other diseases, including hypothyroidism, nephritic syndrome, diabetes mellitus and alcoholism. Therapy consists of treating the basic disorder.

Primary Hyperlipidemias and Associated Clinical Features

For some individuals, the control of fat consumption is an important factor in preventive nutrition. Dietary fat may be regulated by changing the total amount or the type of fat in the diet, or both. Assisting the patient to modify dietary fat intake through effective counseling requires an understanding to the differences between saturated and polyunsaturated fatty acids, cholesterol, medium-chain triglycerides, and various other fractions, as well as of their functions in the human body.

No single diet or drug will be effective in all conditions in lowering the particular elevated lipid abnormality, but in most people with such an abnormality the level can be brought within the upper normal range.

For patients in whom diet alone cannot normalize the specific lipid, there are several medications that have a synergistic effect when taken with prescribed diet. These agents are shown to be biochemically effective, in that elevated lipoprotein concentration tends to return toward normal, and manifestations of the abnormalities, such as xanthomas (yellow papules in the skin caused by lipid deposits), may disappear. Drug treatment also varies with the type of hyperlipidemia. The drugs used are usually grouped into two type those that decrease lipoprotein synthesis such as nicotinic acid and clofibrate, and those that increase lipoprotein breakdown (catabolism), such as cholestyramine, sitosterol and D-thyroxine.

Harmful side effects can occur from the use of these drugs. Drug therapy is, therefore, reserved for the high-risk patient and is not regarded as a viable substitute for dietary modification. The usefulness of drugs in reversing coronary heart disease is still under investigation. It is however, broadly accepted that preventive nutrition can have a significant impact on coronary heart disease.

Hyperglycemia. The relationship of elevated blood glucose and increased evidence of coronary heart disease is substantiated. Hyperglycemia fosters increased platelet aggregation, wich can lead to thrombus formation. A high level of glucose (as is seen in some cases of adult onset diabetes) is said to cause damage to cells of the smooth muscle lining the vessels. The damaged vessel walls foster the growth of atheromas.

Other risk factors such as obesity and hypertension must be brought under control in addition to hyperglycemia. Control of hyperglycemia without modification of other risk factors does not reduce the risk of coronary heart disease.

Behavior Patterns of Coronary Prone Persons. It is believed that stress and certain behaviors contribute to the pathogenesis of coronary ( atheroscleratic) heart disease.

Psychobiologic and epidemiologic studies have investigated behaviors that characterize people who are prone to coronary artery disease: competitive striving for achievement exaggerated sense of time urgency, aggressiveness and hostility. A person who manifests these behaviors is classified as type. A coronary prone. It appears that, in addition to reducing other risk factory (smoking, dietary fats), such a person should take steps to alter life style and long-term habits.

The type A behavior pattern has been widely accepted as a risk factor for coronary heart disease. Contemporary research indicates that it may not be as significant as was once thought but there is not yet conclusive evidence of its precise role.

1.3. Gerontologic Consideration

Atherosclerotic coronary artery disease is not a function of aging. Aging does, however, produce changes in the integrity of the lining of the walls of arteries (arteriosclerosis), thus impeding blood flow and tissue nutrition. These changes are often sufficient to diminish oxygenation and increase myocardial oxygen consumption (MVO₂). The result can be debilitating angina pectoris and eventually congestive heart failure.

Coronary heart disease is often preceded or accompanied by conditions that may incresa one s likelihood of morbidity. These conditions are referred to as risk factors. They are considered nonmodifiable if they are beyond personal control, such as age. If they are amenable to personal control, such as smoking, they are considered to be modifiable. Risk factor identification and modification are major thrusts of coronary heart disease prevention and treatment.