Coronary Artery Disease and Heart Attacks

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We have seen that the myocardium does not extract oxygen and nutrients from the blood within the atria and ventricles but depends upon its own blood supply via the coronary arteries. In coronary artery disease, changes in one or more of the coronary arteries causes insufficient blood flow (ischemia) to the heart. The result may be myocardial damage in the affected region and, if severe enough, death of that portion of the heart—a myocardial infarction, or heart attack. Many patients with coronary artery disease experience recurrent transient episodes of inadequate coronary blood flow, usually during exertion or emotional tension, before ultimately suffering a heart attack. The chest pain associated with these episodes is called angina pectoris (or, more commonly, angina).

The symptoms of myocardial infarction include prolonged chest pain, often radiating to the left arm, nausea, vomiting, sweating, weakness, and shortness of breath. Diagnosis is made by ECG changes typical of infarction and by measurement of certain proteins in plasma. These proteins are present in cardiac muscle and leak out into the blood when the muscle is damaged; the most commonly used are the enzymes creatine kinase (CK), particularly the myocardial specific isoform, CK-MB, and cardiac-specific isoforms of troponin.

Of the more than 1.5 million heart attack victims in the United States each year, approximately half are admitted to a hospital, where they can be given advanced care, and more than 80 percent of these people survive the attack and are discharged.

Sudden cardiac deaths in myocardial infarction are due mainly to ventricular fibrillation, an abnormality in impulse conduction triggered by the damaged myocardial cells and resulting in completely uncoordinated ventricular contractions that are ineffective in producing flow. (Note that ventricular fibrillation is fatal, whereas atrial fibrillation, as described earlier in this

PART THREE Coordinated Body Functions

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

PART THREE Coordinated Body Functions chapter, generally causes only minor cardiac problems.) A small fraction of individuals with ventricular fibrillation can be saved if modern emergency resuscitation procedures are applied immediately after the attack. This treatment is cardiopulmonary resuscitation (CPR), a repeated series of mouth-to-mouth respirations and chest compressions that circulate a small amount of blood to the brain, heart, and other vital organs when the heart has stopped. CPR is then followed by definitive treatment, including defibrillation, a procedure in which electric current is passed through the heart to try to halt the abnormal electrical activity causing the fibrillation.

The major cause of coronary artery disease is the presence of atherosclerosis in these vessels. Atherosclerosis is a disease of arteries characterized by a thickening of the portion of the arterial vessel wall closest to the lumen with (1) large numbers of abnormal smooth-muscle cells, macrophages (derived from blood monocytes), and lymphocytes, (2) deposits of cholesterol and other fatty substances both in these cells and extracellularly, and (3) dense layers of connective-tissue matrix.

The mechanisms by which atherosclerosis reduces coronary blood flow are as follows: (1) The extra muscle cells and various deposits in the wall bulge into the lumen of the vessel and increase resistance to flow; and (2) dysfunctional endothelial cells in the atherosclerotic area release excess vasoconstrictors (for example, endothelin-1) and deficient vasodilators (nitric oxide and prostacyclin). These processes are progressive, sometimes leading ultimately to complete occlusion. Total occlusion is usually caused, however, by the formation of a blood clot (coronary thrombosis) in the narrowed atherosclerotic artery, and this triggers the heart attack.

The processes that lead to atherosclerosis are complex and still not completely understood. It is likely that the damage is initiated by agents that injure the endothelium and underlying smooth muscle, leading to an inflammatory and proliferative response that may well be protective at first but ultimately becomes excessive. This sequence of events is described in Chapter 20 as an example of a maladaptive inflammatory response.

Cigarette smoking, high plasma concentrations of cholesterol and the amino acid homocysteine, hypertension, diabetes, obesity, a sedentary lifestyle, and stress can all increase the incidence and the severity of the atherosclerotic process. These are all termed, therefore, "risk factors" for coronary artery disease, and prevention of this disease focuses on eliminating or minimizing them through lifestyle changes (for example, changing to a diet designed to lower plasma cholesterol concentration) and/or medications. In a sense, menopause can also be considered a risk factor for coronary artery disease since the incidence of heart attacks in women is very low until after menopause. This relationship is explained by the protective effects of estrogen, including the actions of this hormone on plasma cholesterol concentration. The control of plasma cholesterol is described in Chapter 18, and the use of sex-hormone replacement therapy in menopausal women in Chapter 19.

A few words about exercise are warranted here because of several potential confusions. It is true that a sudden burst of strenuous physical activity can sometimes trigger a heart attack. However, the risk is almost totally eliminated in individuals who perform regular physical activity, and much more important, the overall risk of heart attack at any time can be reduced as much as 35 to 55 percent by maintenance of an active lifestyle, as compared with a sedentary one. In general, the more one exercises the better is the protective effect, but anything is better than nothing in this regard. For example, even moderately paced walking 3 to 4 times a week confers significant benefit.

Regular exercise is protective against heart attacks for a variety of reasons. Among other things, it induces: (1) decreased resting heart rate and blood pressure, two major determinants of myocardial oxygen demand; (2) increased diameter of coronary arteries; (3) decreased severity of hypertension and diabetes, two major risk factors for atherosclerosis; (4) decreased total plasma cholesterol concentration with simultaneous increase in the plasma concentration of a "good" cholesterol-carrying lipoprotein (HDL, discussed in Chapter 18); and (5) decreased tendency of blood to clot and improved ability of the body to dissolve blood clots.

Another protective factor against heart attacks is supplements of vitamin E. This vitamin, which functions as an antioxidant, may act by preventing the oxidation of "bad" cholesterol (LDL, discussed in Chapter 18) since such oxidation makes this cholesterol more likely to promote the buildup of plaques. Supplements of folacin (a B vitamin also called folate or folic acid) are also protective, in this case because fo-lacin helps reduce the blood concentration of the amino acid homocysteine, one of the risk factors for heart attacks. Homocysteine is cysteine with an extra CH2, and is an intermediary in the metabolism of me-thionine and cysteine. In increased amounts, it exerts several pro-atherosclerotic effects, including damaging the endothelium of blood vessels. Folacin is involved in the metabolism of homocysteine in a reaction that lowers the plasma concentration of this amino acid.

Finally, there is the question of alcohol and coronary artery disease. In many studies, moderate alcohol

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition



intake has been shown to reduce the risk of dying from a heart attack. The problem is that alcohol also increases the chances of an early death from a variety of other diseases (cirrhosis of the liver, for example) and accidents. Because of these complex health effects, it is presently recommended that people should take no more than 1 drink a day.

The treatment of coronary artery disease and angina with certain drugs can be understood in terms of physiological and pathophysiological concepts described in this chapter, and we will give only a few examples. First, vasodilator drugs such as nitroglycerin (which is a vasodilator because it is converted in the body to nitric oxide) help in the following way: They dilate the coronary arteries and the systemic arterioles and veins. The arteriolar effect lowers total peripheral resistance, thereby lowering arterial blood pressure and the work the heart must expend in ejecting blood. The venous dilation, by lowering venous pressure, reduces venous return and thereby the stretch of the ventricle and its oxygen requirement during subsequent contraction.

To take a second example, drugs that block beta-adrenergic receptors are used to lower the arterial pressure in persons with hypertension, but more importantly, they block the effects of the sympathetic nerves on the heart; the result is reduced myocardial work, and hence oxygen demand because both heart rate and contractility are reduced.

Third, drugs that prevent or reverse clotting within hours of its occurrence are extremely important in the treatment (and prevention) of heart attacks. Use of these drugs, including aspirin, is described in Section G of this chapter.

There are several surgical treatments for coronary artery disease after the area of narrowing or occlusion is identified by cardiac angiography (described earlier in this chapter). Coronary balloon angioplasty is the passing of a catheter with a balloon at its tip into the occluded artery and then expanding the balloon; this enlarges the lumen by stretching the vessel and breaking up abnormal tissue deposits. A second, but related, surgical technique utilizes the permanent placing of coronary stents in the narrowed or occluded coronary vessel. Stents are latticelike stainless steel tubes that provide a scaffold within a vessel to open it and keep it open. A third surgical technique is coronary bypass, in which an area of occluded coronary artery is removed and replaced with a new vessel, often a vein taken from elsewhere in the patient's body.

We do not wish to leave the impression that atherosclerosis attacks only the coronary vessels, for such is not the case. Many arteries of the body are subject to this same occluding process, and wherever the atherosclerosis becomes severe, the resulting symptoms reflect the decrease in blood flow to the specific area. For example, occlusion of a cerebral artery due to atherosclerosis and its associated blood clotting can cause localized brain damage—a stroke. (Recall that rupture of a cerebral vessel, as in hypertension, is the other cause of stroke.) Persons with atherosclerotic cerebral vessels may also suffer reversible neurologic deficits, known as transient ischemic attacks (TIAs), lasting minutes to hours, without actually experiencing a stroke at the time.

Finally, it should be noted that both myocardial in-farcts and strokes due to occlusion may result from the breaking off of a fragment of blood clot or fatty deposit that then lodges downstream, completely blocking a smaller vessel. The fragment is termed an embo-lus, and the process is embolism.


Hemorrhage and Other Causes of Hypotension

I. The physiological responses to hemorrhage are summarized in Figures 14-55, 14-59, 14-61, and 14-62.

II. Hypotension can be caused by loss of body fluids, by cardiac malfunction, by strong emotion, and by liberation of vasodilator chemicals.

III. Shock is any situation in which blood flow to the tissues is low enough to cause damage to them.

The Upright Posture

I. In the upright posture, gravity acting upon unbroken columns of blood reduces venous return by increasing vascular pressures in the veins and capillaries in the limbs.

a. The increased venous pressure distends the veins, causing venous pooling, and the increased capillary pressure causes increased filtration out of the capillaries.

b. These effects are minimized by contraction of the skeletal muscles in the legs.


I. The cardiovascular changes that occur in endurance-type exercise are illustrated in Figures 14-64 and 14-65.

II. The changes are due to active hyperemia in the exercising skeletal muscles and heart, to increased sympathetic outflow to the heart, arterioles, and veins, and to decreased parasympathetic outflow to the heart.

III. The increase in cardiac output depends not only on the autonomic influences on the heart but on factors that help increase venous return.

IV. Training can increase a person's maximal oxygen consumption by increasing maximal stroke volume and hence cardiac output.

PART THREE Coordinated Body Functions

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

PART THREE Coordinated Body Functions


I. Hypertension is usually due to increased total peripheral resistance resulting from increased arteriolar vasoconstriction.

II. More than 95 percent of hypertension is termed primary in that the cause of the increased arteriolar vasoconstriction is unknown.

Heart Failure

I. Heart failure can occur as a result of diastolic dysfunction or systolic dysfunction; in both cases, cardiac output becomes inadequate.

II. This leads to fluid retention by the kidneys and formation of edema because of increased capillary pressure.

III. Pulmonary edema can occur when the left ventricle fails.

Coronary Artery Disease and Heart Attacks

I. Insufficient coronary blood flow can cause damage to the heart.

II. Sudden death from a heart attack is usually due to ventricular fibrillation.

III. The major cause of reduced coronary blood flow is atherosclerosis, an occlusive disease of arteries.

IV. Persons may suffer intermittent attacks of angina pectoris without actually suffering a heart attack at the time of the pain.

V. Atherosclerosis can also cause strokes and symptoms of inadequate blood flow in other areas.


maximal oxygen consumption (VO2max)


10 11 12

Draw a flow diagram illustrating the reflex compensation for hemorrhage.

What happens to plasma volume and interstitial-

fluid volume following a hemorrhage?

What causes hypotension during a severe allergic response?

How does gravity influence effective blood volume? Describe the role of the skeletal-muscle pump in decreasing capillary filtration. List the directional changes that occur during exercise for all relevant cardiovascular variables. What are the specific efferent mechanisms that bring about these changes?

What factors enhance venous return during exercise? Diagram the control of autonomic outflow during exercise.

What is the limiting cardiovascular factor in endurance exercise?

What changes in cardiac function occur at rest and during exercise as a result of endurance training? What is the abnormality in most cases of established hypertension?

State how fluid retention can help restore stroke volume in heart failure.

How does heart failure lead to edema?

Name the major risk factors for atherosclerosis.


The stoppage of bleeding is known as hemostasis (don't confuse this word with homeostasis). Physiological hemostatic mechanisms are most effective in dealing with injuries in small vessels—arterioles, capillaries, venules, which are the most common source of bleeding in everyday life. In contrast, the bleeding from a medium or large artery is not usually controllable by the body. Venous bleeding leads to less rapid blood loss because veins have low blood pressure. Indeed, the drop in pressure induced by raising the bleeding part above the heart level may stop hemorrhage from a vein. In addition, if the venous bleeding is into the tissues, the accumulation of blood may in-

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  • robert
    What body mechanisms lead to cad?
    8 years ago

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