Potentials and limitations of patients after myocardial infarction

Fundamentals of clinical cardiology

Potentials and after myocerdial George E. Burch, M.D.* Nicholas P. DePasguale, New Orleans, La.

A

llmitsrtJoplis ih~l0n

M.D.

lthough controversy still exists concerning the etiology of coronary heart disease, it is a well-accepted fact that by the time most American males reach 50 years of age they have some degree of coronary artery atherosclerosis. Furthermore, although the incidence of most other forms of heart disease has decreased in the last few decades, the incidence of coronary heart disease has increased, at least in the younger age groups. At present, coronary heart disease is probably the most common cause of chronic disability among the working population of the United States. Furthermore, about one third of all deaths in the United States each year are due to acute myocardial infarction. Patients with coronary heart disease may be divided into three groups on the basis of the clinical findings, viz., (1) those with coronary insufficiency (angina1 syndrome), (2) those with myocardial infarction, and (3) those with congestive heart failure. A patient may progress from coronary insufficiency to myocardial infarction and congestive heart failure or may manifest any one or two of the three phases. All of the above-mentioned conditions are important causes of absenteeism in the male working population. The incidence of acute myocardial inFrom

of patkents

farction in the general population is difficult to determine. However, it has been estimated that 1 out of every 38 men over 40 years of age and 1 out of every 115 women in the United States has an acute myocardial infarction each year.” Although the mean age at the time of the initial myocardial infarction in white males is between 58 and 60 years, the risk of myocardial infarction increases rapidly after 40 years of age. It is during these years that many men reach their peak productivity and hold key positions in industry and the professions. In addition, many men in this age group are heads of households with large financial demands, such as the education of children, the payment of insurance premiums and mortgages, etc. The mortality rate of an initial myocardial infarction in patients between 45 and 60 years of age in many representative large series is about 40 per cent. However in some series, particularly those from private hospitals, the mortality rate of initial myocardial infarction has been reported to be as low as 5 per cent. Furthermore, life expectancy in men who survive the first myocardial infarction is fairly good, the average being about 10 years in patients who are less than 50 years old, and 8.5 years in patients who are over 50 years old

the Department of Medicine, Tulane University School of Medicine, and the Charity Hospital of Louisiana. New Orleans. La. This work was supported by grants from the United States Public Health Service, the Rowe11 A. Billups Fund for Research in Heart Disease, and the Rudolf Matas Memorial Fund for the Kate Prewitt Laboratory. Received for publication June 29, 1966. *Address: Department of Medicine, Tulane University School of Medicine, 1430 Tulane Ave., New Orleans. La., 70112.

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at the time of the first infarction2 Thus, the physician will be faced with the problem of evaluating the capacity to work in at least 6 out of every 10 patients between 45 and 60 years of age who sustain an acute myocardial infarction. This is a difficult task which rests almost completely on the physician in charge of the patient. It is now well recognized that the majority of patients who survive an initial myocardial infarction can be returned to complete or partial employment. However, it should be stated at the outset that there are no rules, criteria, or tests for evaluating the work capacity of patients after a myocardial infarction which can be substituted for the physician’s judgment. To be sure, certain tests of function may guide the physician, but the ultimate decision in regard to work capacity is one of clinical judgment rather than mathematically precise criteria. What is cardiac rehabilitation? The term rehabilitation has many meanings. In the minds of most lay people and to many physicians, rehabilitation implies some form of physical training to regain or improve a loss of function resulting from disease, as for example, various exercises in patients with cerebrovascular accidents or paralytic poliomyelitis. In patients with coronary heart disease, physical methods may assist the heart to function with the maximum efficiency possible for the anatomic state of the heart, but once this point is reached, cardiac function cannot be improved by training. There is little reliable information on the value of physical conditioning after myocardial infarction. Experimental studies in dogs have indicated that exercise promotes the development of the coronary collateral circulation after constriction of a coronary artery.3 Nevertheless, a great deal more needs to be learned about the effect of physical training on cardiac performance in postmyocardial-infarction patients before its role in the treatment of coronary heart disease can be evaluated. Committees established to study the problems of rehabilitation of cardiac patients usually describe the aims of cardiac rehabilitation rather than define what rehabilitation means. These aims usually include restoring the patient’s self-reliance for the purpose of returning him to his former employment, or if that is impossi-

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ble, to employment compatible with his working capacity.4 Although these aims are essential to the long-term management of patients after myocardial infarction, they do not constitute cardiac rehabilitation. In this regard, it is important to distinguish between cardiac rehabilitation and rehabilitation of the patient who has had a myocardial infarction. The aims listed above are directed toward rehabilitation of the patient rather than rehabilitation of the heart. What then is cardiac rehabilitation? In our opinion, cardiac rehabilitation in the patient with coronary heart disease consists of the following: (1) preservation, as much as possible, of the structural integrity of the myocardium through adequate treatment; (2) institution of therapy directed toward establishing the greatest possible coronary collateral circulation; (3) institution of therapy directed toward encouraging compensatory myocardial hypertrophy. The first two of these are the most important and apply to all patients with heart disease. The third applies primarily to patients with large dilated hearts. It is disturbing to us that so much of the literature on “cardiac rehabilitation” is concerned with getting the patient back to work, and that there is so little emphasis on preserving and improving the functional state of the cardiac muscle. In the final analysis, it is the efficiency of the heart as a pump which will determine the ability to work. It must never be forgotten that the motor of the pump is the myocardium itself. The efficiency of the heart after a myocardial infarction will be determined to a large extent by the adequacy of treatment. Once functional myocardial motor units are dead, they can never be regained. Thus, in so far as the heart is concerned, rehabilitation and treatment are, to a great extent, the same thing. Obviously, the effectiveness of physical training in improving cardiac efficiency will depend upon the amount of healthy myocardial tissue which exists after recovery from infarction. The potentials and limitations of patients after myocardial infarction are, therefore, greatly influenced by the treatment received during the period of infarction. The three aspects of cardiac rehabilita-

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tion outlined above are discussed briefly below. Preservation of the structural integrity of the myocardium. After occlusion of a coronary artery a variable amount of myocardial tissue is destroyed. This results in a loss of myocardial motor units, so that there is impairment of the heart as a pump. The degree of impairment depends upon the amount of myocardial tissue lost, as well as losses accumulated previously from myocardial fibrosis associated with coronary artery disease, even in the absence of antecedent clinical myocardial infarction. During the early phases of myocardial infarction the area of injury and ischemia is greater than the ultimate area of death. Thus, nonfunctioning, but viable, myocardial fibers regain their ability to function as a result of physicochemical reparative processes. Therapy should be directed toward insuring recovery of the maximum number of injured muscle fibers. Like any other organ, the diseased heart repairs and returns to good health most quickly when it is permitted to rest. Although the heart must continue to work even when it is diseased, it is possible, within limits, to “unload” and thereby rest the heart by means of relatively simple measures, including (1) decreasing the heart rate, (2) decreasing the arterial blood pressure, (3) decreasing the cardiac output, (4) decreasing the size of the heart, and (5) decreasing the velocity of myocardial contraction. The physician should review each of these factors in terms of his patient in order to determine which apply to his patient and whether appropriate therapy to modify a given factor has been instituted. In order to put the heart at rest, i.e., reduce the hemodynamic load to a minimum, it is not sufficient merely to put the patient with acute myocardial infarction to bed. It is also necessary to recognize and alleviate the psychic disturbances associated with the realization by the patient that he has had a myocardial infarction. This can usually be accomplished by calmness and reassurance on the part of the physician and the judicious use of sedatives. It is also important that the patient be placed in a thermally neutral and comfortable environment. A hot and humid environment increases cardiac work, so that

Am. Hravt J. I),,crvrbcr, 1966

even when the patient is at complete bed rest, the heart is not at rest. The importance of this factor is obvious to those who have observed patients with acute myocardial infarction treated during the summer months in hospitals that were not air conditioned. Careful attention must also be paid to such details as providing for small frequent feedings of soft, low-residue foods, making certain that the patient does not develop bladder distention or fecal impaction, limiting the number of visitors, and eliminating disturbing visitors, relieving pain promptly through the use of narcotics, and not allowing the patient to be disturbed by so-called “hospital routine,” such as bathing the patient, changing bed linens, and the like. Complacency in the treatment of acute myocardial infarction has developed because of the fact that many patients survive an acute myocardial infarction no matter how they are treated. The point to be emphasized is that the goal of the treatment of acute myocardial infarction should be not only the survival of the patient, but also his recovery from the infarction with the least amount of myocardial damage. lLlany inadequately treated patients do survive, but they are often left with a dilated heart, congestive heart failure, and angina pectoris. This is not to say that adequately treated patients do not have these residuals, but only that they are less likely to occur in properly treated patients. In our opinion, the single most important aspect of myocardial infarction in so far as prognosis is concerned is the size of the heart several months after an acute myocardial infarction. The patient who survives a myocardial infarction without developing cardiac enlargement can usually look forward to a productive and relatively symptom-free life. On the other hand, the patient who develops a dilated heart as a result of myocardial infarction is likely to be seriously incapacitated. The mechanical disadvantage of the dilated heart has been discussed previously in papers from this laboratory.5s6 It is only necessary to emphasize the fact that, whereas the tension in the wall of the normal-sized heart decreases or remains constant during systolic ejection, the tension in the dilated heart must increase to

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support intraventricular pressure. Furthermore, for a given amount of work, the greater the myocardial tension, the greater the myocardial oxygen consumption, and consequently the less the efficiency of the heart. Instituting therapy directed toward establishing the greatest possible collateral coronary circulation. It is a well-established clinical fact that patients with severe angina pectoris may in time experience a decrease in the severity and number of angina1 attacks. Presumably, improvement is due to the development of the collateral coronary circulation. Furthermore, although it has not been established, it has been suggested that coronary vasodilators promote the formation of collateral vascular channels in the myocardium. Patients with severe angina pectoris should be treated with coronary vasodilators, and their activity should be limited, but not absolutely restricted. Limitation of activity is important if further myocardial damage is to be avoided. On the other hand, exercise may contribute to the development of the collateral circulation. Unfortunately, there are no criteria by which the physician can determine the amount of exercise that is appropriate for his patient. The amount of exercise prescribed must be based on judgment, supported by the physical examination, the subjective response of the patient, and the electrocardiographic and roentgenographic findings. Cigarette smoking should be curtailed and completely eliminated if possible. It is probably also wise to restrict the use of caffeine-containing beverages. When an adequate collateral circulation develops, as is evidenced by a decrease in the frequency and severity of angina1 episodes, the patient may increase his activity gradually. The fact that angina pectoris is a significant cause of absenteeism, as reported in so many studies on the work capacity of patients with coronary heart disease, indicates that present attitudes concerning the “rehabilitation” of cardiac patients need revision. In the long run it is better to delay the return to work of the patient with postinfarction angina pectoris until an adequate coronary collateral circulation has been established than to encourage too early a return to work. Although a patient with angina pectoris

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may be able to stay on the job, especially if he has a healthy psychologic approach toward his work, permanent disability and retirement may occur earlier than if employment had been delayed and activity restricted. The present aggressive attitude of those involved with the rehabilitation of cardiac patients is disturbing, in that too often it appears that the major concern is with getting the patient back to work rather than with what happens to the patient after he returns to work. Nevertheless, the physician must temper his judgment with the realization that the longer the patient remains away from his job, the more difficult it becomes for him to return to work. Instituting therapy directed toward encouraging compensatory myocardial hypertrophy. Patients with coronary heart disease, extensive myocardial damage, and massive cardiac dilatation represent one of the most frustrating problems to the cardiologist. Although patients with large dilated hearts cannot and should not work, the physician occasionally encounters such a patient who is strongly motivated to work. In some instances, because of the nature of the patient’s work, for example, if he is a top executive or an artist, partial return to work may be possible under the physician’s careful supervision. However, the vast majority of patients with extensive myocardial damage and large dilated hearts should not be permitted to work, Such patients often experience symptoms even at rest. Treatment in general consists of diuretics, digitalis, and low-sodium diet, In addition, the physician is often called upon to treat acute episodes of cardiac asthma, pulmonary edema, or myocardial insufficiency. However, this therapy is only supportive, and the clinical course is one of progressive deterioration. There is a pressing need to develop methods to improve cardiac function in patients with large dilated hearts. There is pulmonary evidence to indicate that such patients may be improved by prolonged, absolute bed rest.’ Although the value of prolonged bed rest is well established in the treatment of tuberculosis and rheumatic fever, it has not generally been applied to patients with coronary heart disease. In fact, there is a tendency to en-

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courage patients with dilated hearts and chronic congestive heart failure to get out of bed because of an increased risk of thromboembolic disease. It can only be said that the application of present therapeutic concepts have been largely unsuccessful. Unless new forms of treatment are developed, no improvement in the present gloomy outlook for patients with large dilated hearts can be expected. Although placing patients with dilated hearts at absolute bed rest for a year or more is in some respects a drastic procedure, the seriousness of the disease requires drastic measures. The dilated heart is under a mechanical disadvantage when compared to the normal-sized heart. The tension developed by a given segment of myocardium during systole is related to the intraventricular pressure and the cross-sectional area of the ventricle at the level of the segment.536 During systole the cross-sectional area of the normal-sized heart decreases, so that the product of pressure times crosssectional area, i.e., the tension in the myocardial segment, either remains unchanged or may actually decrease. Thus, the normalsized heart is able to “loaf” during systole. On the other hand, the cross-sectional area of the dilated heart does not decrease sufficiently during systole to prevent a marked increase in myocardial tension as systole progresses. The increased tension which develops in the wall of the dilated heart imposes an unfavorable “load” on the dilated heart. This is a physiologic or static load because it is not associated with the movement of blood. Furthermore, the increased tension also imposes a “metabolic load” on the dilated heart because myocardial oxygen requirement is directly related to tension. Prolonged bed rest is often associated with a decrease in cardiac dilatation. Any decrease in the state of dilatation of the heart automatically “unloads” the heart to some extent. Theoretically, as the heart is improvement in myocardial “unloaded,” function results in a further reduction in the dilated state, which, in turn, results in further unloading of the heart, and so on until the heart returns to normal size. Of course, this cycle is limited by the degree of myocardial damage. However, as collaterals develop, or if one coronary artery is less

narrowed than the other, compensatory localized myocardial hypertrophy mav develop in the areas that have a relativelv good supply of blood. We have described the hearts of patients in whom one coronary artery was occluded and the other was patent.8 The myocardium in the distribution of the occluded coronary artery was thin and fibrotic, and in some instances dilated to the point of formation of an aneurysm. On the other hand, the myocardium in the distribution of the patent coronary artery was markedly hypertrophied. It is reasonable to consider that placing a patient with coronary artery disease and a large dilated heart at complete prolonged bed rest by removing the static and metabolic “load” from the heart will encourage the gradual development of localized myocardial hypertrophv. Of course, the degree of hypertrophy &ll be limited by such factors as the extent to which each coronary artery is involved by the arteriosclerotic process and the effectiveness of the collateral coronary circulation. Rehabilitation of the cardiac patient. As stated above, it is important to distinguish between rehabilitation of the heart and rehabilitation of the patient with heart disease. The determination of the potentials and limitations of patients with cardiac disease depends primarily upon the evaluation of the patient by his physician. It cannot be done from tables, charts, or by boards of physicians. It is unrealistic, first, to classify a patient in a certain therapeutic category, and then to look up in a table how much and the kind of work he can do, even when such tables are used only as guides. Tables of energy expenditure during various tasks are subject to large errors, especially when the task is not sedentary. In fact, under certain conditions, it may be virtually impossible to estimate the metabolic cost of a complex task because of the variation in time spent at different phases of the tasks, each phase requiring a different expenditure of energy. Furthermore, tables of energy expenditure provide information on the total metabolic cost of various activities; they do not indicate the amount of cardiac work performed while carrying out these activities. Nevertheless, it is worth

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while for the physician to acquaint himself with such tables of energy expenditure in order to get a general idea of the relative energy costs of various tasks (Fig. 1). The use of boards of physicians to determine work capacity is a poor practice. No physician, no matter how talented he is, is able to evaluate accurately the work capacity of a patient on the basis of a single examination, except perhaps that of patients who are so seriously ill that incapacity is obvious. Members of such boards are usually aware of this fact, and for this reason tend to rely heavily on functional tests of cardiac efficiency. At present, no test of cardiac efficiency can reliably predict the capacity of a patient to work. When a physician bases his opinion of capacity to work on tests of cardiac efficiency, he does the patient an injustice. The physicians on some boards, particularly those in state welfare departments, never see the patient whom they are evaluating

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and, therefore, must base their decision on the physical examinations of other physicians and the comments of a social worker, who in most instances they do not know personally. The inadequacy of such a practice needs no comment. The decision of whether a patient is to return to work after a myocardial infarction, as well as the time and type of work that he is to return to should be made only by the patient’s physician. This is a responsibility of which he cannot divest himself. He may seek the help of a consultant or even a rehabilitation board, but ultimately it is he who must make the final decision. More attention should be paid to informing the practicing physician of the problems in the evaluation of the potentials and limitations of the patient who has had a myocardial infarction, and less attention to educating the patient about his infarction. Much of the literature prepared for lay people is filled with oversimplifications

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Fig. 1. Average energy costs (in calories per minute) of various Cardiac ProjecV” and Hendrickson and associates.“)

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and half-truths which confuse the patient, The patient’s best source of information is his own physician, not paperback books and brochures. During the early period of treatment of an acute myocardial infarction the physician will continuously evaluate the severity of the infarct and the response of the patient. He will also evaluate the psychologic effect of the infarction on the patient and his family. As the patient improves, he will be gradually allowed to increase his activity until he becomes fully ambulatory. There is no timetable for determining the period of bed rest, sitting in a chair, and finally ambulation. However, it is better to proceed too slowly than too rapidly. During this period, the physician will encourage the patient and his family, so that when the patient is ready to return to work, he will have a good mental outlook. But the physician must be careful. It is just as important for the patient to know his limitations as his potentials. The physician will observe the response of the patient to a progressive increase in activity. On the basis of the physician’s impressions and the patient’s symptoms as activity is increased, the activity will be adjusted to the patient’s capacity. Eventually, a sound judgment in regard to work capacity will be reached. This judgment will be based on observations and impressions formed during the entire period of treatment and convalescence. It will include not only the consideration of the patient, but that of his family, his employer, and his supervisors, his attitude toward his job, and the job itself, as well as many intangibles. A judgment in regard to the potentials and limitations of a patient after a myocardial infarction that is made on any other basis is an unsatisfactory compromise. Conclusion

At present it appears that about 80 per cent of patients who survive an initial myocardial infarction are able to return to work (Fig. 2). However, among such patients, absenteeism due to angina pectoris, congestive heart failure, and cardiac asthma is relatively frequent. In Dimond’s study of 348 patients who returned to work after an initial myocardial infarction, 25

Fig. 2. Fate of cardial infarction Dimond.9)

348 men who and returned

survived to work.

initial (Data

myofrom

per cent sustained a second myocardial infarction within 5 years9 Thus, although every effort should be made to have patients return to work after a myocardial infarction, the physician must recognize the risks of returning to work too soon, as well as the advantages and disadvantages of prolonged inactivity. Until morbidity is reduced, management will continue to be reluctant to employ men who have had a myocardial infarction, particularly for relatively unskilled tasks. The best means of reducing morbidity is adequate treatment during the acute and convalescent phases of the period of myocardial infarction. REFERENCES 1. Master, A. M.: Incidence of acute coronary occlusion, AM. HEART J. 33:135, 1947. 2. Kirkland, H. R.: Prognosis in heart disease, New York J. Med. 55:3443, 1955. R.: Effect of exercise and coronary 3. Eckstein, artery narrowing on coronary collateral circ ulation, Circulation Res. 5:230, 1957. 4. Rehabilitation of patients with cardiovascular diseases, World Health Organization Technical Report Series. No. 270, 1964. 5. Burch, G. E., Ray, C. T., and Cronvich, J. A.: The George Fahr Lecture. Certain mechanical pecularities of the human cardiac pump in normal and diseased states, Circulation 5:504, 1952. 6. Burch, G. E.: The dilated heart, (Editorial) Arch. Int. Med. %:571, 1955. 7. Burch, G. E., and Walsh, J. J.: Cardiac enlargement due to myocardial degeneration of unknown cause. Preliminary report on effect of prolonged bed rest, J.A.M.A. 178:207, 1960. 8. Burch, G. E., and DePasquale, N. P.: Electrocardiogram and spatial vectorcardiogram in

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localized myocardial hypertrophy, Circulation 26:544, 1962. Dimond, G. E.: Assessment of functional recovery of men surviving first myocardial infarction, AM. HEART J. 65:832, 1963. Purdue Farm Cardiac Project, Agricultural Experiment Station: Energy requirements for

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physical work, Research Progress Report No. 30, Lafayette, Indiana, December, 1961. Hendrickson, D., Anderson, J., and Gordon, E. E.: A physiologic approach to the regulation of activity in the cardiac convalescent, Am. J. Occup. Ther. 14:292, 1960.