Perspectives By PAUL DUDLEY WHITE T IS IMPORTANT to differentiate coronary artery disease from coronary heart disease, Coronary atherosclerosis itsel...

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T IS IMPORTANT to differentiate coronary artery disease from coronary heart disease, Coronary atherosclerosis itself, if of only slight to moderate degree or even if severe but compensated by the development of an adequate collateral coronary circulation, may have little or no deleterious effect on the heart muscle itself. When there is such an effect as shown clinically by the symptom of angina pectoris, by clear electrocardiographic evidence, or by a heart attack (coronary thrombosis, myocardial infarction, or both), then the designation coronary heart disease is preferable to coronary artery disease. One of the most fascinating experiences of my medical career, dating back to my graduation from the Harvard Medical School in 1911, has been the evolution of our knowledge about coronary artery disease. As one very early attracted to the study of history in general and, in natural sequence, to that of the history of medicine, I became cognizant in the early years of cardiology in the 1920s of the historic descriptions of the pathologic findings in coronary artery disease and of their effect on the heart muscle. There were the socalled myomalacias and the myocardial scars as well as the clinical manifestations of instantaneous death (dating back to Pliny the Elder in the first century AD), the symptom of angina pectoris (named as such in a lecture by Heberden, 1768), and the entity of coronary thrombosis as an important and not rare clinical condition rather than as an isolated curiosity (Herrick, 1912). Many others, including those primarily interested in pathology, have been involved in the slow elucidation of coronary heart disease. These included Bellini (1683) and Bonet, who published in the second edition of his Sepalchretum (1700) the autopsy finding of occlusion of the coronary vessels in the case of a fat poet who died very soon after the onset of what seems to have been an acute heart attack. Others of note were Lancisi (1707) and Thebesius (1708). The pace quickened in the latter half of the 18th century when in the 1770s Jenner described the relationship of coronary atherosclerosis to Heberden’s angina pectoris. This observation was later confirmed, after the death and autopsy of John Hunter, by Parry ( 1799). Parry had already contributed an important paper in 1788 on this same relationship. In the 19th century, more attention was paid to a description of the arterial lesions. Arteriosclerosis of the coronary arteries was described Scarpa (1804) and named as such by Lobstein (1833). However, the type of arterial disease described was what we now call atherosclerosis, which combined atheroma (Greek for “soft pudding”) with sclerosis (Greek for “hardening”). The word atherosclerosis was first used by Marchand (1904). Virchow’s great



PAUL DCJDLEY WHITE, M.D.: President, International Cardiology Professorof Medicine Emeritus, Harvard Vniuersity, Boston, Mass. 250













contribution to the field was his clarification of thrombosis and embolism, especially related to the pulmonary circulation without specific reference to the coronary circulation. This process of blood clotting is, however, a part of the entity of coronary thrombosis. Acute myocardial infarction as a pathologic finding was mentioned by Senac (1749) and others as “softening” and later called “cardiomalacia” or “myomalacia cordis” (Lobstein, 1833; Weigert, 1880; Ziegler, 1881; and Huber, 1882), but in the previous century it had not been related to coronary atherosclerosis. Cohnheim (1881) d escribed old myocardial infarcts as fibrous myocarditis and myocardial aneurysms related to coronary obstruction and myocardial ischemia, although the clinical entity was not established at that time. Incidentally Cohnheim thought that the coronary circulation was one of end arteries without anastomoses, as pointed out later by Herrick (1912). We now come to individual case reports of acute myocardial infarction prior to Herrick. These included Latham ( 1846), Diiben ( 1859)) Hammer ( 1878), Leyden (1884), most clearly Dock ( 1896), and finally Obrastzow and Straschesko (1910) who d escribed five cases, three with autopsy and two diagnosed during life. Leading clinicians of the day, including Osler (1897 and 1910) and Mackenzie (1923), were well acquainted with cardiology in general and angina pectoris in particular; however, they missed the diagnosis of acute coronary thrombosis with myocardial infarction, Two other writers worthy OF mention with respect to their contributions to our knowledge of coronary heart disease at the very end of the 19th century were Marie (1896) with his thesis on the accurate anatomic description of myocardial infarction, and Huchard with his textbook containing many clinical references, Unfortunately neither author brought together in clear focus both the clinical and pathologic aspects of the disease process.* Thus it was in 1912 that James Herrick did for acute coronary thrombosis with myocardial infarction what Heberden and Jenner did together nearly I50 yr earlier for angina pectoris. The best way to tell of Her&k’s classic work in the field is to quote a few brief passages from his paper of 1912: Obstruction of a coronary artery or of any of its large branches has long been regarded as a serious accident. Several events contributed toward the prevalence of the view that this condition was almost always suddenly fatal. Parry’s writings on angina pectoris and its relation to coronary disease, Jenner’s observations on the same condition centering about John Hunter’s case, Thorvaldsen’s tragic death in the theater in Copenhagen with the finding of a plugged coronary, sharply attracted attention to the relation between the coronary and sudden death. But there are reasons for believing that even large branches of the coronary arteries may be occluded-at times acutely occluded-without resulting death, at least without death in the immediate future. Even the main trunk may at times be obstructed and the patient live. It is the object of this paper to present a few facts along this line, and particularly to describe some of the clinical manifestations of sudden yet not immediately fatal cases of coronary obstruction.

-. .-*I have been helped in some excellent new book The Hisfory fomia Press, 1971.

~-__ of these references and dates of Coronuq Heurf Disease,

by Professor J. 0. Leibowitz’s Berkeley, University of Cah-

One may conclude, therefore, from :I consideration of the clinical histories of nnlnerous cases in which there has been careful autopsy control, from animal experiments and from anatomic study. that there is no inherent reason why stoppage of a large branch of a coronary artery, or evcu of a main trunk, must of necessity cause sudden death. Rather may it be concluded that \vhile sudden death often does occur, yet at times it is postponed for several hours or even days, and in snme instances a complete, i.e., functionally complete, recovery enslles. The variations in the results are to be accounted for in part by variations in the freedom with which anastomosing branches occur The condition of the remaining vessels as to patency and presence of sclerosis must play an important part in deciding how much they are capable of doing in the way of compensatory nutrition to the anemic myocardium; the strength of the heart itself, as determined, perhaps, by old valvular or myocardial disease, wou!d also have its influence. And presumably a sudden overwhelming obstruction, with comparatively normal vessels. would be followed by a profounder shock than the gradual narrowing of a lumen through sclerosis which has accustomed the heart to this pathologic condition and has perhaps caused collateral circulation through neighboring or anastomosing vessels to be compensatorily increased. The influence of the vessels of Thebcsius is also not to be overlooked in this conncction; compensatory circulation through these accessory channels may be of considerable importance in nourishing areas of heart muscle poorly supplied by sclerotic or obstructed arteries. It was almost a decade later that a few pioneers in cardiology became cognizant of Herrick’s remarkable contribution. He himself in a personal conversation told me that he could not explain the long delay, but I believe that I can do so. There were, I am quite sure, four reasons: First, there were not nearly so many cases of acute coronary thrombosis or myocardial infarction then as now. (I shall discuss that shortly.) Second, there were few “science writers” in those days, and medical reporting by either physicians or laymen was a rarity. Third, there were inadequate clinical-pathologic correlations at the turn of the century. Cabot’s famous “CPCs” got started only in the second and third decades of the twentieth century. Fourth, there was a failure to recognize clinically, or at times even pathologically, heart attacks when they did occur, in the days before the electrocardiogram came into play as an important diagnostic tool around 1920 (Smith, 1918 and Pardee, 1920). A few papers at the end of the second decade of the century and early in the third discussed the differential diagnosis of heart attacks, especially with reference to cholelithiasis (Levine and Tranter, 1918; Herrick, 1919; Faulkner, Marble, and White, 1924). Often and quite to be expected, surgeons and physicians who were associated in these early reports have continued to be all through the more recent decades when surgical therapy of cardiovascular lesions began and became established. Now let me present the reasons for my belief that coronary heart disease was actually much less common when I graduated from medical school in 1911 than now in 1971. In the first place our teachers in the course of the 4 yr prior to graduation had extremely little to say about it, not yet having recognized coronary heart attacks as such but labeling most of the few cases they did see as “severe angina pectoris” or simply as “heart failure” or “cardiac” enlargement.” At autopsy “arteriosclerotic heart disease” was an uncommon entity. Perhaps the most striking evidence was the lack of interest in the



characteristic symptom of angina pectoris, which although well-known to my professors, was evidently rated by them as about as uncommon as it had been in the extensive clinical experience of such medical leaders in the previous century as Graham Steel and William Osler. These authorities, as well as my own professors, certainly knew angina pectoris when they met it and I was myself well aware of it on graduation in 1911. During my medical internship in 1912 and 1913 at the Massachusetts Gcnera1 Hospital taking care of adults, many of them middle aged and older, I rarely saw cases of coronary heart disease. This I have noted recently on reading over my own voluminous handwritten case records and autopsy rcports stored in the cave at the Storrow House in Lincoln, Mass. The very few who did have angina pectoris included syphilitic patients with aortitis. It is of special interest that the hundreds of patients in my wards (West Medical 31 and 16) were for the most part, laborers both male and female. These were still the days when that hospital, like nearly all the other large hospitals of the country, was like an ahnshouse for the relatively poor, with no private patients. The few well-to-do patients in the community, who were taken care of at home by my professors, did not come to my attention with one exception. He was a visiting professor from the Midwest whom I was asked to set in 1916 when he was staying at the home of one of our staff members. He did have an undoubted myocardial infarction, wrongly diagnosed by himself and others as cholelithiasis. Another reason for this opinion of mine that coronary heart disease was uncommon in my early medical days was that the first hundred papers in my bibliography, extending from 1913 to 1926, contained only two which were concerned with coronary heart disease (the first, number 77, in 1924, and the second, number 96, in 1926). Certainly if coronary heart disease had been as common as it is today, I would have been forced to study it and write about it earlier in the century, since I was trying to cover the entire field of cardiology in those early days. One other important factor dealing with both the prevalence and the incidence of coronary heart disease is that we did not see so many young people with it as WC do today. Clearly emphasizing this point was an important paper by Samuel Levine published in 1963 and entitled “Angina Pectoris in Father and Son” (Amer. Heart J. 66:49, 1963). In it Levine noted that in 20 families in his practice in which he had seen both father and son, the son on the average developed his angina at an age 13 yr younger and died I4 yr earlier in age. He quite rightly surmised that something must have happened in the last generation to explain this. My own experience is similar, and it behooves us to try to answer this question as soon as we can to save our young men. It is thus clear that the whole answer is not that we have more aged people today than 60 yr ago, although of course we do. An obvious possible, indeed probable, answer is that we have changed our way of life in the last two generations. The automobile, richer food, more tobacco, a faster life, and more pollution of everything have become available to all of us in the United States. Actually we have not extended much, if any at all, our longevity after the age of 70. We still regard octogenarians, nonagenarians, and centenarians as relative rarities, at least if they are able to carry on a reasonably active life.





Two other points I would like to mention are important to those early days of our specialty in the 1920s. First, the pathologist and the cardiologist got closer together (Levine, Sprague, \Veiss, Blumgart, and I were actually students of our noted pathologists Mallory and Lenry in the 1920s). Second, although Herrick had emphasized as early as 1912 the possibility of survival after a heart attack, coronary thrombosis was still regarded as a very serious condition that limited to a few years at best not only the duration of life but also a return to work. Only at the end of that decade did we become optimistic and begin a growing program of rehabilitation. As interest in coronary heart disease increased, the laboratory brought to US a steadily increasing flow of technique and devices to improve our diagnostic acumen and to aid our follow-up. The most important-now that it is SO widely available, simply applied, and scientifically developed-has been electrocardiography with its offspring in the form of vectorcardiography, and its use in exercise testing as in Master’s two-step test (1929, with Oppenheimer). These uses of the electrocardiogram have continued to increase in value until today but alone they are still not sufficient. In the early 1950s La Due and his associates developed a serum enzyme (transaminase) test useful within 36 hr of an attack of acute myocardial infarction, and other such blood tests have followed. In the 1920s or earlier, fever and leukocytosis had been found to be the rule with large myocardial infarcts. Although X-ray studies decades ago had shown evidence of calcification of the coronary arteries and of the aortic arch (lesions of which are frequently combined), such findings did not necessarily establish the diagnosis of coronary heart disease if the collaterals were adequate. A practical application of the pioneer X-ray cardiography of Castellanos (1937) has been introduced by Sones (1962) and others. When skillfully done, this technique outlines not only the internal bore of the coronary arteries but also by motion picture film the abnormal often paradoxical areas of pulsation of the ventricular muscle wall, the state of the valvular ostia, and the presence of intracardiac thrombosis. This last test has been invaluable in assessing the points of surgical attack in such therapy as the saphenous vein coronary bypass operations of today, which have largely replaced more primitive surgical efforts to revascularize the heart muscle. Three more aspects of the evolution of our knowledge and treatment of coronary heart disease remain to be mentioned. The first concerns advances in the growing cooperation of pathologist and internist. An example of considerable value in outlining the convalescent program of a coronary heart attack victim was the study by Mallory, Salcedo, and White (1937) on the speed of healing of myocardial infarction. This report cited a time interval of about 3 wk for the adequate setting of a scar in a medium-sized infarct. This finding confirms the inadequacy of a rest of only a week or IO days in acute myocardial infarction, whether this rest is in bed or in a chair, since most ruptures of the heart wall from recent infarction occur in the middle or at the end of that first week. Neither is it necessary to prescribe 1% to 3 mo of rest for the healing process, unless the infarct is very large or unless mmplications occur. A second important study was reported by Blumgart et al.



(1940) on the great importance of the collateral coronary circulation. Their findings confirmed Herrick’s observations of 1912. The second aspect of the evolution of our knowledge concerns therapy. When I started in medicine, nitroglycerine was the specific treatment of angina pectoris and it still remains so. Long-acting nitrites have been added and are sometunes helpful, as is the beta-blocker propranolol, in hyperactive hearts and circulations if there is no threat of myocardial failure. Other drugs are useful only for complications, but one other medical measure often neglected is just plain rest as needed. Surgical therapy, already mentioned, in the form of specific saphenous vein coronary bypass is a recent valuable addition to our armamentarium. Other surgical measures include excision of a myocardial aneurysm, when it is large and a severe strain for the ventricle, and a similar removal of an acute or subacute myocardial infarct, when it threatens life by grossly hampering the contraction of the healthy part of the ventricular muscle or by its irritability as a source of serious arrhythmia, especially ventricular fibrillation. Cardiac transplantation for hopelessly damaged “coronary hearts” is not to be ruled out entirely in the future, but for the moment it must be regarded as experimental. Even after the rejection process and other current difficulties have been cleared, it should be applied to only carefully selected patients in good general health. The third and final feature of the problems and perspective of coronary heart disease is its prevention, at least in the young and middle aged. Actually this problem deserves the first priority in research, teaching, public health, and private health. Much has been said and written about it in the last two decades. The earliest and still classic accounts include the paper by Glendy, Levine, and White (1937) entitled “Coronary Disease in Youth” (JAMA 109: 1775, 1937), and the book by Gertler et al. (1954) entitled Coronary Heart Disease in Young Adults (Commonwealth Fund and Harvard University Press). We discussed clues to the disease in 100 individuals (97 of them male and three female) affected by coronary heart involvement under the age of 40 yr. These clues included genetic as well as environmental risk factors. Since then we have emphasized the great importance of genetic factors, male sex, mesomorphic build, familial hypercholesterolemia, diabetes in the family, and a family history, in both ancestral branches, of atherosclerotic lesions in heart, aorta, brain, or legs. These young candidates for early coronary heart disease in youth or middle age are teenagers. We must &&ate them about controlling environmental risk factors (diet, muscular exercise, tobacco, and excessive stress) while they are still young. In perspective, this goal of prevention, it seems to me, is an emergency. Meanwhile we can carry out our increasingly expert diagnostic techniques and our outstanding therapeutic measures, both medical and surgical, in the case of those who are already victims. Much can still be done to help many of them.