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Journal of the American College of Vol. 33, No. 5, 1999 © 1999 by the American College of Cardiology ISSN 0735-1097/99/$20.00 Published by Elsevier Science Inc. PII S0735-1097(99)00027-3 REVIEW ARTICLES A View From the Millennium: The Practice of Cardiology Circa 1950 and Thereafter Mark E. Silverman, MD, FACC Atlanta, Georgia

The knowledge and treatment of cardiology as practiced circa 1950 is discussed as abstracted from authoritative textbooks of that time and other sources. Advances in treatment and diagnostic techniques since 1950 are presented. Dramatic changes in cardiology have come at the expense of bedside cardiology which needs to be balanced with the technology. (J Am Coll Cardiol 1999;33:1141–51) © 1999 by the American College of Cardiology

The year 2000 provides a vantage point to look back and see ment, though a primary nonobstructive arteriosclerotic aor- how cardiology has progressed. I have chosen 1950 as a tic condition (Monckeberg’s sclerosis) was described (3). pivotal moment because, as it turned out, that year roughly prolapse was not yet reported. Aortic dissection divides two vastly different eras in cardiology—one in which was a rare etiology of aortic regurgitation; however, primary cardiology was practiced predominately by generalists and dilation of the aortic root was not mentioned. internist-cardiologists who depended upon their bedside was a common problem. skills, a few basic tests, and limited medical and surgical options, and the other a post–World War II exuberant . Acute rheumatic fever was common growth, fueled by government and pharmaceutical funding, between ages 5 and 12. Though noted to be on a slight that would eventually become dominated by highly trained, decline, it was still the leading cause of death from ages 5 to full-time specialists, the cardiac catheter and a proliferation 20 in the . During World War II, 4%–5% of of therapeutic options. young soldiers infected by hemolytic streptococcus devel- To comprehend the enormous changes that have oc- oped acute rheumatic fever. Paul Dudley White commented curred since 1950, I have provided an in-depth discussion of (1), “One of the most important reasons why rheumatic the understanding of disease from that period based heart disease is so serious is the fact that it is particularly a on authoritative American and British texts published pri- disease of youth, crippling and killing many children and marily between 1946 and 1951 (1–10) and other sources young adults.” (11–14). The terminology of that time has been used The cause of rheumatic fever was uncertain, but its throughout. Advances in treatment and technology since connection with certain streptococcal strains was well 1950 are then presented in Tables 1 and 2. known (1). The absence of a clinical history in 40% to 50% of patients was puzzling but suspected to be due to atypical VALVULAR HEART DISEASE and unrecognized attacks. Carditis was suspected when one In 1950, valvular heart disease was understood to be mostly or more of the following was found: a pericardial rub, due to the inflammatory consequences of rheumatic fever. cardiac enlargement, heart failure, aortic or mitral regurgi- Syphilis was still frequent and an important cause of aortic tation, a diastolic mitral murmur (Carey-Coombs murmur) regurgitation. Stretching of the aortic ring, due to hyper- or a presystolic gallop (4). The sedimentation rate, white tension, was thought to produce “functional aortic regurgi- blood cell count and temperature were followed for evidence tation;” “functional mitral regurgitation” was a secondary of continuing rheumatic activity. effect of left ventricular failure and dilatation (3). In most Prophylactic prevention stressed avoidance of respiratory cases, aortic valve calcification and stenosis, even in the infections, prompt penicillin treatment of streptococcal elderly, was attributed to long-standing rheumatic involve- pharyngitis, small doses of sulfonamides or penicillin throughout the winter or spring in susceptible children and tonsillectomy. Treatment for acute rheumatic fever was From the Division of Cardiology, Department of Medicine, Emory University School of Medicine and Chief of Cardiology, Piedmont Hospital, Atlanta, Georgia. limited to salicylates and absolute bed rest for several The research for this article was undertaken on a Burroughs-Wellcome travel grant at months or longer. Fever therapy, up to 106°F, was some- the Wellcome Institute for the History of Medicine, London, England. Manuscript received August 28, 1998; revised manuscript received November 24, times tried for chorea. Corticosteroids, just introduced in 1998, accepted January 5, 1999. 1949, were reported to be successful in early small series (2). 1142 Silverman JACC Vol. 33, No. 5, 1999 The Practice of Cardiology in 1950 April 1999:1141–51

Clinical findings. These were the times of unoperated, forbidden or terminated early if symptoms and signs of advanced rheumatic valvular disease. By 1950, the symp- heart failure appear early or if there have ever been symp- toms and bedside cardiac findings had been extensively toms or signs (1).” It was estimated that 90% of cardiac correlated with the chest X-ray, fluoroscopy and the elec- disease in pregnant women was due to rheumatic valvular trocardiogram. Typical facial appearances were sought—a disease, and that mitral stenosis alone or in combination malar, cyanotic flush on a pale background was suggestive of with aortic valve disease was present in 75% of these cases. mitral stenosis, while a delicate pink “Dresden china” At the turn of the 20th century, the mortality in symp- appearance was noted with aortic stenosis (2). The cardiac tomatic pregnant patients was around 50%, and the fetal examination had become a fine art as practiced by Paul mortality was correspondingly alarming (3). If pregnancy Wood, Samuel Levine, Paul Dudley White and others was restricted to women who were classed as New York (1–4). Heart Association Class I (no limitation of activity) or II The classic auscultatory findings of each valve abnormal- (slight or moderate limitation of activity) who had never ity were well known. Valvular regurgitation was most been in heart failure, then the mortality was nil (3). The commonly called “insufficiency” in the United States (3) and management of symptomatic patients relied upon strict bed “incompetence” in Great Britain (2). Late systolic murmurs rest, salt restriction, digitalis, mercurial diuretics, quinidine were often attributed to an extracardiac or innocent source. and, for acute pulmonary edema, morphine was the choice. Paul Wood said, “It is now known, however, that apical With strict care, the overall mortality, had fallen to 2%–3% systolic murmurs may be cardiac or extracardiac, and if in 1950 (3). cardiac may be due to mitral incompetence...mitral in- competence itself may be organic or functional (2).” HYPERTENSION Laboratory. The chest x-ray included oblique and barium- Hypertension was defined according to the diastolic pres- filled esophageal views to check for cardiomegaly or specific sure alone and was graded as mild (90–110 mm), moderate chamber enlargement. Office fluoroscopy was routinely (110–130 mm) and severe (130–150 mm) (7). Malignant or done. The electrocardiogram was important for rhythm accelerated hypertension indicated a diastolic pressure in the analysis and could point to chamber dilatation or hypertro- severe range associated with funduscopic abnormalities and phy. Right heart catheterization and angiography was pos- rapidly worsening renal function. Systolic blood pressure sible in a few academic centers only beginning in 1945 at the elevation was attributed to rigidity of the great vessels and Johns Hopkins and the Peter Bent Brigham Hospitals (11). dismissed as not serious; a diastolic elevation was vasocon- Treatment. When significant valvular disease was present, strictive in origin and the cause of true hypertension. patients were advised to avoid effort and to seek a sedentary Incidence and etiology. Hypertension was common, said occupation. Charles Bailey in Philadelphia and Dwight to affect 30%–40% of the U.S. and British population over Harken in Boston initiated surgery for acquired valvular age 40, and account for 15%–20% mortality in those times disease with their reports of successful mitral commissurot- when treatment was so limited. As Paul Dudley White omy for mitral stenosis in 1948 (12). commented, “The most common and important of all types Prognosis. Persistent or recurrent rheumatic carditis with of heart disease by and large the world over is that due to cardiomegaly predicted a worse outcome. Auricular fibrilla- systemic hypertension with elevation of diastolic blood tion was ominous. Marked mitral insufficiency brought pressure. It is often serious and frequently followed by about death in “just a few years” at best. Patients with congestive failure and death (1).” significant mitral stenosis could live 10–20 years, and Known etiologies of hypertension were listed as acute and occasionally much longer. Their average age at death was chronic renal disease, endocrine disorders, coarctation of the 35, however, 25% survived to age 50 or longer (2,3). aorta, central nervous system lesions and toxemia of preg- Aortic valve disease due to syphilis carried a worse nancy (3). The classic experimental studies of Goldbatt and prognosis, apparently because of associated ostial coronary the association of renovascular disease and nephritis with stenosis (3). Patients with aortic insufficiency could live for the release of renin and other pressor agents was well 20–30 years (2). Aortic stenosis carried a 5% to 18% risk of understood. Essential hypertension, probably genetically sudden death and a 10% incidence of bacterial endocarditis related, was felt to explain 80% of hypertensive cases (7). (2). The average age of death with predominant aortic Correlations. The association of hypertension with coro- stenosis was 55.8. When heart failure developed, the sur- nary disease, left ventricular hypertrophy and congestive vival was from a few months to 2 years (3). failure, auricular fibrillation and sudden death was clear (3). Pregnancy. Pregnancy and valvular heart disease posed a due to high blood pressure was greatly feared by the special concern. Paul Dudley White mentions, “The impor- public, and one author stated, “There are few fields in tant question concerning heart disease in pregnancy is the medicine in which so much legendary misinformation has prognosis, one of the most difficult problems in medi- played a role in the management of the patient. Because of cine...Norule can be set, except that pregnancy should be the belief that a very high blood pressure is the precursor of JACC Vol. 33, No. 5, 1999 Silverman 1143 April 1999:1141–51 The Practice of Cardiology in 1950 a “stroke,” patients (and their doctors) have been needlessly occur with aortic stenosis or regurgitation, severe anemia, frightened and their life programs unnecessarily interrupted paroxysmal and hyperthyroidism (4). (5).” Incidence. The incidence of coronary disease was increas- Diagnosis and management. A urinalysis, blood urea ing. Professionals, especially , were said to have an nitrogen, X-ray for renal size and an occasional intravenous especially high incidence (2). For unknown reasons, males pyelogram was the limited workup in most cases. Treatment were affected more often and more seriously than females was meager. As Paul Wood lamented, “It must be said at until age 70, when the incidence was equal. After a once that there is no satisfactory treatment for essential or diagnosis of pectoris, the life expectancy was esti- for malignant hypertension (2).” In many cases, no treat- mated to be 5 to 10 years (2,3). ment was given on the belief that the symptomatic patient would live for many years without complications. Further- Diagnosis. The diagnosis of angina pectoris was made by more, physicians did not want to frighten patients by scrupulous attention to classic symptoms and precipitating creating alarm, often informing them of a “tendency” to factors. Rest angina was attributed to an increased work load high blood pressure. Patients were strongly advised to on the heart from digestion, cold reflexes, disturbing dreams achieve mental and physical tranquility by living at a lower or endocrine factors. Pain was often likened to intermittent tempo, resting and sleeping long hours and avoiding the claudication or a ligature put around a limb causing isch- strains of work, heavy meals and emotional upset. A mental emia and a release of noxious metabolites (3). component was strongly suspected and sedatives such as “Coronary insufficiency” was the commonly applied term phenobarbital, chloral hydrate and bromides were used and for an intermediate stage of pain between angina pectoris psychotherapy might be recommended. Alcohol in moder- and infarction. It was attributed to coronary spasm or ation was permitted and thought to be helpful as a sedative prolonged stimulatory factors such as tachycardia, extreme and vasodilator. Salt was stringently restricted, and diets , severe hypertension, , anemia or high with less than 1 g salt daily, such as the Kempner rice diet, altitude, and could cause infarction even in the absence of a were popular though one author stated, “The evils of rigid new thrombus (3,6). sodium restriction usually outweigh the benefit (3).” Drug “Silent” coronary disease, manifested by occluded coro- treatment was limited to thiocyanate and veratrum alka- nary and normal myocardium at autopsy, or elec- loids, both highly toxic drugs that were poorly tolerated. trocardiographic evidence of infarction in the absence of a Surgery, at significant risk, was applied to an adrenal or clinical story, was recognized (1,6). Sudden death was pituitary tumor or coarctation of the aorta. A splanchnic attributed to an attack of acute coronary insufficiency or nerve lumbar sympathectomy was a surgical gamble used in about 10% of patients with advanced hypertension. Dra- coronary vasoconstriction causing ventricular fibrillation or matic benefit was occasionally produced at the cost of standstill in 80% of cases (6). 0.5%–8.8% mortality, impotence and unpleasant orthostatic Examination. The cardiac examination of patients with hypotension (3). angina was not rewarding in the absence of aortic valve disease. With infarction, however, the textbook findings CORONARY ISCHEMIC HEART DISEASE were dramatic, including restlessness, a shock-like appear- The understanding of coronary disease focused on fixed ance, fever up to 102°F, an elevated venous pressure, a rapid obstruction, primarily due to atherosclerotic narrowing of heart rate or irregular rhythm, faint , a gallop the vessel by atheroma, scar and calcification (3,6). A and a friction rub in 10% to 20% (3). “discharge” of an atheromatous abscess could leave behind Tests. The electrocardiogram was the supreme test, though an ulcerating intimal lesion. Thrombosis was initiated by an it was known to be normal with milder forms of stable abrupt intimal hemorrhage from neighboring vasovasorum coronary disease. Exercise testing was done by checking an (6). Infarction depended upon the rate of progression of narrowing and the formation of collateral circulation (1). electrocardiogram before and after climbing a flight of stairs Coronary spasm was postulated to occur at times though to or performing a “Masters 2-step” test (3). Other provocative be uncommon because of the rigidity of the calcified vessels tests included inducing anoxemia with an inhalation of 10% (4). The cause of atherosclerosis was unknown; however, a oxygen and 90% nitrogen and injecting a subcutaneous dose faulty cholesterol metabolism, heredity, aging, diabetes and of adrenalin (4). Calcification of the coronary arteries was “mechanical” factors such as hypertension were clearly sometimes detected by fluoroscopy. Samuel Levine pro- involved (3). moted the use of carotid sinus stimulation during an episode Tobacco was not regarded as a causal factor but known to of (4). If the pain improved, a confident diagnosis provoke anginal attacks when used in excess (2,3). The of angina could be made. An acute infarction was confirmed strain of living, especially in a person with intense emotions by classic electrocardiographic changes and serial measure- or an ambitious drive, was a risk factor. Myocardial isch- ment of a rising white blood cell count and sedimentation emia, in the absence of coronary disease, was recognized to rate. 1144 Silverman JACC Vol. 33, No. 5, 1999 The Practice of Cardiology in 1950 April 1999:1141–51

Treatment. Treatment was limited. A moderate, low-fat ischemia, rheumatic fever, nutritional deficiency, thyrotox- diet, small frequent meals, the avoidance of large rich meals, icosis, scleroderma, toxic drugs, allergy and . reduction of mental stress and careful attention to the Alcohol caused a nutritional deficiency of the heart as seen bowels was advised. Tobacco use was severely restricted by in beriberi heart disease, but was not regarded to be a some, while alcohol was advised for treating angina (2). myocardial depressant or toxic agent. Nitrates in the form of nitroglycerine were highly effective Left ventricular hypertrophy was considered to be due to for angina but considered dangerous with infarction. Xan- the strain of increased work, as seen with hypertension, thine derivatives were sometimes used. Sedatives were valvular disease or thyrotoxicosis (1). An “idiopathic hyper- popular. trophy,” thought to be congenital in origin, had been A “lazy” vacation in a warm climate or prolonged bed rest reported in children, young adults and families (3). was recommended for unstable patients. Intractable angina Most often, cardiomegaly was due to hypertension, val- pectoris gave risk to a number of radical approaches, which vular disease or , and less commonly to included paravertebral alcohol injection, dorsal sympathec- myocarditis, thyrotoxicosis, chronic pulmonary disease, con- tomy or ganglionectomy, the induction of myxedema, anas- genital heart disease, severe anemia and an athletic heart. tomosis of the pectoral muscle or omentum to the heart, Cardiac enlargement was evaluated clinically by percussing instillation of powdered asbestos talc or bone dust into the the heart border relative to the midclavicular or midsternal , ligation of the great cardiac and radiation line and by routinely measuring the cardiothoracic ratio on to the anterior chest (2,12). the chest X-ray. Patients with an acute coronary thrombosis were often, Earlier, the term “chronic myocarditis” had been used but not always, hospitalized in an unmonitored room or freely and inaccurately. By 1950, the term was defined and ward. Morphine was the single most important drug for the restricted. Paul Dudley White commented, “In the attempt treatment. Antiarrhythmic drugs were limited to quinidine to diagnose heart disease more accurately, the term myo- for ectopy and ephedrine for heart block. Digitalis was carditis is wisely being abandoned in large part; we must avoided unless heart failure developed, in which case mer- remember, nevertheless, that there does exist such a condi- curial diuretics and a low-salt diet were also advised. tion as myocarditis which is particularly exemplified by Heparin, 50 mg every 4 h, and oral dicoumarol for three to involvement by rheumatic fever and diphtheria (1).” Specific six weeks were strongly advocated by some beginning the etiologies of myocarditis included rheumatic fever, diphthe- first day for infarction (2,4). Paul Wood, a strong advocate, ria, syphilis, endocarditis, viral, rickettsial and parasitic said, “The onset or sudden deterioration of angina pectoris diseases. An acute interstitial round cell myocarditis of is attended by considerable risk of cardiac infarction as a unknown cause, “Fiedler’s myocarditis,” was associated with result of spreading coronary thrombosis (2). This may be rapid heart rate, heart failure and a poor prognosis with prevented in favourable circumstances by the administration sudden death in young adults (1,3). of anticoagulants.” The mortality of infarction was 23% Thyrotoxic heart disease was highly regarded, perhaps without and 13% with anticoagulants (2). A pulmonary because it was one of the few treatable forms of heart embolus, estimated to cause a 6% to 10% mortality, was disease. greatly feared. Survivors were kept at bed rest for 2 to 6 weeks so that a firm scar could form to prevent softening of PERICARDIAL DISEASE the heart muscle that could lead to rupture, aneurysm or dilation (1). Absolute bed rest, to the point that the patient Pericarditis was often classified by the pathologic findings was not allowed to cut his food or brush his teeth, was into fibrinous (dry), serofibrinous, hemorrhagic, purulent, insisted upon for the first two weeks. Samuel Levine adhesive and constrictive types (1). Clinically, these divided recommended the radical approach of “arm chair treatment” into acute, with or without sterile or purulent effusion and allowing the patient to sit up the first two weeks (4). adhesive, with or without constriction. The most common Depending on the patient’s progress and the sedimentation etiologies were rheumatic fever, tuberculosis, uremia (or rate, a gradual increase in activities was allowed over the nephritis), coronary thrombosis and bacterial infection. A next 2–3 months—a major departure from the 6–12 months benign form of pericarditis, associated with a respiratory of convalescence practiced in the 1930s. Paul Dudley White infection and presumed to be viral, had been recently noted, “The heart itself possesses a striking recuperative recognized. Pericarditis was a sign of severe rheumatic capacity no matter what is done (1).” carditis, and its presence was worrisome. The clinical incidence of pericarditis with a coronary occlusion was MYOCARDIAL DISEASE between 7% and 22%. The combination of polyserositis and pericarditis, was known as “Concato’s Disease (1).” Pneu- Although Charles Friedberg commented (3), “Almost every monia and sepsis-related pericarditis, responsible for many cardiac disease is associated with myocardial involvement,” cases earlier in the century, was on a steep decline as was little attention was paid to a primary form of myocardial tuberculous pericarditis, which was found in 4% to 6% of disease in 1950. Fibrosis of the heart was attributed to autopsies of patients with tuberculosis (1). Constrictive JACC Vol. 33, No. 5, 1999 Silverman 1145 April 1999:1141–51 The Practice of Cardiology in 1950 pericarditis, sometimes called “Pick’s Disease,” was attrib- where obstruction was not apparent, such as coronary uted to tuberculosis in 15% to 75% of cases or a chronic disease. Furthermore, the concept of blood “damming up” infection of unknown cause in the rest (1). was difficult for physiologists to accept. With “forward failure,” myocardial dysfunction was the Diagnosis. A typical pain pattern was appreciated; how- primary fault. Symptoms, then, were due to a deficiency in ever, asymptomatic pericarditis was known to be frequent. cardiac output resulting in an impaired circulation to the The clinical diagnosis in all cases of acute pericarditis rested organ. Dyspnea, for example, was an effect of a lack of upon finding a friction rub. The electrocardiogram provided aerated blood to the head. Retention of salt and water, an helpful ST-T wave confirmation. Pericardial tamponade obvious manifestation of heart failure, was a consequence of was suspected by a falling arterial pressure, tachycardia, reduced renal blood flow. The broad appeal of the forward muffling of the heart sounds, a disappearance of the rub, failure concept was tarnished by the finding of a normal jugular venous engorgement with a cyanotic face, a rise in cardiac output in some patients with heart failure; a low the jugular pressure with inspiration (Kussmaul’s sign), cardiac output in some patients without evidence for heart displacement of the heart border by percussion, a tender failure; and a puzzlingly high cardiac output when heart enlarged liver, a paradoxical tested for mostly by failure was seen with anemia, hyperthyroidism and beri-beri palpation and evidence for consolidation of the lung at the (3). angle of the left scapula (Ewart’s sign). Serial enlargement By 1950, most authors felt that both backward and of the cardiac silhouette with a pear or water flask config- forward heart failure occurred and were modified by com- uration on chest X-ray was strong evidence. Constrictive pensatory mechanisms such as the Starling principle, heart pericarditis was diagnosed by noting an elevated venous rate and the peripheral arterial circulation. As Charles pressure, a small and paradoxical pulse, systolic apical Friedberg stated, “On the basis of present knowledge it is retraction (Broadbent’s sign), a loud third heard sound or possible to evolve a theory of congestive heart failure which knock, ascites and pericardial calcification on chest x-ray. accords with the evidence adduced to support both the Treatment. General pain relief for pericarditis consisted of forward failure and backward failure advocates and which salicylates, bromides, an ice bag on the chest, codeine and obviates their criticisms (3).” morphine. Purulent and tuberculous pericarditis were Etiology. Chronic heart failure was separated into left or treated with antibiotics. A decision to tap for a pericardial right ventricular failure and high-output failure (9). Left effusion, referred to as an exploratory pericardial paracente- ventricular failure was most commonly attributed to hyper- sis, was a major decision since the only diagnostic help was tension followed by coronary disease and valvular disease the examination and chest x-ray. This was a particular (mostly rheumatic but also syphilitic). Less common expla- dilemma in a patient with acute rheumatic fever with a nations included rheumatic and diphtheritic carditis, thyro- pericardial rub, an enlarging cardiac silhouette and a wors- toxicosis, tachyarrhythmia, arteriovenous fistula, cardiac ening clinical state (4). Electrocardiographic monitoring of trauma and pericardial adhesions. Cardiomyopathy, with the needle tip was not yet done. Pericardial drainage or the exception of rheumatic carditis, was not considered. stripping was an available surgical procedure with a consid- Paul Dudley White stated, “Myocardial degeneration and erable mortality (4). fibrosis result chiefly from extensive coronary atherosclerosis (1).” Right heart failure could occur acutely from a massive HEART FAILURE pulmonary embolus or pneumonia or chronically from left heart failure and chronic lung disease, including essential Heart failure was defined as an inability or impairment of pulmonary hypertension. Bernheim’s syndrome, in which the heart muscle to discharge its contents or to maintain a case the ventricular septum bulges into and obstructs the satisfactory circulation of blood to the tissues, resulting in an right ventricle inflow, was an accepted phenomenon (1). A elevation of venous pressure or vascular stasis (3,8). A hyperkinetic circulatory state leading to heart failure was long-standing argument still existed between advocates of known to occur with anemia, thyrotoxicosis, beri-beri, backward heart failure and forward heart failure (3). The arteriovenous fistula, Paget’s disease and severe emphysema. two theories argued over whether the elevated venous pressure was a primary or secondary event. In “backward Clinical features. Chronic left heart failure caused dyspnea failure,” an upstream obstruction in the circulation was on exertion, orthopnea and paroxysmal nocturnal dyspnea. thought to be the central factor. This obstruction, such as In addition, Cheyne-Stokes respiration, cough, “cardiac seen with aortic stenosis or hypertension, increased the back asthma” and acute pulmonary edema occurred. Chronic pressure thereby causing distention and hypertrophy of the right heart failure was manifested by hepatic discomfort and affected left and then right heart chambers. Symptoms, such edema. The examiner felt and percussed for cardiac enlarge- as dyspnea, resulted from an elevated left ventricular pres- ment, as determined by a displaced apical impulse, and sure “damming” the blood in the lungs and reducing the listened for a presystolic, protodiastolic (ventricular) or vital capacity. This backward theory, though supported by summation gallop, accentuation of the pulmonic sound, an pathology, was deficient in not explaining circumstances apical systolic murmur of relative mitral insufficiency and 1146 Silverman JACC Vol. 33, No. 5, 1999 The Practice of Cardiology in 1950 April 1999:1141–51 basilar rales. A hydrothorax was discovered by percussion. of cheerfulness that should surround the patient, a natural Pulsus alternans, a key finding, was determined by slowly attribute of a good doctor and a good nurse and one of the deflating the arm blood pressure cuff until alternate beats, chief elements in the psychotherapy of heart disease (1).” separated by 5–20 mm Hg, were heard (2). With right heart failure, the findings included jugular venous distention, measured in centimeters above the ster- INFECTIONS OF THE HEART nal angle with the patient’s chest elevated at 30–45°, prominent superficial , hepatomegaly, edema, ascites, Cardiovascular syphilis. Cardiovascular syphilis remained jaundice and mild cyanosis. a problem causing 5% to 15% of heart disease in the U.S. and United Kingdom. The infection was clearly in retreat, Laboratory tests. The chest X-ray was scanned for cardiac Paul Dudley White optimistically commenting “This is enlargement, congestion and pleural effusion. Measurement another chapter which we may justifiably hope and expect to of a reduced vital capacity, previously greatly stressed, was in become obsolete during the next generation (1).” decline. Patients were routinely fluoroscoped to look for weak cardiac pulsations. Importance was placed on the CLINICAL FINDINGS. The disease was insidious and clini- measurement of a delayed circulation time, obtained by cally silent for many years. The ostial narrowing could cause injecting ether or Decholin into an arm vein and timing its angina, often nocturnal and prolonged, but rarely infarction. appearance in the breath (ether) or taste buds (Decholin) Progressive aortic regurgitation led to increasing cardiomeg- (3). Venous pressure measurement, obtained through a aly and ultimately to heart failure. Severe dilatation of an saline-filled manometer connected to a needle that had been aneurysm of the ascending aorta could eventually compress inserted into the median basilic vein, was popular for the or erode nearby structures thereby causing cough, hoarse- bedside measurement of venous pressure. Radioactive iso- ness, dysphagia and pain. Distention of the jugular vein only topes were in their infancy and used by a few to measure in the right side of the neck indicated superior venal caval circulation time. The cardiac output could be estimated by obstruction. Sudden death, especially from rupture of an the Fick method, injection of dyes and the ballistocardio- aneurysm and also related to combined ostial stenosis and graph. aortic regurgitation, was not uncommon (2).

Treatment. General measures included limiting strain and LABORATORY CONFIRMATION. The diagnosis was sus- exercise, restricting sodium and water, dieting and resting in pected by finding aortic regurgitation on examination or an bed from days to weeks to many months when necessary. A abnormal bulge or widening of the aorta on chest X-ray. A daily bowel movement was felt desirable. There was no positive Wasserman or Kahn serology clinched the diagno- objection to moderate amounts of alcohol, tobacco, coffee or sis, though a 15% false-negative rate was appreciated (3). tea. Digitalis was the most valuable drug and prescribed in the form of a powdered leaf, digilanid, digitoxin or intra- TREATMENT. Heavy metals (bismuth and arsenical injec- venously. Great emphasis was placed on the exact schedule tions) were still given routinely for the chronic infection. of digitalization as well as observing a heart rate response Penicillin was administered every 3 hours or so for 2–3 when auricular fibrillation was present (1). Digitalis toxicity, weeks. A Jarisch-Herxheimer reaction was feared. Surgery judged by intestinal symptoms, visual changes or new was limited to cellophane encasing of the aneurysm or arrhythmia, was carefully monitored clinically since blood passing a galvanic current through a coiled wire inside the levels were not available. Diuretic therapy was effectively aneurysmal sac (2). delivered only by injection of mercurials given one to several Diphtheria. Diphtheria still occurred causing heart failure, times a week, often by lining patients up in “merc clinics.” shock and atrioventricular block in 10%–20% of afflicted Ammonium salts were felt to improve the response to patients. World War II had seen outbreaks of the disease, mercurials by acidifying the blood. Xanthine derivatives but Paul Dudley White commented, “...happily it has were weak diuretics occasionally used as adjuvants. Chloro- been robbed of so much of its threat in recent years by large thiazide, the first potent oral diuretic, would not become scale prevention...andbytheuseofantitoxin, that much available until 1958 (13). Failing to respond to mercurial less diphtheritic heart disease is nowadays diagnosed than diuretics, a patient might receive oral urea, sedatives, ca- was the rule a generation ago (1,3).” thartics, laxatives or a medical or surgical thyroidectomy (1). Patients with pleural effusions, ascites and marked edema PROGNOSIS AND TREATMENT. Mortality was very high, were often treated mechanically by thoracentesis, paracen- ranging from close to 100% in children under two to 25% in tesis and puncturing or incising the edematous thighs or adults (3). Sudden death was common. The cardiac effects legs, sometimes with the insertion of drainage (Southey) of the illness could vanish entirely or leave fibrosis or chronic tubes. Acute pulmonary edema was handled emergently bundle branch block in its wake. Early use of diphtheria with oxygen, morphine, rotating tourniquets, and venesec- antitoxins and penicillin was the main therapy. Bed rest, tion of 350–1,000 cc. fluids and management of heart failure and shock were all Paul Dudley White adds, “Last but not least is the spirit that were available. Digitalis was considered dangerous. JACC Vol. 33, No. 5, 1999 Silverman 1147 April 1999:1141–51 The Practice of Cardiology in 1950

Bacterial endocarditis. In this period when valvular dis- (especially for a thrill), the symmetry and character of ease was so prevalent, bacterial endocarditis was common, arterial , the jugular waves for pulmonary hyperten- infecting 10% to 25% of patients with rheumatic heart sion and the components and splitting intervals of the disease (3,5). In addition, there was a 15% incidence of second heart sound. Paul Wood emphasized, “No sign will endocarditis with congenital heart defects, most often with repay closer study than the second heart sound at the a bicuspid aortic valve, ventricular septal defect, patent pulmonary area.” ductus arteriosus, pulmonic stenosis and coarctation of the Laboratory. Taussig relied on the chest X-ray with ob- aorta (3). The recent availability of antibiotics for the liques and fluoroscopy to evaluate the chamber size, pulmo- treatment of pneumonia and other infectious illnesses had nary flow and aortic arch position. She considered the reduced the risk of endocarditis. Streptococcal viridans led electrocardiogram to be “a useful adjunct” but not specific the list of responsible organisms with Pneumococcus, Staph- except for dextrocardia and anomalous origin of the left ylococcus aureus, Enterobacillus coli, Gonococcus, and Meningo- coronary from the pulmonary artery. Though angiog- coccus trailing far behind (3,5). raphy of congenital heart disease was available since the late CLINICAL FINDINGS. The disease was suspected when a 1930s and the cardiac catheter diagnosis of atrial septal patient with valvular or congenital disease developed recur- defect had been reported in 1945, Taussig did not provide rent fever of prolonged duration, often associated with catheter or angiographic information. She does describe the chills, sweats, prostration, anorexia, weight loss, anemia or measurement of the pulmonary circulation time by injecting embolic events. In the absence of positive blood cultures, ether and the systemic circulation time by using saccharine active rheumatic fever was in the differential. Embolic or decolyn. phenomena included arterial embolism causing stroke, re- Treatment. The child with congenital heart disease was nal, splenic, intestinal or limb infarct, renal failure secondary often coddled and activities were restricted. Taussig strongly to glomerulonephritis, mycotic aneurysm and pulmonary opposed this approach: “The two most important consider- embolus. ations in the care of patients with congenital malformations TREATMENT. Prophylactic measures meant attention to of the heart are: 1) Allow the individual to lead as normal a dental hygiene; antibiotic coverage started 24 h prior to, and life as possible. 2) Surround him with an atmosphere of continued 48 h after, dental extraction and tonsillectomy confident expectation that he will grow.” and repair of a patent ductus and coarctation. The untreated Immunization for diphtheria, tetanus, pertussis and disease was 97% to 99% fatal, though a few made a smallpox was advised. Dental hygiene was important, and spontaneous recovery, and others developed a chronic form sulfa or penicillin were administered several days before and that could fester for years (1). Sulfonamides, with or without after dental work. heparin, provided only a slight (5% to 6%) improvement in Pregnancy was contraindicated for women with cyanotic mortality. The introduction of penicillin in the early 1940s congenital heart disease, Eisenmenger’s syndrome and atrial had dramatically improved survival up to 80%. Doses of septal defect with a dilated right heart but not with 60,000 to 1 million units of penicillin were given every 3–6 uncomplicated atrial septal defect, patent ductus arteriosus, hours (commonly 1 million units total a day). Paul Dudley ventricular septal defect, pulmonic stenosis or coarctation of White commented, “A high mortality was one characteristic the aorta (1,2). of this disease, prior to the use of penicillin in 1944, but now Cyanotic spells in children were treated with oxygen and recovery is the rule (1).” morphine. Severely cyanotic and polycythemic children were considered at risk for cerebral thrombosis, and hydra- tion was maintained. Exciting developments had recently CONGENITAL HEART DISEASE taken place in congenital heart surgery—the ligation of a patent ductus arteriosus by Gross and Hubbard in 1939, Until the 1940s, congenital heart disease was understood repair of an aortic coarctation by Crafoord and Nylen in primarily from the landmark autopsy information compiled 1945 and pulmonic valvotomy by Holmes Sellors in 1947 by Maude Abbott in 1924 (9,10). The 1947 publication of and Brock in 1948 (12,13). The surgical mortality rate in Congenital Malformations of the Heart by Helen Taussig 1950 was 2% to 3% for patent ductus closure and 10% to illuminated the clinical side of the story (9). In the forward 16% for coarctation repair. The Blalock-Taussig subclavian to her book, Edwards Park comments, “She has done for the artery to pulmonary artery shunt, introduced in 1945, clinician what Dr. Maude Abbott did for the pathologist, dramatically changed the approach to cyanotic congenital namely, made the malformations of the heart understand- heart disease. Intracardiac repair of congenital defects, first able and accessible, but her work has a practical usefulness used with hypothermia, would not be reported until 1945. which Dr. Abbott’s, owing to its nature, could not possess.” Charles Friedberg exulted “...amazing progress has been Examination. The findings on examination for the major- achieved in the surgical treatment of certain congenital ity of patients had been carefully described by Taussig, cardiovascular anomalies, and these advances enhance the Wood and others. Particular attention was paid to palpation important of diagnostic accuracy (3).” 1148 Silverman JACC Vol. 33, No. 5, 1999 The Practice of Cardiology in 1950 April 1999:1141–51

PSYCHONEUROTIC CARDIOVASCULAR DISORDERS was in vogue (2). The ventricular gradient and intrinsicoid deflection were calculated. Criteria for hypertrophy, bundle Major symptoms referable to the heart or chest in an branch block, ischemia, infarction and pericarditis were well apparently normal person with no discernable cardiac find- established. ings was a matter of great concern and debate. Known variously as neurocirculatory asthenia, Da Costa’s Syn- Sinus node. Prolonged asystolic periods without P waves drome, The Soldier’s Heart, Effort Syndrome, Cardiac were called sinoatrial (or auricular) block and sinus arrest, Neurosis, Irritable Heart and Disordered Action of the pauses or standstill. These were blamed on digitalis, quin- Heart, the problem warranted attention because it had to be idine, advanced potassium intoxication, infection and or- distinguished from organic heart disease. The association ganic heart disease, or thought to be a manifestation of a with anxiety, hyperventilation and automatic disturbance high vagal tone or a sensitive carotid sinus. Paul Wood was clear; however, the exact cause of the tachycardia and stated, “There are no symptoms of sino-auricular block per chest pain was not. Paul Wood said, “It should be under- se, but occasionally short periods of cardiac standstill, with stood that there is no essential difference between “effort dizziness or syncope, may occur and appear to be due to syndrome” and “cardiac neurosis,” they are merely clothed bursts of extreme vagal activity (2).” A tachy-brady associ- differently, the former in battle dress, the latter in artificial ation was not yet known. silk (2).” Treatment was felt to be very difficult and required a A-V node. Second-degree atrioventricular block was also complete cardiovascular examination and testing to provide referred to as partial heart block; the two types were unconditional reassurance. Psychiatric referral was often Wenckebach and a more severe form of partial heart block necessary. Paul Wood commented, “The patient’s reaction characterized by a fixed P-R interval with beats dropped should be analysed, and some psychiatric skill and knowl- unpredictably. The term “Mobitz II” was not used. Com- edge are required to do this. It is often possible to show that plete heart block was a major concern because it produced his reaction is based on false values, ideas, or beliefs. Or one dramatic, recurrent Stokes-Adams attacks in those pre- may simply explain just why he so reacts, in order to give pacemaker days. “Nodal rhythm” was the traditional term him insight. It is impossible to outline precisely just what is for an escape beat or rhythm arising above the bundle required, for every case is different, and needs individual branches. Heart block was attributed to coronary disease, treatment (2).” calcific aortic stenosis, hypertensive heart disease, congenital heart disease, a syphilitic gumma, neoplasm, drugs (digitalis, quinidine) and infections or inflammatory disease (notably rheumatic fever and diphtheria). Electrocardiography was an established discipline thanks to Auricular (atrial) . There were three auricu- the monumental contributions of Einthoven, Lewis, Wil- lar/atrial tachycardias: auricular (atrial, nodal) paroxysmal son, Wenckebach and others (14). Paul Dudley White tachycardia, auricular/atrial fibrillation and auricular (atrial) exclaimed that “Electrocardiography is one of the most flutter. A circus movement or an irritable ectopic focus was important methods of cardiovascular examination, ranking invoked as alternate explanations for all three. Dual path- in value third after history taking and physical examination ways were not known. Auricular fibrillation was caused by (1).” Although an exploring bipolar electrode was available rheumatic heart disease, especially mitral stenosis, coronary in the 1930s, the interpretation was usually based upon the disease, hypertension, thyrotoxicosis and old age. The risk original three bipolar leads of Einthoven until the 1940s. of stroke with atrial fibrillation was not yet realized. Atrial Wilson introduced the central terminal in 1934, and in 1935 he standardized the six unipolar precordial leads (14). flutter was seen with mitral stenosis, hypertension, thyro- Goldberger contributed the augmented unipolar limb leads toxicosis, and in healthy individuals. in 1947, which were thought to provide more precise Wolff-Parkinson-White syndrome. After the 1930 classic electrical views of the chambers. After World War II, the description of “physiological bundle branch block with short laborious photographic method of recording electrocardio- P-R interval,” the electrocardiographic features of the grams was replaced by a direct recording using a heated Wolff-Parkinson-White Syndrome and its linkage with stylus to burn the tracing onto wax paper. Electrode jelly or paroxysmal rapid rhythm disturbances and an anomalous paste was applied to conduct the electrical current from the Kent bundle had become well established (14). patient to the metal electrodes. The electrical activity of the heart could also be obtained by esophageal leads, intracar- Ventricular tachycardia. Ventricular tachycardia was a diac recordings and vectorcardiography. The electrical anat- complication of recent myocardial infarction, hypertensive omy and physiology were understood, and the interpretation heart disease, digitalis and was sometimes documented in an of underlying disease and arrhythmias quite advanced. In apparently normal person. An accelerated idioventricular order to explain the morphology of the precordial leads, an rhythm and polymorphic tachycardia/torsade de pointes interpretation of a clockwise or counterclockwise rotation were not in the textbook vocabulary. JACC Vol. 33, No. 5, 1999 Silverman 1149 April 1999:1141–51 The Practice of Cardiology in 1950

Management. Premature beats were generally regarded as cardiologists had an excellent understanding of the clinical having no clinical importance when there was no associated presentation of cardiac problems and placed their diagnostic heart disease. Worry, nervous excitement, effort, hearty faith in a thorough clinical history and examination, sup- meals, caffeine, alcohol and tobacco were sometime impli- ported by the electrocardiogram and chest x-ray film. The cated. Paul Wood felt “Reassurance is important and should essential cornerstone of therapy was an in-depth under- be unconditional and convincing, for it should be remem- standing of the patient based on long-term follow-up care. bered that ectopic beats rarely constitute a complaint except Effective medical therapy was confined to digitalis, mercu- in those prone to morbid anxiety (2).” rial diuretics, morphine, nitroglycerine, quinidine, antico- The treatment of a slow, symptomatic heart rate or long agulants, penicillin, sedatives, rest, special diets and phle- asystolic periods was vexing. Pacemakers were not available. botomy. Cardiopulmonary resuscitation meant open chest Ephedrine and sublingual adrenaline were the only oral cardiac massage and defibrillation with the intracardiac medications, albeit short-lived and unreliable. In the hos- injection of adrenaline and calcium. There were no special pital setting, subcutaneous injections of atropine and adren- care units, defibrillators, cardioverters, pacemakers, potent aline could be helpful. Digitalis was avoided unless heart antihypertensive agents or diuretics to take care of the many failure was pronounced. Adrenocorticotrophic hormone patients with rheumatic and syphilitic valvular disease, (ACTH) and cortisone were sometimes tried for acute heart hypertension or coronary artery disease and their complica- block when infarction or inflammation was the presumed tions (Table 1). The prognosis for patients with advanced cause (1). heart disease was generally grim. Sophisticated testing was Auricular tachycardias were liberally dosed with digitalis limited to the Master’s two-step exercise test and the until the rate was slowed or side effects occurred. Quinidine injection of agents to measure the circulation time. Al- was the workhorse to convert atrial fibrillation or flutter. It though right heart catheterization was available in a few was scheduled every 2 hours for five doses a day with academic centers, it was of little clinical importance because increased doses daily until the rhythm resolved. The asso- surgery was possible for only a few congenital defects (Table ciation of quinidine with sudden death was known but felt 2). to be rare. Paul Dudley White explained, “The more normal Funded and energized by the post–World War II enthu- the heart fundamentally, the more likely is quinidine to act siasm for research, specialty training and technology, cardi- successfully and safely. Hence it is particularly indicated ology has radically changed from a placid, clinically based when the arrhythmia is simply a very annoying disorder of field to what now seems to be a frenzied, procedurally function...since quinidine in large dosages is a poison, it oriented specialty with an emphasis on catheter interven- must be used with care, and by the exercise of care accidents tion, cardiovascular surgery and transplantation and device and fatalities that have been reported in rare cases in the past implantation. Rheumatic fever, syphilis and diphtheria have can largely be avoided (1).” Procainamide was a recent almost vanished as cardiac problems from most areas of the discovery, mentioned only in one textbook, and was felt to world, and have been replaced by a preoccupation with be effective. coronary disease, sudden death and risk factor reduction. Episodes of supraventricular tachycardia were responsive Hypertension, once unmanageable, has been tamed by to breath holding, Valsalva maneuver, gagging or pulling on effective treatment for the majority of patients; malignant the tongue, drinking cold water or ingesting ipecac, com- hypertension, once so feared, is virtually a disease of the pressing the eyeball or the carotid sinus for 10–30 s or an ice past. The management of coronary disease, congestive heart bag applied to the chest. Failing one or several of these failure and congenital heart disease is dramatically better. maneuvers, the administration of subcutaneous anticholin- The cardiologist, once widely knowledgeable about all ergic drugs (mecholyl or prostigmine) was often successful. aspects of heart disease and its evaluation, has become Digitalis and quinidine were used if all else failed. increasingly superspecialized into areas such as noninvasive Quinidine, intravenous magnesium sulfate and oral po- cardiology, angioplasty and electrophysiology. It has been tassium salts were the only resort for recurrent ventricular said that these specialists often know more and more about tachycardia or fibrillation. Open chest defibrillation in the less and less. Paul Wood, in the introduction to his 1950 operating room only had been reported by Claude Beck in textbook, anticipated this prospect worrying, “There is 1947 (13). already plenty of evidence to show that we are in danger of losing our clinical heritage and of pinning too much faith in COMMENT figures thrown up by machines. Medicine must suffer if this tendency is not checked (2).” Unfortunately, his concern has Extraordinary developments have occurred in the field of come to pass as cardiology has been increasingly criticized cardiology over the past 50 years. In 1950, with the for being technically oriented at the expense of bedside skills exception of a few full-time cardiologists at academic and clinical judgment. centers, the heart specialist was primarily a practicing In his 1951 introduction to his 4th edition of Heart general with an interest and limited training in Disease, Paul Dudley White, looked forward with anticipa- heart disease and electrocardiography (11). These part-time tion to the next 50 years: “Thus, on the threshold of a new 1150 Silverman JACC Vol. 33, No. 5, 1999 The Practice of Cardiology in 1950 April 1999:1141–51

Table 1. Advances in Therapy: 1950–2000 Table 2. Advances in Diagnostic Techniques: 1950–2000 1950–1960 1950–1960 Carbonic anhydrase Hypothermia Left heart catheterization inhibitors Selective coronary arteriography Chlorothiazide External cardiac pacing M-mode echocardiography Hexamethonium Mitral valvotomy Serum glutamic oxaloacetic transaminase Reserpine Vineberg procedure 1960–1970 Procainamide Coronary endarterectomy Bicycle and treadmill exercise testing Defibrillation Aortic valvotomy Holter monitoring Senning procedure for Rastelli procedure 1970–1980 transposition Creatine phosphokinase 1960–1970 Nuclear cardiology Lidocaine Implantable pacemaker 2-D echocardiography Alpha methyl dopa Aneurysectomy Doppler echocardiography Spironolactone Prosthetic and homograft Electrophysiologic testing cardiac valves 1980–1990 Furosemide and Cardiac transplantation Signal-averaged electrocardiography ethacrynic acid Positive emission tomography Beta blockers Coronary artery bypass Magnetic resonance imaging surgery ST segment monitoring Bretylium tosylate Coronary care units Color Doppler flow echocardiography Intra-aortic balloon pump Cardiac rehabilitation 1990–2000 Cardioversion CPR (closed chest) Pharmacologic stress testing Mustard procedure for Echo stress testing transposition Coronary angioscopy and ultrasound 1970–1980 Troponin I and T Sodium nitroprusside Mitral valve repair Ultra-fast computerized tomography Hydralazine Potassium cardioplegia Calcium channel blocking Coronary angioplasty agents Nitroglycerine drip Intracoronary thrombolysis coronary circulation (1).” At the year 2000 milestone, (streptokinase) cardiology can look back at its half century of accomplish- Dopamine and Amiodarone ments with great pride and optimism that even coronary dobutamine atherosclerotic disease, the major scourge of today, might Isosorbide dinitrate Propafenone also prove to be as susceptible to future advances as Disopyramide Correction of Tetralogy of rheumatic fever and hypertension did in the past. But, at the Fallot same time, we will also need to balance our remarkable 1980–1990 technical prowess with a rejuvenation of the basic bedside Aspirin for coronary Intravenous thrombolysis oriented skills of cardiology as practiced so skillfully circa disease (t-PA) Ace inhibitors Statin lipid lowering agents 1950. Phosphodiesterase Surgery for Wolff-Parkinson- inhibitors White (WPW) Acknowledgments Flecainide His bundle ablation I thank Diana Silverman for her thoughtful editorial work Automatic implanted Antitachycardia pacemakers and Arthur Hollman, Barry Silverman, Charles Upshaw, defibrillators Tillie Tansey and Desmond Julian for their advice. The 1990–2000 many resources of the Wellcome Institute for the History of Ticlopidine Atherectomy Medicine were invaluable. Carvedilol Intracoronary stents Reprint requests and correspondence: Mark E. Silverman, MD, FACC, 1968 Peachtree Road, NW, Atlanta, Georgia 30309. E-mail: [email protected]. half century we face the full challenge, which we have come a long way to recognize as such. We must, and I am confident that we can, master during the next quarter century much, if not all, of the three greatest threats to the REFERENCES public health of this country and of much of the rest of the 1. White PD. Heart Disease. 4th ed. New York: MacMillan, world, each one more important than any other threat of our 1951. day—namely, rheumatic heart disease, high blood pressure, 2. Wood P. Diseases of the Heart and Circulation. London: and presenile arteriosclerosis, especially as it involves the Eyre and Spottiswoode, 1950. JACC Vol. 33, No. 5, 1999 Silverman 1151 April 1999:1141–51 The Practice of Cardiology in 1950

3. Friedberg C. Diseases of the Heart. Philadelphia: W.B. 9. Taussig H. Congenital Malformations of the Heart. New Saunders, 1950. York: EL Hildreth, 1947. 4. Levine S. Clinical Heart Disease. Philadelphia: W.B. Saun- 10. Brown JW. Congenital Heart Disease. London: Staples Press, ders, 1951. 1950. 5. Levy RL. Disorders of the Heart and Circulation. New York: 11. Fye WB. American Cardiology. Baltimore, MD: The Johns Thomas Nelson. Hopkins University Press, 1996. 6. Boas EP, Boas NF. Coronary Artery Disease. Chicago: The 12. Shumacker HB, Jr. The Evolution of Cardiac Surgery. Year Book Publishers, 1949. Bloomington, IN: Indiana University Press, 1992. 7. Page IH, Corcoran AC. Arterial Hypertension. Chicago: The 13. Acierno LJ. The History of Cardiology. London: Parthenon, Year Book Publishers, 1946. 1994. 8. Fishberg AM. Heart Failure. London: Henry Kimpton, 14. Burch GE, De Pasquale NP. A History of Electrocardiogra- 1940. phy. San Francisco: Norman, 1990.