Author + information
- Received August 28, 1998
- Revision received November 24, 1998
- Accepted January 5, 1999
- Published online April 1, 1999.
- ↵*Reprint requests and correspondence: Mark E. Silverman, MD, FACC, 1968 Peachtree Road, NW, Atlanta, Georgia 30309
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.
The year 2000 provides a vantage point to look back and see how cardiology has progressed. I have chosen 1950 as a pivotal moment because, as it turned out, that year roughly divides two vastly different eras in cardiology—one in which cardiology was practiced predominately by generalists and internist-cardiologists who depended upon their bedside skills, a few basic tests, and limited medical and surgical options, and the other a post–World War II exuberant growth, fueled by government and pharmaceutical funding, that would eventually become dominated by highly trained, full-time specialists, the cardiac catheter and a proliferation of therapeutic options.
To comprehend the enormous changes that have occurred since 1950, I have provided an in-depth discussion of the understanding of heart disease from that period based on authoritative American and British texts published primarily between 1946 and 1951 (1–10)and other sources (11–14). The terminology of that time has been used throughout. Advances in treatment and technology since 1950 are then presented in Tables 1 and 2.
Valvular heart disease
In 1950, valvular heart disease was understood to be mostly due to the inflammatory consequences of rheumatic fever. Syphilis was still frequent and an important cause of aortic regurgitation. Stretching of the aortic ring, due to hypertension, was thought to produce “functional aortic regurgitation;” “functional mitral regurgitation” was a secondary effect of left ventricular failure and dilatation (3). In most cases, aortic valve calcification and stenosis, even in the elderly, was attributed to long-standing rheumatic involvement, though a primary nonobstructive arteriosclerotic aortic condition (Monckeberg’s sclerosis) was described (3). Mitral valve prolapse was not yet reported. Aortic dissection was a rare etiology of aortic regurgitation; however, primary dilation of the aortic root was not mentioned. Endocarditis was a common problem.
Acute rheumatic fever was common between ages 5 and 12. Though noted to be on a slight decline, it was still the leading cause of death from ages 5 to 20 in the United States. During World War II, 4%–5% of young soldiers infected by hemolytic streptococcus developed acute rheumatic fever. Paul Dudley White commented (1), “One of the most important reasons why rheumatic heart disease is so serious is the fact that it is particularly a disease of youth, crippling and killing many children and young adults.”
The cause of rheumatic fever was uncertain, but its connection with certain streptococcal strains was well known (1). The absence of a clinical history in 40% to 50% of patients was puzzling but suspected to be due to atypical and unrecognized attacks. Carditis was suspected when one or more of the following was found: a pericardial rub, cardiac enlargement, heart failure, aortic or mitral regurgitation, a diastolic mitral murmur (Carey-Coombs murmur) or a presystolic gallop (4). The sedimentation rate, white blood cell count and temperature were followed for evidence of continuing rheumatic activity.
Prophylactic prevention stressed avoidance of respiratory infections, prompt penicillin treatment of streptococcal pharyngitis, small doses of sulfonamides or penicillin throughout the winter or spring in susceptible children and tonsillectomy. Treatment for acute rheumatic fever was limited to salicylates and absolute bed rest for several months or longer. Fever therapy, up to 106°F, was sometimes tried for chorea. Corticosteroids, just introduced in 1949, were reported to be successful in early small series (2).
These were the times of unoperated, advanced rheumatic valvular disease. By 1950, the symptoms and bedside cardiac findings had been extensively correlated with the chest X-ray, fluoroscopy and the electrocardiogram. Typical facial appearances were sought—a malar, cyanotic flush on a pale background was suggestive of mitral stenosis, while a delicate pink “Dresden china” appearance was noted with aortic stenosis (2). The cardiac examination had become a fine art as practiced by Paul Wood, Samuel Levine, Paul Dudley White and others (1–4).
The classic auscultatory findings of each valve abnormality were well known. Valvular regurgitation was most commonly called “insufficiency” in the United States (3)and “incompetence” in Great Britain (2). Late systolic murmurs were often attributed to an extracardiac or innocent source. Paul Wood said, “It is now known, however, that apical systolic murmurs may be cardiac or extracardiac, and if cardiac may be due to mitral incompetence … mitral incompetence itself may be organic or functional (2).”
The chest x-ray included oblique and barium-filled esophageal views to check for cardiomegaly or specific chamber enlargement. Office fluoroscopy was routinely done. The electrocardiogram was important for rhythm analysis and could point to chamber dilatation or hypertrophy. Right heart catheterization and angiography was possible in a few academic centers only beginning in 1945 at the Johns Hopkins and the Peter Bent Brigham Hospitals (11).
When significant valvular disease was present, patients were advised to avoid effort and to seek a sedentary occupation. Charles Bailey in Philadelphia and Dwight Harken in Boston initiated surgery for acquired valvular disease with their reports of successful mitral commissurotomy for mitral stenosis in 1948 (12).
Persistent or recurrent rheumatic carditis with cardiomegaly predicted a worse outcome. Auricular fibrillation was ominous. Marked mitral insufficiency brought about death in “just a few years” at best. Patients with significant mitral stenosis could live 10–20 years, and occasionally much longer. Their average age at death was 35, however, 25% survived to age 50 or longer (2,3).
Aortic valve disease due to syphilis carried a worse prognosis, apparently because of associated ostial coronary stenosis (3). Patients with aortic insufficiency could live for 20–30 years (2). Aortic stenosis carried a 5% to 18% risk of sudden death and a 10% incidence of bacterial endocarditis (2). The average age of death with predominant aortic stenosis was 55.8. When heart failure developed, the survival was from a few months to 2 years (3).
Pregnancy and valvular heart disease posed a special concern. Paul Dudley White mentions, “The important question concerning heart disease in pregnancy is the prognosis, one of the most difficult problems in medicine … No rule can be set, except that pregnancy should be forbidden or terminated early if symptoms and signs of heart failure appear early or if there have ever been symptoms or signs (1).” It was estimated that 90% of cardiac disease in pregnant women was due to rheumatic valvular disease, and that mitral stenosis alone or in combination with aortic valve disease was present in 75% of these cases.
At the turn of the 20th century, the mortality in symptomatic pregnant patients was around 50%, and the fetal mortality was correspondingly alarming (3). If pregnancy was restricted to women who were classed as New York Heart Association Class I (no limitation of activity) or II (slight or moderate limitation of activity) who had never been in heart failure, then the mortality was nil (3). The management of symptomatic patients relied upon strict bed rest, salt restriction, digitalis, mercurial diuretics, quinidine and, for acute pulmonary edema, morphine was the choice. With strict care, the overall mortality, had fallen to 2%–3% in 1950 (3).
Hypertension was defined according to the diastolic pressure alone and was graded as mild (90–110 mm), moderate (110–130 mm) and severe (130–150 mm) (7). Malignant or accelerated hypertension indicated a diastolic pressure in the severe range associated with funduscopic abnormalities and rapidly worsening renal function. Systolic blood pressure elevation was attributed to rigidity of the great vessels and dismissed as not serious; a diastolic elevation was vasoconstrictive in origin and the cause of true hypertension.
Incidence and etiology
Hypertension was common, said to affect 30%–40% of the U.S. and British population over age 40, and account for 15%–20% mortality in those times when treatment was so limited. As Paul Dudley White commented, “The most common and important of all types of heart disease by and large the world over is that due to systemic hypertension with elevation of diastolic blood pressure. It is often serious and frequently followed by congestive failure and death (1).”
Known etiologies of hypertension were listed as acute and chronic renal disease, endocrine disorders, coarctation of the aorta, central nervous system lesions and toxemia of pregnancy (3). The classic experimental studies of Goldbatt and the association of renovascular disease and nephritis with the release of renin and other pressor agents was well understood. Essential hypertension, probably genetically related, was felt to explain 80% of hypertensive cases (7).
The association of hypertension with coronary disease, left ventricular hypertrophy and congestive failure, auricular fibrillation and sudden death was clear (3). Stroke due to high blood pressure was greatly feared by the public, and one author stated, “There are few fields in medicine in which so much legendary misinformation has played a role in the management of the patient. Because of the belief that a very high blood pressure is the precursor of a “stroke,” patients (and their doctors) have been needlessly frightened and their life programs unnecessarily interrupted (5).”
Diagnosis and management
A urinalysis, blood urea nitrogen, X-ray for renal size and an occasional intravenous pyelogram was the limited workup in most cases. Treatment was meager. As Paul Wood lamented, “It must be said at once that there is no satisfactory treatment for essential or for malignant hypertension (2).” In many cases, no treatment was given on the belief that the symptomatic patient would live for many years without complications. Furthermore, physicians did not want to frighten patients by creating alarm, often informing them of a “tendency” to high blood pressure. Patients were strongly advised to achieve mental and physical tranquility by living at a lower tempo, resting and sleeping long hours and avoiding the strains of work, heavy meals and emotional upset. A mental component was strongly suspected and sedatives such as phenobarbital, chloral hydrate and bromides were used and psychotherapy might be recommended. Alcohol in moderation was permitted and thought to be helpful as a sedative and vasodilator. Salt was stringently restricted, and diets with less than 1 g salt daily, such as the Kempner rice diet, were popular though one author stated, “The evils of rigid sodium restriction usually outweigh the benefit (3).” Drug treatment was limited to thiocyanate and veratrum alkaloids, both highly toxic drugs that were poorly tolerated.
Surgery, at significant risk, was applied to an adrenal or pituitary tumor or coarctation of the aorta. A splanchnic nerve lumbar sympathectomy was a surgical gamble used in about 10% of patients with advanced hypertension. Dramatic benefit was occasionally produced at the cost of 0.5%–8.8% mortality, impotence and unpleasant orthostatic hypotension (3).
Coronary ischemic heart disease
The understanding of coronary disease focused on fixed obstruction, primarily due to atherosclerotic narrowing of the vessel by atheroma, scar and calcification (3,6). A “discharge” of an atheromatous abscess could leave behind an ulcerating intimal lesion. Thrombosis was initiated by an abrupt intimal hemorrhage from neighboring vasovasorum (6). Infarction depended upon the rate of progression of narrowing and the formation of collateral circulation (1). Coronary spasm was postulated to occur at times though to be uncommon because of the rigidity of the calcified vessels (4). The cause of atherosclerosis was unknown; however, a faulty cholesterol metabolism, heredity, aging, diabetes and “mechanical” factors such as hypertension were clearly involved (3).
Tobacco was not regarded as a causal factor but known to provoke anginal attacks when used in excess (2,3). The strain of living, especially in a person with intense emotions or an ambitious drive, was a risk factor. Myocardial ischemia, in the absence of coronary disease, was recognized to occur with aortic stenosis or regurgitation, severe anemia, paroxysmal tachycardia and hyperthyroidism (4).
The incidence of coronary disease was increasing. Professionals, especially physicians, were said to have an especially high incidence (2). For unknown reasons, males were affected more often and more seriously than females until age 70, when the incidence was equal. After a diagnosis of angina pectoris, the life expectancy was estimated to be 5 to 10 years (2,3).
The diagnosis of angina pectoris was made by scrupulous attention to classic symptoms and precipitating factors. Rest angina was attributed to an increased work load on the heart from digestion, cold reflexes, disturbing dreams or endocrine factors. Pain was often likened to intermittent claudication or a ligature put around a limb causing ischemia and a release of noxious metabolites (3).
“Coronary insufficiency” was the commonly applied term for an intermediate stage of pain between angina pectoris and infarction. It was attributed to coronary spasm or prolonged stimulatory factors such as tachycardia, extreme bradycardia, severe hypertension, shock, anemia or high altitude, and could cause infarction even in the absence of a new thrombus (3,6).
“Silent” coronary disease, manifested by occluded coronary arteries and normal myocardium at autopsy, or electrocardiographic evidence of infarction in the absence of a clinical story, was recognized (1,6). Sudden death was attributed to an attack of acute coronary insufficiency or coronary vasoconstriction causing ventricular fibrillation or standstill in 80% of cases (6).
The cardiac examination of patients with angina was not rewarding in the absence of aortic valve disease. With infarction, however, the textbook findings were dramatic, including restlessness, a shock-like appearance, fever up to 102°F, an elevated venous pressure, a rapid heart rate or irregular rhythm, faint heart sounds, a gallop and a friction rub in 10% to 20% (3).
The electrocardiogram was the supreme test, though it was known to be normal with milder forms of stable coronary disease. Exercise testing was done by checking an electrocardiogram before and after climbing a flight of stairs or performing a “Masters 2-step” test (3). Other provocative tests included inducing anoxemia with an inhalation of 10% oxygen and 90% nitrogen and injecting a subcutaneous dose of adrenalin (4). Calcification of the coronary arteries was sometimes detected by fluoroscopy. Samuel Levine promoted the use of carotid sinus stimulation during an episode of chest pain (4). If the pain improved, a confident diagnosis of angina could be made. An acute infarction was confirmed by classic electrocardiographic changes and serial measurement of a rising white blood cell count and sedimentation rate.
Treatment was limited. A moderate, low-fat diet, small frequent meals, the avoidance of large rich meals, reduction of mental stress and careful attention to the bowels was advised. Tobacco use was severely restricted by some, while alcohol was advised for treating angina (2). Nitrates in the form of nitroglycerine were highly effective for angina but considered dangerous with infarction. Xanthine derivatives were sometimes used. Sedatives were popular.
A “lazy” vacation in a warm climate or prolonged bed rest was recommended for unstable patients. Intractable angina pectoris gave risk to a number of radical approaches, which included paravertebral alcohol injection, dorsal sympathectomy or ganglionectomy, the induction of myxedema, anastomosis of the pectoral muscle or omentum to the heart, instillation of powdered asbestos talc or bone dust into the pericardium, ligation of the great cardiac vein and radiation to the anterior chest (2,12).
Patients with an acute coronary thrombosis were often, but not always, hospitalized in an unmonitored room or ward. Morphine was the single most important drug for the treatment. Antiarrhythmic drugs were limited to quinidine for ectopy and ephedrine for heart block. Digitalis was avoided unless heart failure developed, in which case mercurial diuretics and a low-salt diet were also advised. Heparin, 50 mg every 4 h, and oral dicoumarol for three to six weeks were strongly advocated by some beginning the first day for infarction (2,4). Paul Wood, a strong advocate, said, “The onset or sudden deterioration of angina pectoris is attended by considerable risk of cardiac infarction as a result of spreading coronary thrombosis (2). This may be prevented in favourable circumstances by the administration of anticoagulants.” The mortality of infarction was 23% without and 13% with anticoagulants (2). A pulmonary embolus, estimated to cause a 6% to 10% mortality, was greatly feared. Survivors were kept at bed rest for 2 to 6 weeks so that a firm scar could form to prevent softening of the heart muscle that could lead to rupture, aneurysm or dilation (1). Absolute bed rest, to the point that the patient was not allowed to cut his food or brush his teeth, was insisted upon for the first two weeks. Samuel Levine recommended the radical approach of “arm chair treatment” allowing the patient to sit up the first two weeks (4). Depending on the patient’s progress and the sedimentation rate, a gradual increase in activities was allowed over the next 2–3 months—a major departure from the 6–12 months of convalescence practiced in the 1930s. Paul Dudley White noted, “The heart itself possesses a striking recuperative capacity no matter what is done (1).”
Although Charles Friedberg commented (3), “Almost every cardiac disease is associated with myocardial involvement,” little attention was paid to a primary form of myocardial disease in 1950. Fibrosis of the heart was attributed to ischemia, rheumatic fever, nutritional deficiency, thyrotoxicosis, scleroderma, toxic drugs, allergy and myocarditis. Alcohol caused a nutritional deficiency of the heart as seen in beriberi heart disease, but was not regarded to be a myocardial depressant or toxic agent.
Left ventricular hypertrophy was considered to be due to the strain of increased work, as seen with hypertension, valvular disease or thyrotoxicosis (1). An “idiopathic hypertrophy,” thought to be congenital in origin, had been reported in children, young adults and families (3).
Most often, cardiomegaly was due to hypertension, valvular disease or myocardial infarction, and less commonly to myocarditis, thyrotoxicosis, chronic pulmonary disease, congenital heart disease, severe anemia and an athletic heart. Cardiac enlargement was evaluated clinically by percussing the heart border relative to the midclavicular or midsternal line and by routinely measuring the cardiothoracic ratio on the chest X-ray.
Earlier, the term “chronic myocarditis” had been used freely and inaccurately. By 1950, the term was defined and restricted. Paul Dudley White commented, “In the attempt to diagnose heart disease more accurately, the term myocarditis is wisely being abandoned in large part; we must remember, nevertheless, that there does exist such a condition as myocarditis which is particularly exemplified by involvement by rheumatic fever and diphtheria (1).” Specific etiologies of myocarditis included rheumatic fever, diphtheria, syphilis, endocarditis, viral, rickettsial and parasitic diseases. An acute interstitial round cell myocarditis of unknown cause, “Fiedler’s myocarditis,” was associated with rapid heart rate, heart failure and a poor prognosis with sudden death in young adults (1,3).
Thyrotoxic heart disease was highly regarded, perhaps because it was one of the few treatable forms of heart disease.
Pericarditis was often classified by the pathologic findings into fibrinous (dry), serofibrinous, hemorrhagic, purulent, adhesive and constrictive types (1). Clinically, these divided into acute, with or without sterile or purulent effusion and adhesive, with or without constriction. The most common etiologies were rheumatic fever, tuberculosis, uremia (or nephritis), coronary thrombosis and bacterial infection. A benign form of pericarditis, associated with a respiratory infection and presumed to be viral, had been recently recognized. Pericarditis was a sign of severe rheumatic carditis, and its presence was worrisome. The clinical incidence of pericarditis with a coronary occlusion was between 7% and 22%. The combination of polyserositis and pericarditis, was known as “Concato’s Disease (1).” Pneumonia and sepsis-related pericarditis, responsible for many cases earlier in the century, was on a steep decline as was tuberculous pericarditis, which was found in 4% to 6% of autopsies of patients with tuberculosis (1). Constrictive pericarditis, sometimes called “Pick’s Disease,” was attributed to tuberculosis in 15% to 75% of cases or a chronic infection of unknown cause in the rest (1).
A typical pain pattern was appreciated; however, asymptomatic pericarditis was known to be frequent. The clinical diagnosis in all cases of acute pericarditis rested upon finding a friction rub. The electrocardiogram provided helpful ST-T wave confirmation. Pericardial tamponade was suspected by a falling arterial pressure, tachycardia, muffling of the heart sounds, a disappearance of the rub, jugular venous engorgement with a cyanotic face, a rise in the jugular pressure with inspiration (Kussmaul’s sign), displacement of the heart border by percussion, a tender enlarged liver, a paradoxical pulse tested for mostly by palpation and evidence for consolidation of the lung at the angle of the left scapula (Ewart’s sign). Serial enlargement of the cardiac silhouette with a pear or water flask configuration on chest X-ray was strong evidence. Constrictive pericarditis was diagnosed by noting an elevated venous pressure, a small and paradoxical pulse, systolic apical retraction (Broadbent’s sign), a loud third heard sound or knock, ascites and pericardial calcification on chest x-ray.
General pain relief for pericarditis consisted of salicylates, bromides, an ice bag on the chest, codeine and morphine. Purulent and tuberculous pericarditis were treated with antibiotics. A decision to tap for a pericardial effusion, referred to as an exploratory pericardial paracentesis, was a major decision since the only diagnostic help was the examination and chest x-ray. This was a particular dilemma in a patient with acute rheumatic fever with a pericardial rub, an enlarging cardiac silhouette and a worsening clinical state (4). Electrocardiographic monitoring of the needle tip was not yet done. Pericardial drainage or stripping was an available surgical procedure with a considerable mortality (4).
Heart failure was defined as an inability or impairment of the heart muscle to discharge its contents or to maintain a satisfactory circulation of blood to the tissues, resulting in an elevation of venous pressure or vascular stasis (3,8). A long-standing argument still existed between advocates of backward heart failure and forward heart failure (3). The two theories argued over whether the elevated venous pressure was a primary or secondary event. In “backward failure,” an upstream obstruction in the circulation was thought to be the central factor. This obstruction, such as seen with aortic stenosis or hypertension, increased the back pressure thereby causing distention and hypertrophy of the affected left and then right heart chambers. Symptoms, such as dyspnea, resulted from an elevated left ventricular pressure “damming” the blood in the lungs and reducing the vital capacity. This backward theory, though supported by pathology, was deficient in not explaining circumstances where obstruction was not apparent, such as coronary disease. Furthermore, the concept of blood “damming up” was difficult for physiologists to accept.
With “forward failure,” myocardial dysfunction was the primary fault. Symptoms, then, were due to a deficiency in cardiac output resulting in an impaired circulation to the organ. Dyspnea, for example, was an effect of a lack of aerated blood to the head. Retention of salt and water, an obvious manifestation of heart failure, was a consequence of reduced renal blood flow. The broad appeal of the forward failure concept was tarnished by the finding of a normal cardiac output in some patients with heart failure; a low cardiac output in some patients without evidence for heart failure; and a puzzlingly high cardiac output when heart failure was seen with anemia, hyperthyroidism and beri-beri (3).
By 1950, most authors felt that both backward and forward heart failure occurred and were modified by compensatory mechanisms such as the Starling principle, heart rate and the peripheral arterial circulation. As Charles Friedberg stated, “On the basis of present knowledge it is possible to evolve a theory of congestive heart failure which accords with the evidence adduced to support both the forward failure and backward failure advocates and which obviates their criticisms (3).”
Chronic heart failure was separated into left or right ventricular failure and high-output failure (9). Left ventricular failure was most commonly attributed to hypertension followed by coronary disease and valvular disease (mostly rheumatic but also syphilitic). Less common explanations included rheumatic and diphtheritic carditis, thyrotoxicosis, tachyarrhythmia, arteriovenous fistula, cardiac trauma and pericardial adhesions. Cardiomyopathy, with the exception of rheumatic carditis, was not considered. Paul Dudley White stated, “Myocardial degeneration and fibrosis result chiefly from extensive coronary atherosclerosis (1).” Right heart failure could occur acutely from a massive pulmonary embolus or pneumonia or chronically from left heart failure and chronic lung disease, including essential pulmonary hypertension. Bernheim’s syndrome, in which case the ventricular septum bulges into and obstructs the right ventricle inflow, was an accepted phenomenon (1). A hyperkinetic circulatory state leading to heart failure was known to occur with anemia, thyrotoxicosis, beri-beri, arteriovenous fistula, Paget’s disease and severe emphysema.
Chronic left heart failure caused dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea. In addition, Cheyne-Stokes respiration, cough, “cardiac asthma” and acute pulmonary edema occurred. Chronic right heart failure was manifested by hepatic discomfort and edema. The examiner felt and percussed for cardiac enlargement, as determined by a displaced apical impulse, and listened for a presystolic, protodiastolic (ventricular) or summation gallop, accentuation of the pulmonic sound, an apical systolic murmur of relative mitral insufficiency and basilar rales. A hydrothorax was discovered by percussion. Pulsus alternans, a key finding, was determined by slowly deflating the arm blood pressure cuff until alternate beats, separated by 5–20 mm Hg, were heard (2).
With right heart failure, the findings included jugular venous distention, measured in centimeters above the sternal angle with the patient’s chest elevated at 30–45°, prominent superficial veins, hepatomegaly, edema, ascites, jaundice and mild cyanosis.
The chest X-ray was scanned for cardiac enlargement, congestion and pleural effusion. Measurement of a reduced vital capacity, previously greatly stressed, was in decline. Patients were routinely fluoroscoped to look for weak cardiac pulsations. Importance was placed on the measurement of a delayed circulation time, obtained by injecting ether or Decholin into an arm vein and timing its appearance in the breath (ether) or taste buds (Decholin) (3). Venous pressure measurement, obtained through a saline-filled manometer connected to a needle that had been inserted into the median basilic vein, was popular for the bedside measurement of venous pressure. Radioactive isotopes were in their infancy and used by a few to measure circulation time. The cardiac output could be estimated by the Fick method, injection of dyes and the ballistocardiograph.
General measures included limiting strain and exercise, restricting sodium and water, dieting and resting in bed from days to weeks to many months when necessary. A daily bowel movement was felt desirable. There was no objection to moderate amounts of alcohol, tobacco, coffee or tea. Digitalis was the most valuable drug and prescribed in the form of a powdered leaf, digilanid, digitoxin or intravenously. Great emphasis was placed on the exact schedule of digitalization as well as observing a heart rate response when auricular fibrillation was present (1). Digitalis toxicity, judged by intestinal symptoms, visual changes or new arrhythmia, was carefully monitored clinically since blood levels were not available. Diuretic therapy was effectively delivered only by injection of mercurials given one to several times a week, often by lining patients up in “merc clinics.” Ammonium salts were felt to improve the response to mercurials by acidifying the blood. Xanthine derivatives were weak diuretics occasionally used as adjuvants. Chlorothiazide, the first potent oral diuretic, would not become available until 1958 (13). Failing to respond to mercurial diuretics, a patient might receive oral urea, sedatives, cathartics, laxatives or a medical or surgical thyroidectomy (1). Patients with pleural effusions, ascites and marked edema were often treated mechanically by thoracentesis, paracentesis and puncturing or incising the edematous thighs or legs, sometimes with the insertion of drainage (Southey) tubes. Acute pulmonary edema was handled emergently with oxygen, morphine, rotating tourniquets, and venesection of 350–1,000 cc.
Paul Dudley White adds, “Last but not least is the spirit of cheerfulness that should surround the patient, a natural attribute of a good doctor and a good nurse and one of the chief elements in the psychotherapy of heart disease (1).”
Infections of the heart
Cardiovascular syphilis remained a problem causing 5% to 15% of heart disease in the U.S. and United Kingdom. The infection was clearly in retreat, Paul Dudley White optimistically commenting “This is another chapter which we may justifiably hope and expect to become obsolete during the next generation (1).”
The disease was insidious and clinically silent for many years. The ostial narrowing could cause angina, often nocturnal and prolonged, but rarely infarction. Progressive aortic regurgitation led to increasing cardiomegaly and ultimately to heart failure. Severe dilatation of an aneurysm of the ascending aorta could eventually compress or erode nearby structures thereby causing cough, hoarseness, dysphagia and pain. Distention of the jugular vein only in the right side of the neck indicated superior venal caval obstruction. Sudden death, especially from rupture of an aneurysm and also related to combined ostial stenosis and aortic regurgitation, was not uncommon (2).
The diagnosis was suspected by finding aortic regurgitation on examination or an abnormal bulge or widening of the aorta on chest X-ray. A positive Wasserman or Kahn serology clinched the diagnosis, though a 15% false-negative rate was appreciated (3).
Heavy metals (bismuth and arsenical injections) were still given routinely for the chronic infection. Penicillin was administered every 3 hours or so for 2–3 weeks. A Jarisch-Herxheimer reaction was feared. Surgery was limited to cellophane encasing of the aneurysm or passing a galvanic current through a coiled wire inside the aneurysmal sac (2).
Diphtheria still occurred causing heart failure, shock and atrioventricular block in 10%–20% of afflicted patients. World War II had seen outbreaks of the disease, but Paul Dudley White commented, “ … happily it has been robbed of so much of its threat in recent years by large scale prevention … and by the use of antitoxin, that much less diphtheritic heart disease is nowadays diagnosed than was the rule a generation ago (1,3).”
Prognosis and treatment
Mortality was very high, ranging from close to 100% in children under two to 25% in adults (3). Sudden death was common. The cardiac effects of the illness could vanish entirely or leave fibrosis or chronic bundle branch block in its wake. Early use of diphtheria antitoxins and penicillin was the main therapy. Bed rest, fluids and management of heart failure and shock were all that were available. Digitalis was considered dangerous.
In this period when valvular disease was so prevalent, bacterial endocarditis was common, infecting 10% to 25% of patients with rheumatic heart disease (3,5). In addition, there was a 15% incidence of endocarditis with congenital heart defects, most often with a bicuspid aortic valve, ventricular septal defect, patent ductus arteriosus, pulmonic stenosis and coarctation of the aorta (3). The recent availability of antibiotics for the treatment of pneumonia and other infectious illnesses had reduced the risk of endocarditis. Streptococcal viridans led the list of responsible organisms with Pneumococcus, Staphylococcus aureus, Enterobacillus coli, Gonococcus, and Meningococcustrailing far behind (3,5).
The disease was suspected when a patient with valvular or congenital disease developed recurrent fever of prolonged duration, often associated with chills, sweats, prostration, anorexia, weight loss, anemia or embolic events. In the absence of positive blood cultures, active rheumatic fever was in the differential. Embolic phenomena included arterial embolism causing stroke, renal, splenic, intestinal or limb infarct, renal failure secondary to glomerulonephritis, mycotic aneurysm and pulmonary embolus.
Prophylactic measures meant attention to dental hygiene; antibiotic coverage started 24 h prior to, and continued 48 h after, dental extraction and tonsillectomy and repair of a patent ductus and coarctation. The untreated disease was 97% to 99% fatal, though a few made a spontaneous recovery, and others developed a chronic form that could fester for years (1). Sulfonamides, with or without heparin, provided only a slight (5% to 6%) improvement in mortality. The introduction of penicillin in the early 1940s had dramatically improved survival up to 80%. Doses of 60,000 to 1 million units of penicillin were given every 3–6 hours (commonly 1 million units total a day). Paul Dudley White commented, “A high mortality was one characteristic of this disease, prior to the use of penicillin in 1944, but now recovery is the rule (1).”
Congenital heart disease
Until the 1940s, congenital heart disease was understood primarily from the landmark autopsy information compiled by Maude Abbott in 1924 (9,10). The 1947 publication of Congenital Malformations of the Heartby Helen Taussig illuminated the clinical side of the story (9). In the forward to her book, Edwards Park comments, “She has done for the clinician what Dr. Maude Abbott did for the pathologist, namely, made the malformations of the heart understandable and accessible, but her work has a practical usefulness which Dr. Abbott’s, owing to its nature, could not possess.”
The findings on examination for the majority of patients had been carefully described by Taussig, Wood and others. Particular attention was paid to palpation (especially for a thrill), the symmetry and character of arterial pulses, the jugular waves for pulmonary hypertension and the components and splitting intervals of the second heart sound. Paul Wood emphasized, “No sign will repay closer study than the second heart sound at the pulmonary area.”
Taussig relied on the chest X-ray with obliques and fluoroscopy to evaluate the chamber size, pulmonary flow and aortic arch position. She considered the electrocardiogram to be “a useful adjunct” but not specific except for dextrocardia and anomalous origin of the left coronary artery from the pulmonary artery. Though angiography of congenital heart disease was available since the late 1930s and the cardiac catheter diagnosis of atrial septal defect had been reported in 1945, Taussig did not provide catheter or angiographic information. She does describe the measurement of the pulmonary circulation time by injecting ether and the systemic circulation time by using saccharine or decolyn.
The child with congenital heart disease was often coddled and activities were restricted. Taussig strongly opposed this approach: “The two most important considerations in the care of patients with congenital malformations of the heart are: 1) Allow the individual to lead as normal a life as possible. 2) Surround him with an atmosphere of confident expectation that he will grow.”
Immunization for diphtheria, tetanus, pertussis and smallpox was advised. Dental hygiene was important, and sulfa or penicillin were administered several days before and after dental work.
Pregnancy was contraindicated for women with cyanotic congenital heart disease, Eisenmenger’s syndrome and atrial septal defect with a dilated right heart but not with uncomplicated atrial septal defect, patent ductus arteriosus, ventricular septal defect, pulmonic stenosis or coarctation of the aorta (1,2).
Cyanotic spells in children were treated with oxygen and morphine. Severely cyanotic and polycythemic children were considered at risk for cerebral thrombosis, and hydration was maintained. Exciting developments had recently taken place in congenital heart surgery—the ligation of a patent ductus arteriosus by Gross and Hubbard in 1939, repair of an aortic coarctation by Crafoord and Nylen in 1945 and pulmonic valvotomy by Holmes Sellors in 1947 and Brock in 1948 (12,13). The surgical mortality rate in 1950 was 2% to 3% for patent ductus closure and 10% to 16% for coarctation repair. The Blalock-Taussig subclavian artery to pulmonary artery shunt, introduced in 1945, dramatically changed the approach to cyanotic congenital heart disease. Intracardiac repair of congenital defects, first used with hypothermia, would not be reported until 1945. Charles Friedberg exulted “ … amazing progress has been achieved in the surgical treatment of certain congenital cardiovascular anomalies, and these advances enhance the important of diagnostic accuracy (3).”
Psychoneurotic cardiovascular disorders
Major symptoms referable to the heart or chest in an apparently normal person with no discernable cardiac findings was a matter of great concern and debate. Known variously as neurocirculatory asthenia, Da Costa’s Syndrome, The Soldier’s Heart, Effort Syndrome, Cardiac Neurosis, Irritable Heart and Disordered Action of the Heart, the problem warranted attention because it had to be distinguished from organic heart disease. The association with anxiety, hyperventilation and automatic disturbance was clear; however, the exact cause of the tachycardia and chest pain was not. Paul Wood said, “It should be understood that there is no essential difference between “effort syndrome” and “cardiac neurosis,” they are merely clothed differently, the former in battle dress, the latter in artificial silk (2).”
Treatment was felt to be very difficult and required a complete cardiovascular examination and testing to provide unconditional reassurance. Psychiatric referral was often necessary. Paul Wood commented, “The patient’s reaction should be analysed, and some psychiatric skill and knowledge are required to do this. It is often possible to show that his reaction is based on false values, ideas, or beliefs. Or one may simply explain just why he so reacts, in order to give him insight. It is impossible to outline precisely just what is required, for every case is different, and needs individual treatment (2).”
Electrocardiography was an established discipline thanks to the monumental contributions of Einthoven, Lewis, Wilson, Wenckebach and others (14). Paul Dudley White exclaimed that “Electrocardiography is one of the most important methods of cardiovascular examination, ranking in value third after history taking and physical examination (1).” Although an exploring bipolar electrode was available in the 1930s, the interpretation was usually based upon the original three bipolar leads of Einthoven until the 1940s. Wilson introduced the central terminal in 1934, and in 1935 he standardized the six unipolar precordial leads (14). Goldberger contributed the augmented unipolar limb leads in 1947, which were thought to provide more precise electrical views of the chambers. After World War II, the laborious photographic method of recording electrocardiograms was replaced by a direct recording using a heated stylus to burn the tracing onto wax paper. Electrode jelly or paste was applied to conduct the electrical current from the patient to the metal electrodes. The electrical activity of the heart could also be obtained by esophageal leads, intracardiac recordings and vectorcardiography. The electrical anatomy and physiology were understood, and the interpretation of underlying disease and arrhythmias quite advanced. In order to explain the morphology of the precordial leads, an interpretation of a clockwise or counterclockwise rotation was in vogue (2). The ventricular gradient and intrinsicoid deflection were calculated. Criteria for hypertrophy, bundle branch block, ischemia, infarction and pericarditis were well established.
Prolonged asystolic periods without P waves were called sinoatrial (or auricular) block and sinus arrest, pauses or standstill. These were blamed on digitalis, quinidine, advanced potassium intoxication, infection and organic heart disease, or thought to be a manifestation of a high vagal tone or a sensitive carotid sinus. Paul Wood stated, “There are no symptoms of sino-auricular block per se, but occasionally short periods of cardiac standstill, with dizziness or syncope, may occur and appear to be due to bursts of extreme vagal activity (2).” A tachy-brady association was not yet known.
Second-degree atrioventricular block was also referred to as partial heart block; the two types were Wenckebach and a more severe form of partial heart block characterized by a fixed P-R interval with beats dropped unpredictably. The term “Mobitz II” was not used. Complete heart block was a major concern because it produced dramatic, recurrent Stokes-Adams attacks in those pre-pacemaker days. “Nodal rhythm” was the traditional term for an escape beat or rhythm arising above the bundle branches. Heart block was attributed to coronary disease, 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).
Auricular (atrial) tachycardias
There were three auricular/atrial tachycardias: auricular (atrial, nodal) paroxysmal tachycardia, auricular/atrial fibrillation and auricular (atrial) flutter. A circus movement or an irritable ectopic focus was invoked as alternate explanations for all three. Dual pathways were not known. Auricular fibrillation was caused by rheumatic heart disease, especially mitral stenosis, coronary disease, hypertension, thyrotoxicosis and old age. The risk of stroke with atrial fibrillation was not yet realized. Atrial flutter was seen with mitral stenosis, hypertension, thyrotoxicosis, coronary artery disease and in healthy individuals.
After the 1930 classic description of “physiological bundle branch block with short P-R interval,” the electrocardiographic features of the Wolff-Parkinson-White Syndrome and its linkage with paroxysmal rapid rhythm disturbances and an anomalous Kent bundle had become well established (14).
Ventricular tachycardia was a complication of recent myocardial infarction, hypertensive heart disease, digitalis and was sometimes documented in an apparently normal person. An accelerated idioventricular rhythm and polymorphic tachycardia/torsade de pointes were not in the textbook vocabulary.
Premature beats were generally regarded as having no clinical importance when there was no associated heart disease. Worry, nervous excitement, effort, hearty meals, caffeine, alcohol and tobacco were sometime implicated. Paul Wood felt “Reassurance is important and should be unconditional and convincing, for it should be remembered that ectopic beats rarely constitute a complaint except in those prone to morbid anxiety (2).”
The treatment of a slow, symptomatic heart rate or long asystolic periods was vexing. Pacemakers were not available. Ephedrine and sublingual adrenaline were the only oral medications, albeit short-lived and unreliable. In the hospital setting, subcutaneous injections of atropine and adrenaline could be helpful. Digitalis was avoided unless heart failure was pronounced. Adrenocorticotrophic hormone (ACTH) and cortisone were sometimes tried for acute heart block when infarction or inflammation was the presumed cause (1).
Auricular tachycardias were liberally dosed with digitalis until the rate was slowed or side effects occurred. Quinidine was the workhorse to convert atrial fibrillation or flutter. It was scheduled every 2 hours for five doses a day with increased doses daily until the rhythm resolved. The association of quinidine with sudden death was known but felt to be rare. Paul Dudley White explained, “The more normal the heart fundamentally, the more likely is quinidine to act successfully and safely. Hence it is particularly indicated when the arrhythmia is simply a very annoying disorder of function … since quinidine in large dosages is a poison, it must be used with care, and by the exercise of care accidents and fatalities that have been reported in rare cases in the past can largely be avoided (1).” Procainamide was a recent discovery, mentioned only in one textbook, and was felt to be effective.
Episodes of supraventricular tachycardia were responsive to breath holding, Valsalva maneuver, gagging or pulling on the tongue, drinking cold water or ingesting ipecac, compressing the eyeball or the carotid sinus for 10–30 s or an ice bag applied to the chest. Failing one or several of these maneuvers, the administration of subcutaneous anticholinergic drugs (mecholyl or prostigmine) was often successful. Digitalis and quinidine were used if all else failed.
Quinidine, intravenous magnesium sulfate and oral potassium salts were the only resort for recurrent ventricular tachycardia or fibrillation. Open chest defibrillation in the operating room only had been reported by Claude Beck in 1947 (13).
Extraordinary developments have occurred in the field of cardiology over the past 50 years. In 1950, with the exception of a few full-time cardiologists at academic centers, the heart specialist was primarily a practicing general physician with an interest and limited training in heart disease and electrocardiography (11). These part-time cardiologists had an excellent understanding of the clinical presentation of cardiac problems and placed their diagnostic faith in a thorough clinical history and examination, supported by the electrocardiogram and chest x-ray film. The essential cornerstone of therapy was an in-depth understanding of the patient based on long-term follow-up care. Effective medical therapy was confined to digitalis, mercurial diuretics, morphine, nitroglycerine, quinidine, anticoagulants, penicillin, sedatives, rest, special diets and phlebotomy. Cardiopulmonary resuscitation meant open chest cardiac massage and defibrillation with the intracardiac injection of adrenaline and calcium. There were no special care units, defibrillators, cardioverters, pacemakers, potent antihypertensive agents or diuretics to take care of the many patients with rheumatic and syphilitic valvular disease, hypertension or coronary artery disease and their complications (Table 1). The prognosis for patients with advanced heart disease was generally grim. Sophisticated testing was limited to the Master’s two-step exercise test and the injection of agents to measure the circulation time. Although right heart catheterization was available in a few academic centers, it was of little clinical importance because surgery was possible for only a few congenital defects (Table 2).
Funded and energized by the post–World War II enthusiasm for research, specialty training and technology, cardiology has radically changed from a placid, clinically based field to what now seems to be a frenzied, procedurally oriented specialty with an emphasis on catheter intervention, cardiovascular surgery and transplantation and device implantation. Rheumatic fever, syphilis and diphtheria have almost vanished as cardiac problems from most areas of the world, and have been replaced by a preoccupation with coronary disease, sudden death and risk factor reduction. Hypertension, once unmanageable, has been tamed by effective treatment for the majority of patients; malignant hypertension, once so feared, is virtually a disease of the past. The management of coronary disease, congestive heart failure and congenital heart disease is dramatically better.
The cardiologist, once widely knowledgeable about all aspects of heart disease and its evaluation, has become increasingly superspecialized into areas such as noninvasive cardiology, angioplasty and electrophysiology. It has been said that these specialists often know more and more about less and less. Paul Wood, in the introduction to his 1950 textbook, anticipated this prospect worrying, “There is already plenty of evidence to show that we are in danger of losing our clinical heritage and of pinning too much faith in figures thrown up by machines. Medicine must suffer if this tendency is not checked (2).” Unfortunately, his concern has come to pass as cardiology has been increasingly criticized for being technically oriented at the expense of bedside skills and clinical judgment.
In his 1951 introduction to his 4th edition of Heart Disease, Paul Dudley White, looked forward with anticipation to the next 50 years: “Thus, on the threshold of a new 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 public health of this country and of much of the rest of the world, each one more important than any other threat of our day—namely, rheumatic heart disease, high blood pressure, and presenile arteriosclerosis, especially as it involves the coronary circulation (1).” At the year 2000 milestone, cardiology can look back at its half century of accomplishments with great pride and optimism that even coronary atherosclerotic disease, the major scourge of today, might also prove to be as susceptible to future advances as rheumatic fever and hypertension did in the past. But, at the same time, we will also need to balance our remarkable technical prowess with a rejuvenation of the basic bedside oriented skills of cardiology as practiced so skillfully circa 1950.
I thank Diana Silverman for her thoughtful editorial work and Arthur Hollman, Barry Silverman, Charles Upshaw, Tillie Tansey and Desmond Julian for their advice. The many resources of the Wellcome Institute for the History of Medicine were invaluable.
☆ The research for this article was undertaken on a Burroughs-Wellcome travel grant at the Wellcome Institute for the History of Medicine, London, England.
- Received August 28, 1998.
- Revision received November 24, 1998.
- Accepted January 5, 1999.
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