University of Minnesota

History of Heart Attack: Diagnosis and Understanding

Is heart attack a modern plague or does it come down from antiquity? Who first described the clinical picture and who first tied it to disease of the coronary arteries? When and by whom was the connection established between atherosclerosis or fatty arteries, and thrombosis and the syndromes of angina pectoris and myocardial infarction? What accounts for the long delay in recognizing the phenomenon of infarction with survival? Where and when did the idea about the potential of preventing heart attack arise?

John Hunter, a brilliant English physician of the eighteenth century, was probably the first in Western medicine to paint the clinical picture of chest pain, called angina pectoris, and sudden death. Noting that his own symptoms were aggravated by anger, he complained that his life was “in the hands of any rascal who chose to annoy or tease” him. He proved the case by dying abruptly after an argument with–we know not whether a rascal–a fellow member of his St. George’s Hospital board (Liebowitz 1970, 102).

The history of coronary syndromes and sudden death, and apoplexy or stroke, goes back to antiquity and has been thoroughly treated by historians and experts from many disciplines. By the beginning of the twentieth century, a heart attack with myocardial infarction was well known to cause death, but comprehension of it as a syndrome that one might survive was much delayed. When that awareness finally came and diffused into the practicing community in the 1920s and after, it had a major effect on the recognition of coronary disease as epidemic after World War II, which, in turn, gave preamble and impetus to CVD epidemiology and preventive cardiology. Because coronary disease was newly epidemic, it was reasoned by a few pioneers that its causes, and conceivably its preventives, must therefore lie in changed environment.

The Clinical-Pathological Picture of Coronary Heart Disease

Angor in the chest–angina pectoris–was depicted in accounts from ancient literature but described as related to coronary artery disease only in the latter part of the eighteenth century. The syndrome of myocardial infarction–prolonged chest pressure or variously referred pain, followed by collapse with rapid death or with survival–was finally and clearly put forward in the early part of the twentieth century. In the English-speaking world, this recognition is mainly attributed to James Herrick, a Chicago internist, because of his effective observations of the clinical and electrocardiographic evolution of the phenomenon. Herrick also documented his views and findings by creating coronary occlusion in animals and became a persistent protagonist of the syndrome at medical meetings in the years following his largely ignored classic JAMA publication in 1912. But others elsewhere, including Obrastzow and Staschesko (1910) in Europe, had similar early insights.

Part of the historical delay and confusion in recognizing heart attacks apparently lay in the Greek word, kardialgia, which could mean either abdominal or precordial pain. Biblical and Talmudic references abound, however, about chest pain of a life-threatening nature, and Hippocrates mentions sudden death related to an episode of chest distress (Leibowitz 1970).

Leibowitz points out that the great Italian anatomist Morgagni failed to tie it all together, but nevertheless clearly described in 1761 the late pathology found in survivors of myocardial infarction in his well-known dictum: “The force of the heart decreases so much more in proportion as the greater number of its parts becomes tendonous instead of being fleshy” (ibid., 4).

The communication most recognized as a starting point for the modern history of coronary artery disease is the presentation by William Heberden before the College of Physicians in London on July 21, 1768, titled, “Some Account of a Disorder of the Breast.” There he gave an incomplete picture but one that Leibowitz and other historians consider adequate to accept his claim about a “morbid entity not hitherto named in the history of diseases . . . ” Heberden and his younger colleague, Edward Jenner, related the cause of angina pectoris to insufficient coronary circulation; and Jenner was the first to mention, in a letter to Heberden, the finding of a thrombus in a coronary artery at autopsy and to tie it to a clinical history in the patient of angina pectoris. Charles Parry, in a reading before the Royal Society in July 1788, also attributed angina to partial obstruction of the coronaries (ibid., 4-5).

René Marie in France in 1896 provided a classical description of clinical coronary disease, and George Dock in the U.S. the same year reported having made the clinical diagnosis during life in a patient with an anatomical myocardial infarction at autopsy. Even as the literature expanded and became more sophisticated during this period, however, the “medical profession at large was,” according to Leibowitz, “not yet prepared to accept and absorb these discoveries which ultimately led to the diagnosis of myocardial infarction” (ibid., 10).

Electrocardiography to the Rescue

As modern science developed from the telescope and the microscope, so modern cardiology and its partner, epidemiology, owes much to technology, not least to the electrocardiograph (ECG). After centuries of irregular progress toward understanding the clinical, physiological, and pathological pictures of atherosclerosis, coronary occlusion, and myocardial infarction, their integration was immensely facilitated by the remarkable recording device, the string galvanometer of Wilhelm Einthoven of Leiden, which magnified the surface potentials produced by the electrical activity in the heart beat and indicated its disturbances. Nevertheless, it was the pioneering British clinical investigator, Sir Thomas Lewis, who in the 1920s made the ECG an essential and practical instrument allowing diagnosis not only of disturbances of heart rhythm but also an inadequate blood supply (ischemia) and muscle damage (infarction), the hallmarks of coronary heart disease.

Paul Dudley White, as a youthful clinical fellow from Boston, came to study with the famous clinical investigator, Sir Thomas, in the 1920s and, as did other contemporaries, brought home to the U.S. the apparatus and the popular art of electrocardiology (see Chapter 9).[1]

James Herrick’s description of non-fatal myocardial infarction, bringing together the ECG findings, symptoms, and experimental coronary occlusions, is widely recognized to have changed medical ways of dealing with coronary disease in the United States. With great modesty, Herrick wrote in 1942: “These facts had been written about before. They had to be rediscovered.” Liebowitz, in fact, gives equal credit to Polish researchers Obrastzow and Straschesko in 1910, “for having initiated the definitive understanding of cardiac infarction as a clinically recognizable morbid entity, which was later acknowledged to be a very common condition and of paramount statistical importance” (ibid., 11).

Thus was recognition of coronary occlusion, thrombosis and damage to the myocardium clearly differentiated from the ancient notion of sudden death and angina pectoris of effort. As important, original, and well-documented as these two classic papers were on cardiac infarction, neither stirred excitement when they were first published. Referring to his presentation before the American Medical Association in 1912, Herrick later wrote, “When it was presented, it was discussed by only one person, there was no repercussion for six years. It had fallen like a dud” (Means 1961, 108).

Even by the 1920s, cardiologists had not widely embraced the concept of infarction with survival. The 1925 edition of Sir James MacKenzie’s classic text, Diseases of the Heart, makes no mention of coronary thrombosis. And although Lewis described McKenzie’s death in January of 1925 as due to myocardial infarction, he failed to recognize or accept the same diagnosis for his own severe attack in 1927. H. M. Marvin, the young American physician who was called to Lewis’s home at that urgent moment, recalled diagnosing an infarct upon finding the modern leader of cardiology in severe pain. But even after an electrocardiogram confirmed Marvin’s diagnosis, Lewis, ausculting his own pericardial rub, remarked that he had not been aware that pericarditis caused such pain (still not accepting the diagnosis of infarction!) (Morris 2002).

When he eventually faced the reality of his infarct, Sir Thomas became profoundly depressed, resigning himself to the view of the time that the diagnosis meant a sedentary and short future. In fact, he lived for many more productive years and came to revise his prognosis of the phenomenon in later editions of his text, to read: “Many patients are known to recover to good health, leading active lives or relatively active lives” (Lewis 1948, 60).

Paul White in his text, Heart Disease, first published in 1941, was next among the cardiological elite to maintain that one could recover from an infarct and carry on a full life. But progress in defining and diagnosing routinely, during life, the presence, localization, and extent of myocardial infarction came only with the widespread use of the electrocardiogram with the addition of Wilson’s chest leads to the three limb leads in the 1940s. Laboratory confirmation came along via measurement of elevated white blood count and then, starting in the 1950s with Ladue and Wroblewski, through identification of enzymes released by infarcted myocardium in rough proportion to the muscle damage and the ability to measure accurately the course of their blood levels in an evolving clinical case (1955).

The variegated phenomena in the “chain of causation” for heart attack and its consequences were connected by understanding of the underlying atherosclerosis and arterial plaque formation, with stenotic or ulcerative and thrombotic obstruction of coronary vessels. Thus, the full-blown picture of myocardial infarction was not high in the awareness of even the best medical diagnosticians until well into the twentieth century. And not until the confirmatory evidence of electrocardiographic findings indicating muscle ischemia and damage was it widely recognized that not only did people die suddenly from this condition, but that many did not die and some lived extended lives with healed muscle and collateral circulation.

In hindsight, discussion of either the pathogenesis or treatment of coronary heart disease now seems conspicuously absent from the great classic texts on cardiology until Paul White’s in 1941. And even White, as late as his third edition in 1948, makes no mention of prevention. Indeed, the recognition of coronary disease as a common, epidemic (and therefore preventable) condition is a recent phenomenon. It came from reports that acute coronary events rose before and subsided greatly during World War II and re-emerged following the war. Then it was noted to increasingly involve middle-aged and younger men in industrial societies.

It seems likely that the dramatic circumstance of the emerging epidemic, perhaps along with its predominance in men stricken suddenly in their prime years, precipitated the intense study of coronary disease in clinics and laboratories and gave impetus to studies in populations, manifestations of the new disciplines of CVD epidemiology and preventive cardiology. Wide awareness of the real potential for universal primary prevention of heart attack would not come until much later, mainly due to evidence from the prospective, cross-cultural and experimental studies of CVD epidemiology in the 1960s to ‘80s. (Henry Blackburn)

[1]Recommended reading on the history of electrocardiography includes Bruce Fye’s 1994 article in The American Journal of Cardiology, “A history of the origin, evolution and impact of electrocardiography,” and the 1990 edition of Burch and DePasquale’s book: A History of Electrocardiography.


Burch, G. E., and N. P. DePasquale. 1964. A history of electrocardiography. Chicago: Yearbook Medical Publishers.

Fye, W. B. 1994. A history of the origin, evolution and impact of electrocardiography.
The American Journal of Cardiology 73 (13):937-949.

Herrick, J. B. 1912. Certain clinical features of sudden obstruction of the coronary arteries. Journal of the American Medical Association 27:100-116.

La Due, J. S., and F. Wroblewski. 1955. The significance of serum glutamic oxalacetic transaminase activity following acute myocardial infarction. Circulation 2:871-877.

Leibowitz, J. O. 1970. The history of coronary heart disease. Berkeley: University of California Press.

Lewis, T. 1948. Diseases of the heart. 4th ed. London: Macmillan.

Means, J. H. 1961. The Association of American Physicians: Its first seventy-five years. New York: McGraw-Hill.

Morris, Jeremy. 2002. Interview by Henry Blackburn. Tape recording. June 3. Hampstead, England. University of Minnesota CVD History Interviews.*

Obrastzow, W. P., and N. D. Straschesko. 1910. Zur kenntis der thrombose der koronararterien des herzens [Toward understanding coronary artery thrombosis]. Zeitschrift für klinische medizin 71:116-132.

White, P. D. 1951. Heart disease. 4th ed. New York: Macmillan.