It has been claimed that no mention of CHD occurs in ancient manuscripts and that the first recognisable description is that by William Harvey in 1648 (Seely, 1985). This view is, however mistaken. Up until the end of the seventeenth century CHD is regarded as a rare event – five cases of presumably sudden cardiac deaths or heart attacks in Rome around 1700 prompted a papal enquiry (Seely, 1985). CHD was well known to the ancient Egyptians (Baldry, 1971) and adult arterial disease was common in former times (Cockburn, 1975). In Egypt circa 1500 BC the Ebers Papyrus was familiar with what appears to be angina pectoris – in the ancient library of Ashurbanipal (Assyrian king, 668-631 BC) tablets refer to CHD? The ancient Hindus recognised heart disease in their Vedic books, with sudden death known to the ancient Maya in the Popol Vuh (Sandison, 1967; Goetz, 1950).
The Ebers Papyrus was familiar with angina pectoris having noted dyspneoa, tachycardia and extrasystoles possibly noted (Ghaliougui, 1963). The Ebers is a copy of earlier texts (Ebell, 1939) and which refers to “…pains in his arm, in his breast and in one side of his cardia” and that “…it is death that threatens him.” indicating angina (Sigerist, 1951; 1961). Descriptions in the Ebers of coronary diseases (Sandison, 1967) apart, another event possibly illustrates the oldest known possible SCD case (Bruetsch, 1959). A tomb wall illustration depicts the death of the VIth Dynasty (2645-2475 BC) nobeleman Sesi – an artists description that is credited with representing a sudden collapse and death by the Egyptologist von Kissing in 1914 (Bruetsch, 1959).
Atheroma was extremely common in ancient Egypt (Wadsworth, 1984a; 1984b) which caused hemiplegia and gangrene of the feet – shown by the mummy of the Vth Dynasty vizier Weshptah who had evidence of a stroke (Thomson Rowling, 1961). Calcification of temporal and other vessels has been found (Wadsworth, 1984a) with signs of hypertensive arteriosclerosis with associated atheromatous damage (Sandison, 1967). Post-mortem study of the Pun II mummy (Ptolemaic, circa 150 BC) showed an aorta in excellent condition with large and small atheromatous plaques present in portions of aorta removed from the chest cavity but no coronary arteries were seen. (Cockburn, 1975). Such evidence is available because Egyptian embalmers left the heart in situ (Sandison, 1967).
Atheromatous degeneration is often confused with ‘arteriosclerosis’ (Sigerist, 1951; Thorvald, 1963). Atheroma (endarteritis deformans) is assumed inevitable by old age and consists of patchy intimal lesions associated with degeneration and accumulation of lipids in the deeper arterial lamellae (Sandison, 1967). Arteriosclerosis is a more diffuse condition, aetiologically distinct from atherosclerosis, affecting the arterial tree with concentric thickening and hyalinisation (Sandison, 1967). Blood vessels are well preserved in dried bodies and mummies, with calcified temporal arteries and aorta described (Sandison, 1980), in addition to degenerated aorta, epicardial and renal vessels, and myocardial fibrosis.
Preserved canopic material (circa XVIII Dynasty) provided hepatic, pulmonary and mesenteric arteries with elastic thickening (Shaw, 1938). Pharoah Merneptah had severe aortic atherosclerosis (Shattock, 1909a, 1909b; Smith, 1908). Hard calcareous plates in the aorta (XXI Dynasty specimen) and numerous calcareous and other lesions (including calcific atheroma) were found in a XXVIII-XXX Dynasty mummy (Ruffer, 1910, 1911a, 1911b, 1921). The individual was not of advanced years. A Greek period male mummy (circa 50 years) had aortal and brachial artery atheroma; a XXVII Dynasty specimen had calcareous changes in the thoracic aorta, as did a dessicated Coptic (Ruffer, 1910, 1911a, 1911b). A female mummy aged about 50 (the Lady Teye) from the XXI Dynasty was found at Deir-el-Bahari (Long, 1931). The specimen showed coronary disease, myocardial fibrosis and “…nodular arteriosclerosis…” of the aorta (Long, 1931).
Modern histological techniques have identified atherosclerosis, atheroma with lipids, and medial calcification in ancient human remains (Wadsworth, 1984a). The technique necessarily delineates the laminae of vessels (Sandison, 1962) with identification of persistent sudanophilic lipid to determine atherosclerosis (Sandison, 1959). Staining is possible as mummifird material is often well preserved (Sandison, 1957, 1962, 1970). It is possible to identify fibrosis, intimal thickening and atheroma and confirm histlogically the studies by Ruffer and those studies done on the remains of Francisco Pizarro (McGhee, 1894).
Remains of the heart and preserved blood vessels were found in dried Basket Maker Indian bodies and in dessicated Peruvians (Wilder, 1904). Another Basket Maker Indian study found no cardiovascular pathology (Wilson, 1927) but a Peruvian mummy (dated 700 AD) showed atherosclerosis and thrombosis (Williams, 1927). A body from a beach in Alaska (C14 dated to circa 405 AD) was of an elderly woman with moderate coronary atheroma, but no AMI evidence, and aortal arteriosclerosis (Zimmerman, 1980). The caution was added that “…presence of such degenerative changes in the blood vessels may not necessarily have been associated with the occurrence of ischemic heart disease.” The ancient Maya recognised sudden death (Goetz, 1951) – in the Popol Vuh mention is made of the Gods or Lords Xic and Patan. Their work was to “…cause men to die on the road, which is called sudden death, making blood to rush to their mouths until they died vomiting blood.” (Goetz, 1978). The Quiche Maya names of demons were also disease names e.g., Ahal Xic whose work to men was “…to seize upon them, squeeze their throats and chests, so that the men died on the road, making the blood rush to their throats when they were walking. This was the work of Xic and Patan.” (Goetz, 1978).
Ancient Sumerian textual tablets contain the word sbennu* (cited as STT I 89, iv 192-5 by Kinnier Wilson, 1967) thus: “…if his chest often hurts him, and however much it hurts or however long it retains the pain …and he becomes nervous and fearful, a ‘bennu*-attack has seized him. For such a man an attack may occur at a gateway, at an animal enclosure or at a river.” The text is thought to refer to angina precipitated by slopes, sudden noises or cold. In ancient Greek myth shooting arrows connoted ‘sudden death’ with Apollo selecting male victims ( e.g., the helmsman of Menelaus) and Artemis despatching females (Laodamia and the mother of Andromache) – combining to dispose of Niobe and her children.
Non-specific heart disease is mentioned in the ancient Hindu Vedda (Sigerist, 1961; Zimmer, 1948; Jayne, 1925). In ancient China heart disease (hsiu chi, hsiu ping) killed General Tz-Chung in 569 BC (Lu Gwei Djen, 1967). Presumed to be anxiety precipitated angina the condition became known as ‘shan’ – found in the text called ‘Nei Ching’ – with a parallel description ‘hsin thung’ in the text ‘Shan Hei Ching’ from the middle Chou period (Lu Gwei Djen, 1967).
The Hippocratic School recognised angina pectoris (Sandison, 1967) with descriptions “…of circulatory collapse and coronary thrombosis in the fifth century AD by Coelius Aurelianus.” (Siegel, 1961). Angina was noted in the ‘Coan Prognosis’ of Corpus Hippocrasticorum, and said to be recognised by Coelius Aurelianus in 400 AD (Sandison, 1967). A sharp pain `cardimona’ was delineated from ‘cardiaca passio’ or cardiac passion – an acute, violent and dissolutionary condition deemed atrial fibrillation (Siegel, 1961). Cardimona is thus angina pectoris. Aretaeus a physician from Cappadocia and contemporary of Galen considered cardiaca passio to be syncope of the heart – a dangerous condition leading to sudden death (Aretaeus ‘On the Causes and Signs of Acute Diseases’, ii, 3, cited in Harris, 1973) as it “…unties the bonds of life which are knotted in the heart.” Aretaeus described heart failure and correctly noted its symptoms and signs, whilst Soranus noted ‘cardiac passion’ leading to terminal heart failure, and Asclepiades differentiated heart disease and palpitations (Siegel, 1951). Seneca (died 65 AD) noted his heart condition in terms indicating coronary disease (Sandison, 1967).
The palaeopathological evidence for CHD is found directly from mummies and dessicated remains with the majority from Egypt, Peru and north European peat bogs (Sandison, 1967). There is thus ample proof of the antiquity of atherosclerosis (Zimmerman, 1980) though whether it was a population control measure among earlier peoples as claimed (Nye, 1966) is debatable. Distinct evidence shows vascular disease present in Egypt for thousands of years from Predynastic to the Coptic period (Sandison, 1967). Life expectancy in Egypt was less than forty years but despite this individuals showed CHD evidence with onset in relatively young persons (Sandison, 1967).
CHD (IHD) has many manifestations. Angina pectoris was first described during mid-seventeenth century (Liebowitz, 1970; Trowell & Burkitt, 1975) and subsequently given clinical entity status by the physician Heberden in 1768 (Liebowitz, 1970). The coronary arteries received scant attention until Vesalius’s `Six Tables’ of 1538 (Baldry, 1971), but their function was not noted until William Harvey (in ‘De motu cordis’) stated they nourished the myocardium. The Earl of Clarendon provided an accurate description (1632) of the life and death of his father who suffered from angina (Sandison, 1967). Giovanni Morgagni studied heart disease and published ‘De Sedibus’ in 1761 (Baldry, 1971) finding: (1) an old man with coronary arteries so hard and thickened as to resemble bone; (2) at post-mortem of a 42 year old woman victim of sudden death noted her long history of episodes of constricting chest pain, left arm numbness, breathing difficulties, all precipitated by exertion and relieved by rest. Not only is this possibly a case of exertional angina pectoris but the premenopausal age of the woman may suggest an underlying hyperlipidaemia conducive to premature coronary disease?
William Herberden (1710-1801) was a noted London physician who in 1768 presented a paper (‘Some Account of a Disorder of the Breast’) to the Royal College of Physcians (Gibbs, 1987a). Angina was not widely recognised until Heberden’s lecture and first written about by him in the Transactions of the College in 1772 (Baldry, 1971). In 1768 Heberden described angina pectoris after observing over 100 patients, commenting males were more susceptible – especially after their 55th year (Gibbs, 1987a). Heberden’s ‘Commentaries on the History and Cure of Diseases’ (published posthumously in 1802) stated angina as derived from the Greek ‘agkhone’ (strangling) which he applied synonymously to the chest (Baldry, 1971). Heberden was left the corpse of an unknown correspondent (a doctor having predicted his own death from a heart disorder) which the physician John Hunter (1728-1793) dissected but did not find cause of death. But, one Edward Jenner (1749-1823) witnessed the post-mortem and noted that the coronary arteries had not been studied (Gibbs, 1987a). Later, Hunter did report (1776) coronary ossification in a fatal case of angina pectoris and stated the same later to Caleb Parry (1755-1822). Heberden is cited by Parry (a Bath physician) in a paper written in 1788 (published 1799) where he attributes angina pectoris to coronary artery disease (Gibbs, 1987a).
Heberden pioneeringly described variant angina, recognised prolonged pain at rest (unstable angina), plus sudden collapse and death (AMI and SCD), noting that the condition was more common in males over 50 (out of 100 patients only three were women), and noted one post-mortem incidence of rudiments of aortal ossification (Baldry, 1971). Edward Jenner and Caleb Parry formulated the coronary artery theory of angina – several cases of angina pectoris had died suddenly but they did not publish for fear of distressing John Hunter (Gibbs, 1987a) whom Jenner had diagnosed as having angina. Jenner (also a West Country doctor) like Parry studied the hearts of his angina patients, both corresponded about the importance of coronary artery narrowing, Jenner observing that “…the coronaries were become bony canals” and “…how much the heart must suffer from their not being able fully to perform their functions…” (cited in Baldry, 1971).
John Hunter suffered from angina pectoris for twenty years and was found at post-mortem to have coronary disease (Sandison, 1967). Hunter eventually died of severe paroxysmal chest pains in 1793 (Gibbs, 1987a) and his post-mortem records state “The coronary arteries had their branches which ramify through the substance of the heart in the state of bony tubes, which were with difficulty divided by the knife, and their transverse sections did not collapse, but remained open.” (cited in Gibbs, 1987a). In 1799 Parry published “An Inquiry into the Symptoms and Causes of the Syncope Anginosa, commonly called Angina Pectoris; illustrated by dissections” containing the concept that blood flow through diseased coronary arteries was inadequate for exertional demands and produced angina (Baldry, 1971). This concept was taken up by the Glasgow physician Allan Burns (“Observations on Some of the Most Frequent and Important Diseases of the Heart”, 1809) who concluded “When, therefore, the coronary arteries are ossified every agent capable of increasing the action of the heart, such as exercise, passion and ardent spirits, must be a source of danger.” (cited in Baldry, 1971). In the preface to Hunters posthumous book (“A Treatise on the Blood, Inflammation and Gunshot Wounds.” 1794) Everard Home described Hunters symptoms and death plus white opaque areas, or old infarcts, in Hunter’s heart wall (Baldry, 1971), but the condition was not regarded as a distinct entity until Adam Hammer (1818-78) made the first diagnosis in 1876.
Rupture of the heart (`ruptura cordis’) has been noted historically (Bayle, 1824) with descriptions of nervous agitation resembling SCD and necropsy showing a myocardium resembling a ruptured infarct (brown colour surrounding perforation). In the same paper Bayle mentioned, but did not cite, reports by Corvisart and Laennec, but did list similar findings by Morgagni (Lett. lxiv, 14, 15. and “Adversaria Anatomica”), plus other references to Bolinus, Bonet, Senac. Bayle noted additional references for ruptura cordis’ as ‘Memoires de L’Academie des Sciences’ (1732, p. 428, a Dr Ferrcus in Corvisart’s 3rd edition), to Dr’s Bland and Rostan in the ‘Nouveau Journal de Medicine, 7th volume (1820), and the 68th number of ‘Bibliotheque Medicale’ which cited ten cases (in Paris) of *ruptura cordis’ – representing possible infarcts, SCD and AMI), see Table A below:
death in 1-2 hours
death in 1-14 hours
Table A Cases of heart rupture in Paris, early 19th century, indicating possible CHD. Source: Bayle, 1824.
Further reports (Lancet, 1826) mention ‘ruptura cordis’ and infarcts plus a possible venticular aneurysm. Furthermore (Berard, 1826, p. 172) a description of an inflammation of coronary arteries that “…cuts like cheese or lard” linked to a case of ‘ruptura cordis’ (see also Lancet, 1826, p. 69).
William Stokes, Dublin surgeon (1804-1878) wrote a chapter on the `Fatty Degeneration of the Heart’ in his (Dublin, 1854) “The Diseases of The Heart and Aorta” (Gibbs, 1987b). Sir Dominic John Corrigan, another Irish surgeon, wrote “On Aortitis, as One of the Causes of Angina Pectoris” in the Dublin Journal of Medical Sciences, 1887 (Gibbs, 1987a). The first description of proximal aorta disease causing angina.
Myocardial infarction was introduced as a term in 1896 by Rene Marie, a French physician, but only achieved common usage after a paper by Lian in 1921 (Johansson, 1982). The first clinical description of myocardial infarction was made in 1859 by Swedish physicians Malmsten and von Duben (Malmsten, 1859, cited in Johansson, 1982). Von Duben described canalised coronary thrombus and fat-intermingled detritus. Again in 1861 Malmsten believed one should consider coronary thrombosis as a cause of SCD (Johansson, 1982). Coronary vasospasticity has been noted historically by Latham (1876) with the postulation that spasm was a mechanism underlying angina, with Huchard’s suggestion (1889) that spasm superimposed on organic lesions explained some aspects of IHD (Mulcahy, 1988c).
In 1887 a Dr Hammer was called to diagnose a collapsed 34 year-old man (see “A Case of Thrombotic Occlusion of One of the Coronary Arteries of the Heart”, 1878, cited in Baldry, 1971). The post-mortem found a clotted jelly-like whitish plug (thrombus) blocking one of the coronary arteries. Again, in 1910 the first paper on angina pectoris was written by James Herrick (1861-1954) and in 1912 the Journal of the American Medical Association published his “Clinical Features of Sudden Obstruction of the Coronary Arteries” where he showed sudden occlusion in the young was more likely to be fatal than insidious narrowing over time (Baldry, 1971).
Sir William Osler – an Oxford professor of medicine – emphasised for the first time that certain types of individual had raised susceptibility to coronary artery disease due to a mix of hereditary and environmental causes (Baldry, 1971, Gibbs, 1988b). In 1910 Osler found CHD prevalent among upper classes (Baldry, 1971) – the reverse of the current class gradient – and that certain families “…with a hereditary predisposition developed a special strain of tissue with a particular liability to react anginally.” occurring over successive generations (cited in Baldry, 1971). In essence Sir William Osler foreshadowed current aetiological and epidemiological thinking on CHD noting thus familial aggregation and the multifactorial nature of the disease.
Originally published as Appendix 180 in my MPhil Thesis entitled Population Variation for Risk Factors for Ischaemic Heart Disease. CNAA at Oxford Polytechnic and Oxford Brookes University, 1987 to 1992.
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