Heart Disease
Heart disease, also known as cardiovascular disease, refers to a range of conditions that affect the heart and blood vessels. It is a broad term that encompasses various conditions, including coronary artery disease, heart failure, arrhythmias, and valvular heart diseases, among others. Heart disease is a leading cause of death worldwide.
Recent History
January 1, 1950
NHI holds first heart disease conference with NHLBI and establishes scientific control of the field.
NHI morphed over the years into the National Heart, Lung, and Blood Institute (NHLBI) that exists today. And every step of the way, this new institute moved in concert with its close sibling, the AHA.
In 1950, for instance, the two jointly held the first national conference on heart disease, in Washington, DC.
August 2, 1950
Blood lipids and human atherosclerosis
Dr John Gofman created the original diet-heart and lipid hypothesis, but included carbohydrates as a factor driving cardiovascular disease.
https://www.crossfit.com/health/ancel-keys-cholesterol-con-part-4
Dr Tim Noakes:
In a previous column (3), I described how already in 1950, John Gofman, MD, had formulated the diet-heart and lipid hypotheses (4) two years before Keys would commandeer the ideas as his own.
Gofman posed as a double challenge for Keys and his future disciples. First, Gofman was far more qualified than Keys to undertake research into the dietary and other factors causing heart disease. But perhaps more importantly, Gofman’s diet-heart hypothesis gave equal weight to dietary fats and dietary carbohydrates as the factors driving atherosclerosis and the development of CHD.
According to Gofman:
What is solidly established is that the Sf° 20-400 lipoprotein levels [i.e., blood triglyceride or VLDL concentrations] on the average, can be raised by increasing the dietary carbohydrate intake and can be lowered by decreasing it. … Furthermore, many individuals who are characterized habitually by some type of error in their metabolism that makes their Sf° 20-400 lipoproteins habitually extremely high will experience a marked reduction in the blood levels of these lipoproteins when the carbohydrate intake is lowered. (5, p. 123, my addition)
Gofman continues:
These same lipoproteins are essentially unaffected, in the average case, by changing from animal to vegetable fats. This information is extremely crucial, for in many individuals the risk of coronary heart disease comes primarily from the Sf° 20-400 lipoproteins [VLDL or triglycerides]. For such individuals, any attempt to lower heart attack risk by shifting from animal fat to vegetable fat in the diet would be illogical. There would be no reason whatever to expect any benefits since one would be changing the diet in a manner directed toward affecting the Sf° 0-20 [LDL] lipoproteins, which is not the problem at hand for these persons. For such individuals, the preventive efforts would have to be directed toward lowering the carbohydrate intake, which will, on the average reduce the Sf° 20-400 lipoprotein levels. With respect to the effect of carbohydrates on the Sf° 20-400 lipoproteins, it is a matter of the amount of carbohydrate that is eaten rather than the total number of calories ingested. For example, if one maintains individuals at exactly the same number of calories per day, so that they do not alter the weight in any way, but takes out some of the carbohydrates in their diet and replaces them by vegetable oil, one finds that the Sf° 20-400 lipoprotein levels will fall. Achievement of this result of lowering the Sf° 20-400 lipoproteins requires neither any alteration in caloric intake nor any alteration in body weight. (5, p. 124, my additions and emphasis)
Subsequently, in 1958 Gofman pointed out a key logical flaw that has since been ignored (6). He noted that a number of studies had found increasing the dietary intake of vegetable oils produced a fall in blood cholesterol concentrations, and this has been interpreted as beneficial. But the addition of vegetable oils also reduced total carbohydrate intake, and since carbohydrate increases the Sf° 20-400 lipoprotein levels, which contain approximately 13% of cholesterol by weight, the shift from a higher- to a lower-carbohydrate diet might be the real reason why increasing the intake of vegetable oils causes a reduction in blood cholesterol concentrations.
Thus, Gofman warned: “No consideration was given by them to the possibility that the lowering of cholesterol levels might have been the result of the simultaneous removal of a large amount of carbohydrate from the diet” (6, p. 277).
Gofman next describes the effects of a low-carbohydrate (100 g/day) diet in a 65-year-old male subject with a previous myocardial infarction (Figure 2).
Figure 2: The effects of a low-carbohydrate diet in a myocardial infarction survivor. Note the low-carbohydrate diet produced a very large decrease in the Sf° 20-400 lipoprotein levels, now known as the VLDL-lipoproteins, which transport predominantly triglycerides. Total blood cholesterol concentration was unaffected by this dietary change. Despite this, the patient’s atherogenic index (AI) had fallen, placing him in a more favorable metabolic state according to Gofman’s understanding. Reproduced from data on Table V in reference 6, p. 279.
As Gofman wrote: “It can be seen from these data that a massive fall in the serum Sf° 20-400 lipoprotein levels occurs on the low-carbohydrate diet, without significant changes in the Sf° 0-20 lipoprotein levels. Accompanying this fall in lipoproteins is a highly marked and favourable reduction in the atherogenic index value” (6, p. 278-279).
Thus, the real originator of the diet-heart and lipid hypotheses stated that a low-carbohydrate, high-fat diet can be used in persons with established coronary atherosclerosis, presumably to reverse that disease.
He continued:
These same principles of carbohydrate restriction have been applied successfully in several types of extreme derangement of lipoprotein level control of the Sf° 20-400 lipoprotein class, namely, in xanthoma tuberosum, essential hyperlipidemia, and in diabetes mellitus … . For such a [post-myocardial infarction] patient, it is quite clear that management of the problem of coronary disease by dietary means involves the use of a low-carbohydrate diet, and not a low-fat, high-carbohydrate diet which is so often prescribed when attention is not paid to the lipoprotein findings. (6, p. 279-280, my emphasis)
The importance of this is that this evidence anticipated Peter Kuo’s “discovery” of carbohydrate-sensitive hyper(tri)glyceridemia (7) and its reversal with a low-carbohydrate diet by nine years (Figures 6 and 7 in reference 8).
In his conclusions Gofman wrote:
The increase in risk of future myocardial infarction associated with elevation of lipoproteins of the Sf° 20-400 lipoprotein classes provides the basis for a rational application of dietary measures in this disease … . Dietary carbohydrate intake is a prime factor controlling the serum level of the Sf° 20-100 and Sf° 100-400 lipoprotein classes. Restriction of dietary carbohydrates can provoke marked falls in the serum level of these lipoproteins … . The serum cholesterol measurement can be a dangerously misleading guide in evaluation of the effect of diet upon the serum lipids … . Rational management of patients with coronary heart disease or of individuals attempting to avoid coronary disease depends upon knowledge of the lipoprotein distribution in the individual patient. (6, p. 282-283)
Elsewhere Gofman wrote: “Neglect of [the carbohydrate factor] can lead to rather serious consequences, first in the failure to correct the diet in some individuals who are very sensitive to the carbohydrate action; and second, by allowing certain individuals sensitive to the carbohydrate action to take too much carbohydrate as a replacement for some of their animal fats” (9, p. 156-157).
In one of his last publications, a 1960 editorial, he again emphasized his concern about the carbohydrate factor:
Several investigators have shown that a low-fat high-carbohydrate diet produces opposite trends in the blood cholesterol and the blood lipid levels. The cholesterol level falls because the low fat diet depresses the level of the cholesterol rich Sf° 0-20 lipoproteins. The triglyceride level rises because the high carbohydrate intake elevates the level of the triglyceride-rich Sf° 20-400 lipoproteins. Both the triglyceride-bearing and cholesterol-bearing lipoproteins have been associated with the development of coronary disease. It therefore behoves the physician utilizing the dietary approach to understand the likelihood that a focus on the fat intake without an appreciation of the effect of carbohydrate intake will not lower all the blood lipids associated with the development of coronary heart disease. (10, p. 83)
January 1, 1954
Preliminary Survey of Dietary Intakes and Blood Levels of Cholesterol and the Occurrence of Cardiovascular Disease in the Eskimo.
Very little exact information is available regarding the occurrence of arteriosclerosis in Eskimos. None of the 16 Eskimos analyzed here showed any evidence of arteriosclerosis by clinical or roentgenological examination, and cardiovascular disease was extremely rare among the large number of Eskimo patients examined by the author during a two-year period in Alaska.
4. Discussion.
Since hypertension in man has been stated to be typically associated with increased incidence and severity of atherosclerosis (Katz and Stamler, 1953), it would be of interest to compare the incidence of hypertension in Eskimos with that of Whites although the interrelationship between hypertension and atherosclerosis is by no means clear. In a survey of 104 Alaskan Eskimos the author found that both the systolic and diastolic blood pressures were lower in Eskimos than in Whites of corresponding age. Eighty per cent of the recorded systolic blood pressures were below 116 mm Hg. and no systolic blood pressure higher than 162 mm was ever recorded in our "normal" Eskimo subjects. In a series of 117 Eskimo patients, only one of the patients had systolic blood pressure above 145 mm (a 60-year old woman having a blood pressure of 200/80 mm) (Rodahl, 1954). It may be noted in this connection that Alexander (1949) found hypertension to be practically non-existent among Aleuts, and his electrocardiographic and clinical examination of 296 Aleuts, including 23 above the age of 60, revealed almost no cardiovascular disease.
Gotman et al. (1950) have found that some hypertensives show elevated plasma concentrations of Sf 10-20 lipoproteins even if the blood cholesterol concentration is normal, although these changes in the "giant molecule" levels are not correlated with the degree of hypertension.
Very little is known regarding the plasma lipids in Eskimos, and the plasma lipid studies in Eskimos so far reported have yielded inconsistent data. This may not be surprising when considering the wide range of conditions, dietary and otherwise, encountered in the different groups of Eskimos. Corcoran and Rabinowitch (1937) who studied two groups of Canadian Eskimos, one group subsisting on a meat diet and one group subsisting on a mixed diet, found in both groups lower concentrations of plasma lipids and of cholesterol than the normal values for Whites, and the meat group had slightly higher plasma lipid levels than the group on a mixed diet. In this connection it may be noted that serum cholesterol in Whites is decreased in severe caloric undernutrition (Keys, 1953-b). Periods of semi-starvation may occur among the Eskimos, which thus may affect the blood lipid levels. Sinclair et al. ( 1949) have reported plasma lipid findings in the Canadian Eskimos that are similar to the figures considered normal in Americans. Wilber and Levine (1950) found moderately elevated plasma lipid levels of Alaskan Eskimos. It may also be noted that Alexander (1949) found mean plasma cholesterol levels of 176-197 mg/l 00 ml in two groups of Aleuts.
In view of the small number of Eskimos examined in the present study no definite conclusion can be drawn from this limited material. These preliminary investigations indicate, however, that while some Eskimos, such as the Nunamiuts, may have very high cholesterol intakes, the average figures for dietary cholesterol and fat for the four Eskimo groups examined are comparable to those of the average American man; their blood cholesterol levels are the same, while the Sf 12-20 lipoproteins (Gofman fraction) were lower in concentration than Whites of corresponding age. If it were convincingly demonstrated that the Eskimos in reality have a lower incidence of cardiovascular disease than Whites, it would appear that these findings support Gofman's postulates that the high concentration of the cholesterol-bearing protein molecules are associated with atheroclerosis.
It should be noted, however, that very little exact information is available regarding the occurrence of arteriosclerosis in Eskimos. None of the 16 Eskimos analyzed here showed any evidence of arteriosclerosis by clinical or roentgenological examination, and cardiovascular disease was extremely rare among the large number of Eskimo patients examined by the author during a two-year period in Alaska. Similarly, Dr. Paul Haggland, who has operated on a large number of Eskimos in Alaska during the last 15 years, has never seen arteriosclerosis or atherosclerosis in Eskimos (personal communications). He had the occasion to perform autopsy on one female and two male Eskimos, aged 60-65 years, and found no arteriosclerosis. Dr. Earl Albrecht, Territory Commissioner of Health, states that arteriosclerosis is rare in Eskimos, based on clinical evidence (personal communications).
Bertelsen (1940) is, on the other hand, of the opinion that arteriosclerosis is fairly common in Greenland, particularly if one considers the average span of life for the Greenland Eskimos. Hoygaard (1941) writes with regard to the Angmagssalik Eskimos, Southeast Greenland, that "arteriosclerosis was frequently found even in persons below 40".
Brown (1951) states with regard to the Southampton Island Eskimos and the Igloolik Eskimos: "We have found well-marked general arteriosclerosis and also coronary heart disease proved by electrocardiogram and, in one case, by post mortem. Some of the cases of coronary heart disease were in congestive failure."
During our study of the patho-physiology of the Alaskan Eskimos from 1950 to 1952, x-rays were taken of the chest and extremities of 84 Eskimos, using a portable x-ray apparatus. All chest x-rays were taken at a distance of 180 cm; all x-rays of the limbs (left arm and left leg) were taken at a distance of 90 cm. Professor Johan Torgersen, Institute of Anatomy, Oslo University, has very kindly examined all these roentgenograms, with a particular reference to possible roentgenological evidence of arteriosclerosis and other cardiovascular abnormalities. He finds, as a typical feature of all roentgenograms examined, that the bone structure in the Eskimo is unusually massive with sharply defined, well-calcified bone lamellae. The muscle attachments are as a rule very large. The occurrence of arthritis deformans is no less frequent in these Eskimos than in Whites of similar age (:5 cases in 84 Eskimos, 51 males and 33 females, with an average age of 28 years). Four Eskimo subjects at Barter Island had cartilaginous exostoses on the tibia (fig. 2).
From this material (see Table 5) it appears that the occurrence of roentgenological evidence of arteriosclerosis in these Eskimos is neither more nor less than what one would expect to find in Whites of similar age groups. Out of 9 Eskimos over 47 years of age, roentgenological evidence of atherosclerosis of the arch of the aorta was detected in 3 cases, 2 males and 1 female. Of the entire material one Eskimo showed calcium deposits in the arteries (see fig. 1). In one 60-year old Eskimo woman with a blood pressurc of 200/80, thcre was slight enlargemcnt of the left ventricle of the heart. It is thus evident that further studies are necessary in order to settle the question of arteriosclerosis in the Eskimo and the relation between dietary cholesterol, serum cholesterol levels and cardiovascular disease ill these people.
5. Summary and Conclusions.
The cholesterol content of some common Eskimo foods has been determined and the serum cholesterol level as well as the serum concentration of Sf 12-20 lipoproteins in 16 healthy Alaskan Eskimos are reported. On the basis of these preliminary data it appears that some Eskimos have high cholesterol intakes compared with healthy American men, but that their blood cholesterol levels are the same. On the other hand, the Sf 12-20 lipoproteins in Eskimos are lower in concentration than in Whites of corresponding age. From the available evidence it appears that the incidence of cardiovascular disease among the Alaskan Eskimos may be lower than in whites. A more complete analysis of this problem is in progress.
July 27, 1957
John Yudkin
DIET AND CORONARY THROMBOSIS HYPOTHESIS AND FACT
Yudkin thinks that heart disease is caused by dietary sugar.
Ancel Keys was alert to the idea that sugar might be an alternative dietary explanation to his own as a cause of heart disease. From the late 1950s to the early 1970s, he held an ongoing debate in the scientific literature with John Yudkin, a professor of physiology at Queen Elizabeth College, London University, who at the time was the man behind the sugar hypothesis. "Keys was very opposed to the sugar idea," Daan Kromhout recalled in an interview, though he could not say why. Philosophers of science would say that the job of a scientist is to be as skeptical as possible about his or her own ideas, but Keys was evidently just the opposite. "He was so convinced that fatty acids were the thing in relation ot atheroschlerosis, he saw everything from that perspective," says Kromhout. "He was a very driven person and had his own point of view." About the views of others, Keys could be aggressively disaparing: Yudkin's idea that sugar causes heart disease is a "mountain of nonsense," he concluded at the end of a nine-page criticque in Artherosclerosis. "Yudkin and his commercial backers were not deterred by the facts; they continue to sing the same discredited tune," he wrote later.
Keys specifically defended his Seven Countries study from the idea that sugar might explain some of the mortality differences he observed.
Nina Teicholz - TBFS - page 42
Ancient History
Cairo, Cairo Governorate, Egypt
3100
B.C.E.
Atherosclerosis across 4000 years of human history: the Horus study of four ancient populations
Probable or definite atherosclerosis was noted in 47 (34%) of 137 mummies and in all four geographical populations
Summary
Background
Atherosclerosis is thought to be a disease of modern human beings and related to contemporary lifestyles. However, its prevalence before the modern era is unknown. We aimed to evaluate preindustrial populations for atherosclerosis.
Methods
We obtained whole body CT scans of 137 mummies from four different geographical regions or populations spanning more than 4000 years. Individuals from ancient Egypt, ancient Peru, the Ancestral Puebloans of southwest America, and the Unangan of the Aleutian Islands were imaged. Atherosclerosis was regarded as definite if a calcified plaque was seen in the wall of an artery and probable if calcifications were seen along the expected course of an artery.
Findings
Probable or definite atherosclerosis was noted in 47 (34%) of 137 mummies and in all four geographical populations: 29 (38%) of 76 ancient Egyptians, 13 (25%) of 51 ancient Peruvians, two (40%) of five Ancestral Puebloans, and three (60%) of five Unangan hunter gatherers (p=NS). Atherosclerosis was present in the aorta in 28 (20%) mummies, iliac or femoral arteries in 25 (18%), popliteal or tibial arteries in 25 (18%), carotid arteries in 17 (12%), and coronary arteries in six (4%). Of the five vascular beds examined, atherosclerosis was present in one to two beds in 34 (25%) mummies, in three to four beds in 11 (8%), and in all five vascular beds in two (1%). Age at time of death was positively correlated with atherosclerosis (mean age at death was 43 [SD 10] years for mummies with atherosclerosis vs 32 [15] years for those without; p<0·0001) and with the number of arterial beds involved (mean age was 32 [SD 15] years for mummies with no atherosclerosis, 42 [10] years for those with atherosclerosis in one or two beds, and 44 [8] years for those with atherosclerosis in three to five beds; p < 0.0001).
Interpretation
Atherosclerosis was common in four preindustrial populations including preagricultural hunter- gatherers. Although commonly assumed to be a modern disease, the presence of atherosclerosis in premodern human beings raises the possibility of a more basic predisposition to the disease.
37 mummies from populations of four disparate geo- graphic regions were studied by whole body CT scanning: 76 ancient Egyptians (predynastic era, ca 3100 BCE, to the end of the Roman era, 364 CE, 13 excavation sites), 51 early intermediate to late horizon peoples in present day Peru (ca 200–1500 CE, five excavation sites), five Ancestral Puebloan of the Archaic and Basketmaker II cultures living in southwest America (ca 1500 BCE to 1500 CE, five excavation sites), and five Unangan people living in the Aleutian Islands of modern day Alaska (ca 1756–1930 CE,
one excavation site). These geographical areas were selected because of access to mummies with appropriate age and varied cultural attributes. Mummies were selected for imaging on the basis of their good state of preservation and the likelihood of being adults. Mummies were not selected for study in a random fashion.
Luxor, Luxor Governorate, Egypt
2475
B.C.E.
The Earliest Record of Sudden Death Possibly Due to Atherosclerotic Coronary Occlusion
WALTER L. BRUETSCH
The sudden death of an Egyptian noble man is portrayed in the relief of a tomb from the Sixth Dynasty (2625-2475 B.C.). Since there is indisputable evidence from the dissections of Egyptian mummies that atherosclerosis was prevalent in ancient Egypt, it was conjectured that the sudden death might have been due to atherosclerotic occlusion of the coronary arteries.
It may be presumptuous to assume that an Egyptian relief sculpture from the tomb of a noble of the Sixth Dynasty (2625-2475 B.C.) may suggest sudden death possibly due
to coronary atherosclerosis and occlusion. Much of the daily life of the ancient Egyptians has been disclosed to us through well-preserved tomb reliefs. In the same tomb that contains the scene of the dying noble, there is the more widely known relief "Netting Wildfowl in the Marshes." The latter sculpture reveals some of the devices used four thousand years ago for catching waterbirds alive. It gives a minute account of this occupation, which in ancient Egypt was both a sport and a means of livelihood for the professional hunter.
The relief (fig. 1), entitled "Sudden Death," by the Egyptologist von Bissing2 represents a nobleman collapsing in the presence of his servants. The revelant part of the explanatory text, as given by von Bissing, follows (translation by the author):
The interpretation of the details of the theme is left to the observer. We must attempt to comprehend the intentions of the ancient artist who sculptured this unusual scene. In the upper half (to the right) are two men with the customary brief apron, short hair covering the ears, busying themselves with a third man, who obviously has collapsed. One of them, bending over him, has grasped with both hands the left arm of the fallen man; the other servant, bent in his left knee, tries to uphold him by elevating the head and neck, using the knee as a support. Alas, all is in vain. The movement of the left hand of this figure, beat- ing against the forehead, seems to express the despair; and also in the tightly shut lips one can possibly recognize a distressed expression. The body of the fallen noble is limp. . . . Despite great restraint in the interpretation, the impression which the artist tried to convey is quite obvious. The grief and despair are also expressed by the figures to the left. The first has put his left hand to his forehead. (This gesture represents the Egyptian way of expressing sorrow.) At the same time he grasps with the other arm his companion who covers his face with both hands. The third, more impulsively, unites both hands over his head. ... The lord of the tomb, Sesi, whom we can identify here, has suddenly collapsed, causing consternation among his household.
In the section below (to the left) is shown the wife who, struck by terror, has fainted and sunk totheflor. Two women attendants are seen giving her first aid. To the right, one observes the wife, holding on to two distressed servants, leaving the scene. . . .
von Bissing mentions that the artist of the relief must have been a keen observer of real life. This ancient Egyptian scene is not unlike the tragedy that one encounters in present days, when someone drops dead of a "heart attack." The physician of today has almost no other choice than to certify the cause of such a death as due to coronary occlusion or thrombosis, unless the patient was known tohave been aflictedwith rheumatic heart disease or with any of the other more rare conditions which may result in sudden death.
Atherosclerosis among the Ancient Egyptians
The most frequent disease of the coronary arteries, causing sudden death, is atherosclerosis. What evidence is available that atherosclerosis was prevalent in ancient Egypt?
The first occasion to study his condition in peoples of ancient civilizations presented itself when the mummified body of Menephtah (approx.1280-1211B.C.), the reported "Pharaoh of the Hebrew Exodus" from Egypt was found. King Menephtah had severe atherosclerosis. The mummy was unwrapped by the archaeologist Dr. G. Elliot Smith, who sent a piece of the Pharaoh's aorta to Dr. S. G. Shattock of London (1908). Dr. Shattock was able to prepare satisfactory microscopic sections which revealed advanced aortic atherosclerosis with extensive depositions of calcium phosphate.
This marked the beginning of the important study of arteriosclerosis in Egyptian mummies by Sir Mare Armand Ruffer, of the Cairo Medical School(1910-11). His material included mummies ranging over a period of about 2,000 years (1580 B.C. - 525 A.D.).
The technic of embalming in the days of ancient Egypt consisted of the removal of all the viscera and of most of the muscles, destroying much of the arterial system. Often, however, a part or at times the whole aorta or one of the large peripheral arteries was left behind. The peroneal artery, owing to its deep situation, frequently escaped the em- balmer'sknife. Otherarteries,suchasthe femorals, brachials, and common carotids, had persisted.
In some mummies examined by Ruffer the abdominal aorta was calcified in its entirety, the extreme calcification extending into the iliae arteries. Calcified plaques were also found in some of the larger branches of the aorta. The common carotid arteries frequently revealed patches of atheroma, but the most marked atheroselerotic alterations were in the arteries of the lower extremities. The common iliae arteries were not infrequently studded with calcareous plaques and in some instances the femoral arteries were converted into rigid tubes. In other mummies, however, the same arteries were near normal.
What is known as Mdnekeberg's medial calcification was also observed in some of the mummified bodies. In a histologic section of a peronieal artery, the muscular coat had been changed almost wholly by calcification. In one of Ruffer's photographic plates, a part of a calcified ulnar artery is shown. The muscular fibers had been completely replaced by calcification.
In the aorta, as in present days, the atherosclerotic process had a predilection for the points of origin of the intercostal and other arteries. The characteristics and the localization of the arterial lesions observed in Egyptian mummies leaves litle doubt that atherosclerosis in ancient times was of the same nature and degree as seen in today's postmortem examinations.
As to the prevalence of the disease, Ruffer ventured to say that the Egyptians of ancient times suffered as much as modern man from arterial lesions, identical with those found in our times. Ruffer was well qualified to make this statement having performed many autopsies on modern Egyptians, Moslems, and other people of the Middle East. In going over his material and examining the accompanying photographic plates of arteries, one can have litle doubt that what Ruffer had observed in Egyptian mummies represented arteriosclerosis as it is known today.
Although the embalming left no opportunity to examine the coronary arteries inl mummified bodies, the condition of the aorta is a good index of the decree of atheroselerosis present elsewhere. In individuals with extensive atheroselerosis of the aorta, there is almost always a considerable degree of atherosclerosis in the coronary arteries. If Ruffer's statement is correct that the Egyptians of 3,000 years ago were afflicted with arteriosclerosis as much as we are nowadays, coronary occlusion must have been common among the elderly population of the pre-Christian civilizations.
Furthermore, gangrene of the lower extremities in the aged has been recognized since the earliest records of disease. Gangrene of the extremities for centuries did not undergo critical investigation until Cruveilhier (1791- 1873) showed that it was caused by atherosclerotic arteries, associated at times with a terminal thrombus.
SUMMARY
The record of a sudden death occurring in an Egyptian noble of the Sixth Dynasty (2625-2475 B.C.) is presented. Because of the prevalence of arteriosclerosis in ancient Egyptian mummies there is presumptive evidence that this incident might represent sudden death due to atheroselerotic occlusion of the coronary arteries.
Cairo, Cairo Governorate, Egypt
1580
B.C.E.
ON ARTERIAL LESIONS FOUND IN EGYPTIAN MUMMIES
Arteries of Egyptian mummies from 1580 B.C.E. to 525 A.D. have extensive calcification of the arteries, the same nature as we see today, and unlikely to be due to a very heavy meat diet, which was always a luxury in ancient Egypt. Instead, the diet was mostly a course vegetarian one.
DISCUSSION OF RESULTS.
Nature of the lesions. There can be no doubt respecting the calcification of the arteries, and that it is of exactly of the game nature as we see at the present day, namely, calcification following on atheroma.
The small patches seen in the arteries are atheromatous, and though the vessels have without doubt been altered by the three thousand years or so which have elapsed since death, nevertheless the lesions are still recognisable by their position and microscopical structure.
The earliest signs of the disease are always seen in or close below the fenestrated membrane,-that is, just in the position where early lesions are seen at the present time. The disease is characteiised by a marked degeneration of the muscular coat and of the endothelium. These diseased patches, discrete at first, fuse together later, and finally form comparatively large areas of degenerated tissue, which may reach the surface and open out into the lumen of the tube. I need not point out how completely this description agrees with that of the same disease as seen at the present time.
I have already mentioned the absence of leucocytes and cellular infiltration, and need not therefore return to it here.
In my opinion, therefore, the old Egyptians suffered as much as we do now from arterial lesions identical with those found in the present time. Moreover, when we consider that few of the arteries examined were quite healthy, it would appear that such lesions were as frequent three thousand years ago as they are to-day.
I do not think we can accuse a very heavy meat diet. Meat is and always has been something of a luxury in Egypt, and although on the tables of offerings of old Egyptians haunches of beef, geese, and ducks are prominent, the vegetable offerings are always present in greater number. The diet then as now was mostly a vegetable one, and often very coarse, as is shown by the worn appearance of the crown of the teeth.
Nevertheless I cannot exclude a high meat diet as a cause with certainty, as the mummies examined were mostly those of priests and priestesses of Deir el-Bahari, who, owing to their high position, undoubtedly lived well. I must add, however, that I have seen advanced arterial disease in young modern Egyptians who ate meat very occasionally. In fact, my experience in Egypt and in the East has not strengthened the theory that meat-eating is a cause of arterial disease.
Finally, strenuous muscular exercise can also be excluded as a cause, aa there is no evidence that ancient Egyptians were greatly addicted to athletic sport, although we know that they liked watching professional acrobats and dancers. I n the ca6e of the priests of Deir el-Bahari, it is very improbable, indeed, that they were in the habit of doing very hard manual work or of taking much muscular exercise.
I cannot therefore at present give any reason why arterial disease should have been so prevalent in ancient Egypt. I think, however, that it is interesting to find that it was common, and that three thousand years ago it represented the same anatomical characters as it does now.
FIG. 1.-Pelvic and arteries of thigh completely calcified (XVIlIth-XXth Dynasty).
Fro. 2.-Completely dcifiedprofundaarteryaftersoakinginglycerine(XXIstDynasty). FIQ. 8.-Partly calcified aorta (XXVIIth Dynasty).
Fro. 4.-Calcified patches in aorta (XXVIIth Dynasty).
Fio. 5.-Calcified atheromatous ulcer of subclavian artery (XVIIIth-XXth Dynasty). Fro. &-Patch of atheroma i n anterior tibia1 artery (glycerine). The centre of the patch
is calcified (XXIst Dynasty).
FIG. 7.-Atheroma of brachial artery (glycerin) (XXIst Dynasty).
Fro. &-Unopened ulnar artery, atheromatous patch shining through (glycehne) (XXIst Dynasty). 31
FIG. 9.-Section through almost completely calcified posterior peroneal artery (low power). Van Gieson staining. a,al, n2, Remnants of endothelium and
fenestrated membrane. b, Calcified patches.
Many more are seen.
Same stain. (Leitz, Oc. 1, x &.)
FIG. 10.-Section
FIG. 11.-Section m(Leitz, Oc. 1, x *.)
a,Remains of endothelium.
b, Fenestrated membrane.
c, Muscular coat.
d,f,Membrane coat undergoing degenerntion.
e, Completely degenerated remnants of muscular coat.
atheroniatous patch of n h a r artery. Same stain. (Leitz, (Reference letters the same as in Fig. 11.)
FIG. 12.-Section Oc. 1, x fa.)
through calcified patch of ulnar artery. a,d, Calcified patches.
b, Partially calcified m wular coat. c, Annular muscular fibre.
through atheromatous patch of anterior tibia1 artery. Same stain through
FIG. 13.-Section at edge of atheromatous patch. Hreniatoxylin stain (Leitz, Oc. 1, XTh.1 a,Leucocytes (1). The atheromatous part on the left stains intensely dark with hamatoxylin.
Cairo, Cairo Governorate, Egypt
945
B.C.E.
Cardiology in Ancient Egypt by Eugene V. Boisaubin, MD
Egyptians describe coronary ischemia: "if thou examinest a man for illness in his cardia and he has pains in his arms, and in his breast and in one side of his cardio... it is death threatening him."
The classic pattern of cardiac pain--radiation to the left arm--was so well known that the ancient Egyptians and Copts even identified the left ring finger as the "heart" finger.
Altogether, ancient Egyptians were aware of a variety of abnormal cardiac conditions, particularly of angina pectoris and sudden death, arrhythmia, aneurysm, congestive heart failure, and venous insufficiency. Numerous remedies for afflicitions of the heart are found throughout the Ebers payrus.
There were a range of them using different foods, some even including carbohydrates like dates or honey and dough, but interesting, there is another combination of "fat flesh, incense, garlic, and writing fluid".
Extensive histologic analysis of mummies began, however; well before the development of the scanning electron microscope. In 1912, Shattock' made sections of the calcified aorta of Pharaoh Merneptah; and the work of Sir Marc Armand Rufer, published posthumously in 1921, is our most valuable early source of information about vascular disease in ancient Egyptians. Ruffer was able to study a relatively large number of tissue specimens from mummies, mainly from New Kingdom (1600-1100 BC) burials, but covering a wide period of time. In a mummy of the 28th to 30th Dynasty (404-343 BC), he observed atheromas in the common carotids and calcific atheromas in the left subclavian, common iliac, and more peripheral arteries. Ruffer concluded from the state of the costal cartilage that this mummy was not that of an old person. A mummy of a man of the Greek period (ca. 300 to 30 BC), who died at not over 50 years of age, showed atheromas of the aorta and brachial arteries. Since the discoveries of Rufer, numerous other mummies, whose ages at death ranged from the 4th to the 8th decade, have shown similar vascular changes (Fig.4).
In 1931, Long described a female mummy of the 21st Dynasty (1070-945 BC), found at Deir-el- Bahari-that of the lady Teye, who died at about 50 years of age. The heart showed calcification of one mitral cusp, and thickening and calcification of the coronary arteries. The myocardium is said to have had patchy fibrosis, and the aorta "nodular arteriosclerosis." The renal capsule was thickened, many of the glomeruli were fibrosed, and the medium-sized renal vessels were sclerotic. The condition appears to be that of hypertensive arteriosclerotic disease associated with atheromatous change. In the 1960s, Sandison examined and photographed mummy arteries using modern histologic methods (Fig.5). Arteries in the mummy tissues were described as tape-like, but could be dissected easily, whereupon arteriosclerosis, atheroma with lipid depositions, reduplication of the internal elastic lamina, and medial calcification were readily visible under microscopy.
Still more recently, one of the most extensively studied Egyptian mummies has been PUMIL from the Pennsylvania University Museum(hence its initials), now on loan to the National Museum of Natural History at the Smithsonian. It is believed to be from the later Ptolemaic period, circa 170BC. The heart and portions of an atherosclerotic aorta were found in the abdominal cavity. Histologically, large and small arterioles and arteries from other organs showed areas of intimal fibrous thickening typical of sclerosis. These findings are particularly striking since the estimated age of PUM I at time of death was between 35 and 40 years.
