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, 1906
The Jungle
Meat sales in the United States to fall by half in 1906
Ironically—or perhaps tellingly—the heart disease “epidemic” began after a period of exceptionally reduced meat eating. The publication of The Jungle, Upton Sinclair’s fictionalized exposé of the meatpacking industry, caused meat sales in the United States to fall by half in 1906, and they did not revive for another twenty years. In other words, meat eating went down just before coronary disease took off. Fat intake did rise during those years, from 1909 to 1961, when heart attacks surged, but this 12 percent increase in fat consumption was not due to a rise in animal fat. It was instead owing to an increase in the supply of vegetable oils, which had recently been invented.
Nevertheless, the idea that Americans once ate little meat and “mostly plants”—espoused by McGovern and a multitude of experts—continues to endure. And Americans have for decades now been instructed to go back to this earlier, “healthier” diet that seems, upon examination, never to have existed.
January 1, 1910
Über den Gehalt normaler und atheromatöser Aorten an Cholesterin und Cholesterinestern.
German chemist Adolf Otto Reinhold Windaus discovered atheromatous arterial lesions (arterial plaques) contain six times as much free cholesterol and 20 times as much esterified cholesterol as do healthy arteries
In 1910, as part of his pioneering studies of the role of cholesterol in human metabolism, German chemist Adolf Otto Reinhold Windaus discovered atheromatous arterial lesions (arterial plaques) contain six times as much free cholesterol and 20 times as much esterified cholesterol as do healthy arteries (2). Windaus would also later describe the pathways by which cholesterol is converted to vitamin D. For his work, he was awarded the Nobel Prize in chemistry in 1928.
The assumption at the time was, predictably, that the cholesterol in arterial plaques must arise from the cholesterol circulating in the bloodstream. In time, this finding gave rise to Gofman/Keys’ lipid hypothesis, which holds that elevated blood cholesterol concentrations (caused by eating a high-fat diet especially rich in “artery-clogging” saturated fats) drive cholesterol across the arterial lining, a single layer of cells known as the endothelium, and into the subendothelial space, causing the initiation of fatty streaks (Figure 1). These then progress to the development of more advanced atherosclerosis, termed arterial plaques (Figure 2), which among other complications can cause heart attacks and strokes.
Figure 1: This diagram explains the currently accepted theory of how endothelial damage, largely of unknown cause, allows LDL-cholesterol to cross the endothelium and enter a postulated and hypothetical acellular space, the subendothelial space. There, the LDL-cholesterol is taken up by macrophages, causing the development of the earliest form of atherosclerosis, known as the fatty streak. Note that for the atherosclerotic process to happen in this way, the tunica intima must be devoid of all cells other than the single layer of endothelial cells that coat its upper surface, separating it from the blood contained in the lumen of the artery. According to this model, the subendothelial space is essentially a wide-open vacant space waiting expectantly to accommodate these (complex) processes that produce atherosclerosis. Reproduced with additions from reference 4, p. 3.
The finer details in Figure 1 are not critical to the argument. What is important is the way in which the different cellular structures are depicted.
Here, the crucial point is that, according to the currently popular explanation of atherosclerosis (4), until the endothelium is damaged (by currently unknown biological events), allowing the unrestrained entry of LDL-cholesterol, the tunica intima is depicted as a single, thin layer of endothelial cells sitting on top of an acellular space (devoid of cells). This is an important consideration, since the presence of any cells in the subendothelial space must impede the entry of LDL-cholesterol directly from the bloodstream and will hinder the ability of the macrophages to detect and consume the cholesterol, as depicted in Figure 1.
Figure 2 depicts how this model explains the progression of the fatty streak to full-blown atherosclerotic plaque. Note again that the subendothelial space is devoid of cells before the hypothetical endothelial damage allows the free entry of LDL-cholesterol into this conveniently located anatomical space.
Figure 2: This figure shows how the fatty streak (Figure 1) progresses to the atherosclerotic plaque according to the lipid hypothesis. For the lipid hypothesis to be true, until after the initial “injury” to the endothelium has allowed the entrance of blood-derived LDL-cholesterol, the tunica intima must, as shown in this figure and in Figure 1, contain no cells other than the thin layer of endothelial cells on its upper surface. Notice that in this figure, smooth muscle cells (SMC) migrate from the tunica media into the tunica intima to further progress the development of the atherosclerotic plaque. Reproduced with additions from reference 4, p. 8.
In 1910, neither Windaus nor anyone else was aware that cholesterol cannot simply pass through healthy arterial walls, however hard it may be “shoved” (3). Currently, the most popular theory for atherosclerosis is that shown in Figures 1 and 2. This theory holds that the endothelial cells lining the lumen of the artery wall must first be damaged before the passing of cholesterol through the wall can happen. This is termed “endothelial cell dysfunction” (4), but the immediate cause of “endothelial cell dysfunction,” if this is indeed the mechanism, remains shrouded in secrecy even today, 110 years after Windaus’ discovery.
This theory also predicts that cholesterol enters damaged arteries down a concentration gradient, so the degree of a person’s arterial disease can be predicted quite simply as their average blood cholesterol concentration multiplied by the number of years the blood cholesterol concentration has been “elevated” (3, 5).
Also, still unknown then was that atherosclerosis is a patchy disease that selectively targets only specific areas of different arteries. This is exemplified by what happens in the coronary arteries supplying blood to the heart muscle (6).
It also was then unknown that in some populations, there may be advanced atherosclerosis in the cerebral (brain) arteries with minimal involvement of the coronary (heart) arteries (7, 8). In such cases, a person is at greater risk of stroke than heart attack. In other cases, as is more prevalent in the U.S., the opposite applies.
January 1, 1928
Heart disease is first recorded in 1928 in Britain.
In Britain, the Scottish doctor Walter Yellowlees hunted down every last case of heart disease he could find and came to the conclusion that in prewar Britain the condition was “a very rare disease.” The first case of an infarction in the Edinburgh Royal Infirmary was recorded in 1928
January 1, 1934
Dr. L. A. White Letter
Dr. L. A. White practiced in Alaska and rarely found hypertensive, arteriosclerotic, diabetes, cancer, strokes, or coronary heart disease among the natives between 1934-1948.
Dr. L. A. White of 642 Eugene Medical Center, Eugene, Oregon, wrote me on February 21, 1958:
“... It has been almost 17 years since I practiced in Alaska. I was at Unalaska [Aleutian Islands] 1934-48, having previously spent 17 months at Metlakatla [Alaska Panhandle], then several months in '39 at Klawock [Panhandle]; finally one and a half years at Bethel [Lower Kuskokwim]. My work led me to these conclusions: (1) hypertensive and arteriosclerotic diseases were practically nonexistent among the native peoples; (2) diabetes was extremely rare; (3) malignant disease was extremely rare — in fact, I had only one proven case (Bethel, 1940). I saw no strokes nor coronary heart disease ...”
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.
