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Coronary Heart Disease: From Mummies to 21(st) Century

© 2017 Heart Views | Published by Wolters Kluwer - Medknow
Coronary Heart Disease: From Mummies to 21st Century
Rachel Hajar, M.D.
Department of Cardiology, Heart Hospital, Hamad Medical Corporation, Doha, Qatar
Ischemic heart disease and stroke have remained
the world’s leading cause of death over the past
15 years. Our understanding of the pathogenesis
of coronary heart disease has been slow and was not
elucidated until the beginning of the 20th century. This
article will review how the diagnosis and treatment of
coronary heart disease was viewed from ancient times
to the present day.
Coronary heart disease was initially thought to be
a disease of modern humans, with the cause being
attributed to contemporary lifestyles. However, the
disease is not as new as we thought. An article in
the Lancet[1] in 2013 with whole body computed
tomography (CT) scans of mummies from four different
geographical regions (ancient Egypt, ancient Peru,
Ancestral Puebloan of Southwest, and the Unangan of
Address for correspondence:Dr.RachelHajar,
History of Medicine
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Medicine in ancient Egypt
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the Aleutian Islands) showed that atherosclerosis may
be very ancient. The time period spanned more than
4000 years. The investigators found probable or denite
atherosclerosis in 34% of the 137 mummies studied.
The authors conclude that the disease was common in
premodern humans.
CT scan – a 20th century technology – enabled
investigators to see the coronaries of the mummies
without performing dissection. Autopsy was not
performed in ancient times and recording of clinical
observations was not regularly practiced. The rst to
perform human dissections were the Greek physicians
Herophilus and Erasistratus in Alexandria, Egypt.[2]
Later, Roman law prohibited dissection and autopsy
of the human body, and therefore no new dissection
studies were done until the 14th century. When regular
anatomical dissection of humans during the Renaissance
took place in Europe, descriptions of coronary artery
disease (CAD) came to light. Anatomic and clinical
correlation was, however, nonexistent.
How do we know if a particular disease was
identied in antiquity? From ancient writings of course,
Homer (800 BC) remarked in the Odyssey: “In Egypt,
the men are more skilled in medicine than any of human
kind” and “The Egyptians were skilled in medicine
more than any other art.”[3] The medicine of the ancient
Egyptians is very old, dating from the beginnings of
civilization and was considered highly advanced for
its time. Egyptian medical skills and knowledge later
influenced medical traditions, including that of the
Greeks. Galen acknowledged the contribution of ancient
Egyptian medicine to Greek medicine.
Was ischemic heart disease known in ancient
Egypt? Information relating to medicine comes from
several sets of extensive ancient medical documents
dating as far back as 3000 BC. One of these medical
documents is known as the Ebers Papyrus, wherein
appears the following paragraph:
"Shouldst though examine a patient with stomach
disease suffering from pain in the arms, the breast, and
on the side of the stomach, say: ‘Death threatens." And
if though examinst a man for illness in his cardia, and
he has pains in his arm, in his breast, and in side of
his cardia, and it is said of him: It is [w3d] illness, then
thou shalt say thereof: It is due to something entering
the mouth it is death that threatens him. Thou shalt
prepare for him: Stimulating herbal remedies…”[4]"
Hence, it would seem that the clinical syndrome of
angina pectoris existed in ancient Egypt. Unfortunately,
there is no record of any anatomic and clinical correlation.
Even though there are reports of atherosclerosis in
mummies, there was no attempt to correlate clinical
symptoms with pathology. The symptoms in a particular
mummy simply were not available. For example, the
Pharaoh Merneptah[5] had large bone-like plaques in
his aorta which was submitted for analysis in 1909 to
Shattock, a British pathologist. The historical records
are silent whether the pharaoh suffered from any
symptoms. Shattock made frozen sections and conrmed
that the aorta was affected with calcification.[6] Even
though calcifications have been found in the arterial
tree of mummies before, pathologists thought these
calcications were “normal and incidental” ndings due
to age, and therefore natural and not a disease process.[7]
There is also an accurate but incidental description of
angina pectoris in old Arabic love literature revealed in a
poem written by Qais ibn Al-Mulawah. It comes from the
love story Majnoon Lila. The story is famous in Arabic
literature as well as in Arab folk stories. A madman in Arabic
is called “Majnoon,” so Majnoon Lila, means “Crazy about
Lila.” The poet’s name is Qais who lived in the 7th century.
A Mughal miniature illustration of Majnoon Lila
In a nutshell, Majnoon Lila is about a young
poet, Qais ibn Al-Mulawah, who fell in love with a girl
named Lila. The father of Lila refused to consent to
their marriage even though Lila also loved Qais.[8]
Lila was forced to marry another man and moved out
of town. Qais ran away to live in the desert, alone,
losing interest in family, friends, and society. He was
considered sick with “love madness.” He wrote poems
about his love to Lila. In his poems, he described his
tears, sleeplessness, lack of appetite, racing heart
beats or palpitations, and fainting episodes when
Lila left.[8]
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He died immediately after writing a poem to his
beloved Lila saying:
“My heart is rmly seized
By a bird’s claws;
My heart is tightly squeezed,
When Lila’s name ows.
My body is tightly bound,
When the wide world I found
Is like a nger ring around.”[8]
Graphic illustration of angina pectoris[8]
An Arab cardiologist, Dr. H. A. Hajar Albinali, the
author of an Arabic book Majnoon Lila: Between Medicine
and Literature, translated the above poem into English.
He claimed that it was the rst clear and best description
of angina in the history of medicine. He concluded in his
book from that poem and other symptoms that the poet
had CAD and died with myocardial infarction.[8]
In Europe, it is customary to reference angina pectoris
to William Heberden, but he was not the rst to describe
atherosclerosis. The medical literature is replete with
narratives of the rst descriptions of a particular disease
by different physicians.
Among the rst to describe atherosclerosis was
Leonardo da Vinci, who reportedly stated that “vessels in
the elderly restrict the transit of blood through thickening
of the tunics.”[9] Leonardo was not a physician, but he
was a great artist and leading intellectual of the Italian
Renaissance; he is known as the embodiment of a
“Renaissance man.” He believed that studying science
made him a better artist. He is renowned for painting
the Mona Lisa. Leonardo’s experiments, anatomical
drawings, and notes (often in mirror writing) provide early
descriptions of the structure and function of the heart
and circulation. His interest in anatomy was inspired by
the anatomist Marcantonio della Torre (1473–1511) who
was professor of anatomy in Pisa and then Padua and
who commissioned da Vinci to provide the illustrations
for his text on anatomy based on dissection.[10]
It was, however, William Heberden who brought
angina pectoris to the attention of the medical
profession when he presented his paper, “Some
Account of a Disorder of the Breast,” at the Royal
College of Physicians in London in 1768.[11] Many
aspects of his description are true to this day. He
describes both typical exertional angina as well as
variant angina which affected a patient only when he/
she was in bed and was relieved by sitting up. He also
points out the inuence of mental stress. Although it
is a classic, it is not the first description of angina.
Heberden wrote:
Those who are aficted with it are seized, while
they are walking, and more particularly when they walk
soon after eating, with a painful and most disagreeable
sensation in the breast, which seems as if it would take
their life away, if it were to increase or to continue: The
moment they stand still, all this uneasiness vanishes.”[9]
William Heberden (1710–1801)
Heberden coined the term “angina pectoris” from
Greek ankhonē which means “strangling” and Latin
pectoris, meaning “chest.” That historical term – “angina
pectoris” – is still used in this modern era of medicine.
Of interest, John Hunter, the 18th century Scottish
surgeon and anatomist, suffered from angina pectoris
and he was the rst in Europe to mention the effect of
emotions in precipitating an attack of angina. Hunter
unintentionally proved that when he suddenly collapsed
after a dispute with a colleague and died. Marked
atheroma (presumably in his coronary) was found
on autopsy.[12] John Hunter’s death occurred during
a period of emerging understanding of the relation
between angina pectoris and CAD. However, physicians
continued to describe the coronary lesions on pathology
specimens without correlating them to clinical signs.
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In 1761, the Italian anatomist Giovanni Morgagni
described the lesions as “hardening of the arteries” for
the rst time. Edward Jenner (1729–1823), a British
physician and pioneer of smallpox vaccine, and his
contemporary colleague, Caleb Parry (1755–1822),
linked the excruciating “disorder of the breast” to the
“hardening of the arteries.” However, the disease was
looked on, as still, only of pathologic interest.[7]
In 1856, Rudolf Virchow, the “father of pathology,”
dened the physiological elements in thrombosis within the
vascular system and the risk factors that predispose arteries
and veins to thrombus formation. Virchow’s concepts on
thrombosis remained relevant to the current medicine,
especially in cardiology.[13] Only after Virchow postulated
the features of thrombosis did scientists begin to consider
the clinical implications of coronary heart disease seriously.
Near the end of the 19th century, cardiovascular
physiologists noted that occlusion of a coronary artery
in the dog caused “quivering” of the ventricle which was
rapidly fatal. In 1879, the pathologist Ludvig Hektoen
concluded that myocardial infarction is caused by
coronary thrombosis “secondary to sclerotic changes
in the coronaries.” In 1910, two Russian clinicians
described ve patients with the clinical picture of acute
myocardial infarction (AMI), which was confirmed
at postmortem examination. Two years later, James
Herrick established the importance of bed rest and used
electrocardiography (ECG) to diagnose the condition.[14]
The diagnosis and treatment of CAD underwent
many milestones since the publication of William
Harvey’s De Motu Cordis in 1628 wherein he described
the circulation and the function of the heart.[14] These
milestones stimulated physicians in successive centuries
to explore and put forth theories on the pathogenesis
of coronary heart disease, and in the process, made
discoveries on how to improve diagnostic accuracy
and treatment.
In the 19th century, Claude Bernard catheterized
animals, measuring the pressures in the great vessels
and cardiac chambers. Werner Forssman, in 1929,
performed cardiac catheterization on himself which led
to the exploration of cardiac hemodynamics by Andre
Frederic Cournand and Dickinson Richards. These
three investigators were awarded the Nobel Prize in
Physiology or Medicine in 1956.[14]
The coronary arteriogram truly revolutionized our
understanding and management of cardiac patients.
Dr. Mason Sones of Cleveland Clinic introduced the
selective injection of contrast media into the coronary
arteries in 1958.[15] In the catheterization laboratory in
Cleveland Clinic that day, a 26-year-old patient was
being evaluated for rheumatic mitral and aortic valve
disease when the catheter whiplashed into the ostium
of the right coronary artery. Sones was reportedly in
the catheterization laboratory at the time and reportedly
exclaimed, “we’ve killed him!”[15]
Rudolph Virchow (1821–1902)
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However, there was no fatal ventricular arrhythmia;
the monitor showed only prolonged asystole after
sinus arrest that promptly responded to repeated deep
coughs. Two days later, Sones proceeded to a planned
selective injection of the coronary arteries.[15] The
expected ventricular arrhythmias failed to occur and
the technique of selective coronary arteriography was
born. The traditional thinking before the introduction
of the technique was that, if you injected dye into one
coronary artery at a time, the resultant asymmetrical
hypoxia of the coronary circulation would create an
electrical imbalance and fatal ventricular arrhythmia
would ensue.[15]
The images of the coronary arteries obtained with
arteriography provided objective evidence to support or
refute the clinical diagnosis of angina pectoris.
Two radiologists, Drs. Judkins and Amplatz,
designed catheters and used the Seldinger percutaneous
technique to gain access to the femoral artery and
engaged the ostia of either the left or right coronary
artery. Their technique required less training than the
Sones’ technique which facilitated the widespread use
of coronary angiography in cardiology as a diagnostic
The coronary angiogram continues to play an
integral role in diagnosis, management, and planning
future treatment of CAD. It was the rst reliable in vivo
marker for the presence of obstructing coronary lesions.
It provided objective evidence to support or refute the
clinical diagnosis of angina pectoris. It became the
standard diagnostic tool for dening vessel anatomy and
led to the rst studies of the natural history of patients
with CAD. It also led to studies conrming the benet of
coronary artery bypass grafting (CABG) over medical
treatment in subsets of patients. It was instrumental
in the introduction of percutaneous transluminal
coronary angioplasty and delineation of restenosis.
It has the ability to compare percutaneous coronary
intervention (PCI) versus CABG for revascularization
In our time, much progress has been learned about the
pathogenesis and treatment of ischemic heart disease.
Once CAD is diagnosed, the ndings from coronary
angiography guide the strategy for the best treatment.
The options of medical therapy, angioplasty, stenting,
or CABG depend largely on the severity of disease.
In general, at present, patients with coronary
narrowings that do not limit coronary artery blood
flow receive medications and lifestyle modification to
help prevent progression. If a patient has coronary
atherosclerosis that limits blood flow in the coronary
arteries, balloon angioplasty and stenting can be offered.
In patients with multiple areas of coronary artery narrowing
or blockage, CABG surgery is generally recommended.
Below is a brief summary of the modern advances
in the therapy of CAD and AMI.
Before 1961, patients with AMI were placed in
nonmonitored beds in the hospital and far away from
nurses’ stations, so the patients would not be disturbed.
Patients were found dead in their beds. The risk of death
occurring in the hospital was approximately 30%.[14]
Development of the coronary care unit (CCU)[16] took
place in 1961. Establishment of the CCU provided
continuous ECG monitoring of the patient, closed chest
cardiac resuscitation, external defibrillation, and
reduced in-hospital mortality by half among patients
admitted with AMI. Other influences that reduced
mortality were prompt and early diagnosis with sensitive
and specic biomarkers[13] and development of surgical
methods for revascularization.
The coronary arteriogram provided the foundation
for surgical treatment of CAD by means of
coronary revascularization. The development and
renement CABG for the treatment of CAD required
close collaborations among surgeons, engineers,
cardiologists, anesthesiologists, and hematologists.
The heart–lung machine developed by Gibbon[17] was
originally introduced into cardiac surgery for the repair
of intracardiac defects but was soon adopted by cardiac
Normal coronary angiogram
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surgeons for adult coronary revascularizations because
of its ability to create a motionless, bloodless operative
field. Tens of millions of patients benefitted from
coronary revascularization on cardiopulmonary bypass.
However, advances in medical therapy and
PCI have led to shrinking numbers of CABG being
There have been many advances in the medical
therapy of CAD and AMI. Since the 1970s, large-scale
trials have shown that the risk of death is lowered with
aspirin, cholesterol-lowering drugs, β-blockers, and
angiotensin-converting enzyme inhibitors. However,
life-threatening heart failure still occurs late in patients with
large infarcts. Prognosis in such patients has been improved
with an implantable debrillator, cardiac resynchronization
therapy, pacemakers, and left ventricular assist devices.
Fibrinolytic therapy has been a major advance
in the treatment of AMI, leading to improved early
survival, less heart failure, less ventricular remodeling,
and fewer arrhythmias.[18] Streptokinase (SK) was
the first thrombolytic drug to be used in myocardial
infarction. Researchers have known for some time of
SK’ ability to dissolve clots. Fibrinolysis induced by
SK resulted in the breakdown of brin. SK was used
initially for brinous pleural exudates, hemothorax, and
tuberculous meningitis. Some researchers started using
SK in patients with AMI, offering hope that CAD could
be “cured.” Experimental intracoronary infusion of SK
produced conicting results initially. Hence, the Italian
Group for the Study of Streptokinase in Myocardial
Infarction (Gruppo Italiano per la Sperimentazione
della Streptochinasi nell’Infarto Miocardico) (GISSI)
trial in 1986 addressed this issue by recruiting more
than 10,000 patients and proved that SK reduced early
mortality in patients with AMI.[19]
The thrombolytic era was found on a fundamental
concept that most cases of AMI are the result of
sudden obstruction of an epicardial coronary artery
by intracoronary thrombus superimposed on a
ruptured or ssured atherosclerotic plaque. The
GISSI study validated SK as an effective therapeutic
method, and therefore xed protocols for its use in
AMI were established. SK has been supplanted by
tissue plasminogen activator in developed nations,
but SK remains essential to the management of AMI
in developing nations.[18,19] The Second International
Study of Infarct Survival showed that the addition of
aspirin (an antiplatelet drug) led to further reductions
in mortality.[20]
Medications are prescribed to reduce the risk of death by
reducing the risk of heart attack, stroke, and heart failure.
Lifestyle changes help prevent the continuing buildup of
fatty deposits in the coronary arteries. These changes
include smoking cessation, a diet low in fat and cholesterol,
weight loss, regular exercise, stress management, diabetes
control, and blood pressure control. These medications and
lifestyle changes are equally important for those patients
who also undergo coronary revascularization with PCI, with
or without stents or CABG.
In the recent years, PCI treatment (introduced by the
German radiologist Andreas Gruentzig in 1977) for
CAD is oftentimes preferred over CABG because the
comparative effects of these two revascularization
methods on long-term mortality are still unclear. PCI
is also less invasive. However, the journal JAMA Inter
Med[21] in 2014 published a meta-analysis of randomized
clinical trials comparing CABG versus PCI. The study
found that, in patients with multivessel coronary disease,
CABG leads to an unequivocal reduction in long-term
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mortality and myocardial infarctions and to reductions
in repeat revascularizations, regardless of whether
patients are diabetic or not.[21]
Coronary angioplasty and stenting together with
newer, more potent platelet inhibitors such as P2Y and
glycoprotein IIb/IIIa platelet receptor blockers further
reduced in-hospital mortality from AMI to about 7%.[14]
The efcacy of these treatments depends on a short
interval between the onset of symptoms and the patient
arrival at the hospital.
CAD and AMI have been with us since antiquity. We
understand now that coronary ischemia and AMI
are the result of a sudden obstruction of a coronary
artery by intracoronary thrombus superimposed on a
ruptured atherosclerotic plaque. Advances in modern
therapy are based on this concept. However, the
clinical problem of CAD and AMI is still being actively
investigated in an effort to refine management and
hopefully nd a cure.
Financial support and sponsorship
Conicts of interest
There are no conicts of interest.
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... Coronary artery disease (CAD) has been passing the long history of evolution from ancient times [1] until now [2]. Though enormous research has been dedicated to this disorder, it ranks first among death causes worldwide [3] with the highest prevalence in Central and Eastern Europe [4]. ...
Full-text available
Background and aim. Unstable angina is classified into new-onset, progressive, and angina at rest. Though hemostasis plays a crucial role in the pathogenesis of coronary artery disease, including unstable angina, limited data exist regarding peculiarities of fibrinolytic parameters in the above-mentioned types of unstable angina. Our study aims to investigate if there is a difference in the fibrinolytic state between the groups of patients with new-onset, progressive unstable angina in comparison with stable angina patients depending on medical history data, electrocardiographic and hemodynamic features. Materials and methods. In our cross-sectional study, we recruited 93 coronary artery disease patients (mean age 62.32 (6.94) years, 41 males (44.1%)). They were divided into 3 groups: stable angina patients (n=22) (control), new-onset unstable angina patients (n=21), and progressive unstable angina patients (n=50). The groups were comparable by baseline characteristics. Blood samples were obtained before treatment onset. The concentrations of tissue plasminogen activator and inhibitor of plasminogen activator (type 1) were measured by the ELISA method. We registered 14 points at the admission department, particularly age, sex, body mass index, smoking, presence of the family history of cardiovascular disorders, ST-segment depression, T-wave variability, arrhythmias, left bundle branch blockage, heart rate, systolic and diastolic blood pressure, Sokolov-Lyon voltage criteria, and unstable angina type (new-onset or progressive). After comparison of fibrinolytic parameters’ concentrations among groups under investigation, we defined the main independent predictors among observed 14 parameters to create optimal regression models for assessment of fibrinolytic parameters concentrations. Results and conclusion. The groups under investigation differ significantly in concentration of tissue plasminogen activator (P
... In 1958, physician at Cleveland, Sones' mistakenly injected the coronary artery ostia, creating the first coronary angiogram, the catheterisation technique was being used at the time for delineating valvular pathology. This led to visualising the anatomy of these vessels and its appearances in the diseased state; which eventually gave way to management options delineation 3 . In South Asian countries, with progressive urbanization the burden of coronary artery disease is likely to have doubled in the past two decades. ...
Full-text available
Objective: The objective was to establish patterns of diseased vessels amongst the study population. Methodology: This retrospective descriptive study analyzed the data of 396 patients who underwent diagnostic angiographies at a large tertiary care public hospital in Islamabad, from January-2018 till October 2018. All data was coded and recorded in SPSS and was quantitatively run to find percentages and tests of significance were done. Results: We found that single vessel disease was the most common at 31.6%, and that the left anterior descending was the most commonly involved vessel with the most significant coronary artery disease, 86.6% and 71.4% respectively. Conclusion: Hypertension and diabetes has a great burden on our South Asian population and contribution to the development of coronary artery disease. Severe disease present in one vessel should alert physicians to the possibility of multi-vessel involvement and multi vessel progression in the disease progress. Delineation of the vessel involvement pattern in South Asians forms the basis for formulating local guidelines and strategies for tackling coronary artery disease.
The study of epidemiology is vital in identifying the connections which exist between lifestyle, environment, and disease, thus providing knowledge of the factors, distribution, and pathology of disease. As the leading cause of death in the United States since 1900, save 1918, cardiovascular disease, and specifically coronary heart disease, continue to overwhelm mortality and morbidity statistics. In the United States, one in four deaths are attributed to cardiovascular disease, and it is the leading cause of death in both males and females. Additionally, coronary heart disease kills approximately 10 times more females than breast cancer. The estimated direct and indirect cost of cardiovascular disease is $220 billion. Cardiovascular disease is also the leading cause of death worldwide. Coronary heart disease accounts for almost half of the deaths attributed to cardiovascular disease and kills over 18 million Americans per year (that is almost equivalent to the population of New York City, Los Angeles, Chicago, and Houston combined). Although the absolute number of deaths due to coronary heart disease has increased, the age standardized death rate has decreased. Coronary heart disease is a condition that is multifaceted, influenced by social status, genetics, lifestyle, and environmental factors. Risk factors such as hypertension, physical inactivity, tobacco use, and diet are modifiable risk factors, whereas genetics, age, race, and sex are nonmodifiable risk factors associated with coronary artery disease. Public education must continue to dominate efforts to reduce the major modifiable risk factors. As we continue to monitor the distribution of cardiovascular disease and coronary heart disease in populations, epidemiology will provide us with more knowledge to thwart such a devastating disease worldwide.KeywordsCoronary artery diseaseCoronary heart diseaseCardiovascular diseaseEpidemiologyDemographyHeart attackStatisticsRisk factorsCADCHDCVD
Cardiovascular diseases (CVD) remain one of the leading causes of mortality worldwide. Despite recent advances in diagnosis and interventions, there is still a crucial need for new multifaceted therapeutics that can address the complicated pathophysiological mechanisms driving CVD. Extracellular vesicles (EVs) are nanovesicles that are secreted by all types of cells to transport molecular cargo and regulate intracellular communication. EVs represent a growing field of nanotheranostics that can be leveraged as diagnostic biomarkers for the early detection of CVD and as targeted drug delivery vesicles to promote cardiovascular repair and recovery. Though a promising tool for CVD therapy, the clinical application of EVs is limited by the inherent challenges in EV isolation, standardization, and delivery. Hence, this review will present the therapeutic potential of EVs and introduce bioengineering strategies that augment their natural functions in CVD. Extracellular vesicles (EVs) are membrane‐bound nanovesicles secreted by cells to mediate biological functions. In the cardiovascular system, EVs maintain homeostasis and promote repair mechanisms following cardiovascular diseases onset. However, poor standardization and targeting specificity challenge the clinical potential of EV therapy. New bioengineering strategies have been developed to augment the natural bioactive properties of EVs and enhance therapeutic efficacy.
Atherosclerosis, a chronic inflammatory disease of the arteries that appears to have been as prevalent in ancient as in modern civilizations, is predisposing to life-threatening and life-ending cardiac and vascular complications, such as myocardial and cerebral infarctions. The pathogenesis of atherosclerosis involves intima plaque buildup caused by vascular endothelial dysfunction, cholesterol deposition, smooth muscle proliferation, inflammatory cell infiltration and connective tissue accumulation. Hypertension is an independent and controllable risk factor for atherosclerotic cardiovascular disease (CVD). Conversely, atherosclerosis hardens the arterial wall and raises arterial blood pressure. Many CVD patients experience both atherosclerosis and hypertension and are prescribed medications to concurrently mitigate the two disease conditions. A substantial number of publications document that many pathophysiological changes caused by atherosclerosis and hypertension occur in a manner dependent upon circadian clocks or clock gene products. This article reviews progress in the research of circadian regulation of vascular cell function, inflammation, hemostasis and atherothrombosis. In particular, it delineates the relationship of circadian organization with signal transduction and activation of the renin-angiotensin-aldosterone system as well as disturbance of the sleep/wake circadian rhythm, as exemplified by shift work, metabolic syndromes and obstructive sleep apnea (OSA), as promoters and mechanisms of atherogenesis and risk for non-fatal and fatal CVD outcomes. This article additionally updates advances in the clinical management of key biological processes of atherosclerosis to optimally achieve suppression of atherogenesis through chronotherapeutic control of atherogenic/hypertensive pathological sequelae.
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Cardiovascular disease is the leading cause of mortality and morbidity worldwide. The 2011 annual report from the World Health Organization mentioned that, coronary heart disease and cerebro-vascular disease which were reported as the top two causes of mortality in 2004, are predicted to remain the major cause of death in the next 20 years. Coronary heart disease(CHD) and atherosclerosis were once thought to be a disease of modern humankind linked to modern lifestyle. However, researchers dispute this and has confirmed that atherosclerosis was common in preindustrial inhabitants too. Further, vascular system studies of mummies give substantial evidence of atherosclerosis as ancient human disease and clinical syndrome of angina pectoris existed in ancient Egypt. In 1768 the paper presented at the Royal College of Physicians in London on “Some account of a disorder of the breast” was an eye opener to medical professionals and later this excruciating “disorder of breast” was linked to the “hardening of the arteries’’. In the past it was generally believed that MI virtually always resulted in death and identified in postmortem. In1878, the first case of coronary occlusion diagnosed during life was described. ECG was used to diagnose the condition in 1912 and the use of current 12-leads ECG became accepted practice since the 1950s. In addition to clinical evaluation and ECG, cardiacbiomarkers play a pivotal role in diagnosis and management of acute coronary syndrome. Aspartateaminotransferase became the first biomarker used to diagnose and subsequently CK-MB isoenzyme, lactatedehydrogenase and myoglobin played very significant roles. Troponin is now considered the ‘gold standard’biochemical test for the diagnosis. The definition, diagnosis, management and prognosis of coronary heartdisease have changed over the decades with the development of medical science and knowledge. It istherefore interesting to appraise the historical aspect of evolution of CHD definitions and diagnosis. Moreover,clinicians should have updated knowledge on the evolution of definition, diagnosis, management andprognosis of this condition.
Coronary artery disease (CAD) is a condition of an inadequate supply of oxygenated blood to a portion of the myocardium. It typically occurs when there is an imbalance between supply and demand of myocardial oxygen. The most common cause of myocardial ischemia is atherosclerotic disease of an epicardial coronary artery or arteries which is sufficient to cause a regional reduction in myocardial blood flow and inadequate perfusion of the myocardium supplied by the involved coronary artery. Fifty CAD subjects (23 females and 27 males) were enrolled in this study in addition to thirty healthy control subjects (13 female and 17 male). This study aimed to measure the serum levels of interleukin IL- 33, C- reactive protein and troponin in CAD and their association with lipid profile by using enzyme-linked immune sorbent assay (ELISA). T results showed that high-density lipoprotein (HDL) was statistically high while differences in cholesterol, triglyceride and low-density lipoprotein (LDL) were statistically non-significant between CAD patients and controls. Moreover, the serum level of IL-33 and CRP were statistically higher in patients than controls, while troponin levels were not significantly different. In addition, the present study demonstrates that IL-33, CRP, and Troponin were not associated with lipid profile. The relationship of IL-33 with CRP and troponin was non-significant.
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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. Funding: National Endowment for the Humanities, Paleocardiology Foundation, The National Bank of Egypt, Siemens, and St Luke's Hospital Foundation of Kansas City.
In this review of heart disease, Nabel and Braunwald focus on two themes - coronary artery disease and myocardial infarction - and explain how our understanding has evolved over the past two centuries. The authors consider therapies that have led to improved survival.
The original description of Heberden's angina pectoris is put forward to stress the importance of proper history-taking in identifying patients. In a market-driven approach to improve cost-effectiveness in healthcare, angina pectoris as an entity seems stripped to its bare minimum: chest and pain. The diagnostic yield of exercise testing, however, depends on the pre-test likelihood of disease and therefore knowledge of its clinical utility and pitfalls is essential to refine an initial and subjective diagnosis based on anamnesis. Nowadays chest pain units attempt to improve diagnostic accuracy by submitting all sorts of patients to the (stress) test. In the end protocol-driven policies like these may very well prove to be contraproductive when fundamentals are ignored. (Neth Heart J 2010;18:561-4.).
The history of atherosclerosis and cardiovascular disease dates back to ancient times. From the teachings of Galen to the response-to-injury hypothesis of Russel Ross, we have now arrived at the concept of the vulnerable plaque. Next to the development of new treatment options for patients with atherosclerosis, also novel diagnostic imaging techniques have been developed to visualise the arterial wall and to characterise plaque composition. In this article the historical context of atherosclerosis and the attempts towards a noninvasive therapy for patients with atherosclerotic diseases are described. (Neth Heart J 2009;17:140-4.).
In the first half of the third century B.C, two Greeks, Herophilus of Chalcedon and his younger contemporary Erasistratus of Ceos, became the first and last ancient scientists to perform systematic dissections of human cadavers. In all probability, they also conducted vivisections of condemned criminals. Their anatomical and physiological discoveries were extraordinary. The uniqueness of these events presents an intriguing historical puzzle. Animals had been dissected by Aristotle in the preceding century (and partly dissected by other Greeks in earlier centuries), and, later, Galen (second century A.D.) and others again systematically dissected numerous animals. But no ancient scientists ever seem to have resumed systematic human dissection. This paper explores, first, the cultural factors--including traditional Greek attitudes to the corpse and to the skin, also as manifested in Greek sacred laws--that may have prevented systematic human dissection during almost all of Greek antiquity, from the Pre-Socratic philosopher-scientists of the sixth and fifth centuries B.C. to distinguished Greek physicians of the later Roman Empire. Second, the exceptional constellation of cultural, political, and social circumstances in early Alexandria that might have emboldened Herophilus to overcome the pressures of cultural traditions and to initiate systematic human dissection, is analyzed. Finally, the paper explores possible reasons for the mysteriously abrupt disappearance of systematic human dissection from Greek science after the death of Erasistratus and Herophilus.
During the past 25 years, 24 randomized trials of intravenous (IV) fibrinolytic treatment have been reported, involving a total of some 6000 patients in the acute phase of myocardial infarction. Most tested IV streptokinase (SK), but a few tested IV urokinase (UK). In the past 2 or 3 years numerous small randomized trials of intracoronary (IC) SK have been started, 9 of which, involving a total of about 1000 such patients have been reported. Because all of these IV and IC trials were small (the largest including only 747 patients), their separate results appear contradictory and unreliable. But, an overview of the data from these trials indicates that IV treatment produces a highly significant (22%±5%, (P<0.001) reduction in the odds of death, an even larger reduction in the odds of reinfarction, and an absolute frequency of serious adverse effects to set against this that is much smaller than the absolute mortality reduction. The apparent size of the mortality reduction in the IV trials was similar whether anticoagulants were compulsory or optional, whether treatment was in a coronary cure unit or an ordinary ward and, surprisingly, whether treatment began early ( <6 h from onset of symptoms) or late (generally 12–24 h). In addition, there was no evidence that UK was more effective than the less expensive SK, or that, despite their technical complexity, the new IC regimes were more effective than the old IV regimes. Even the IV schedules that have been studied in randomized trials were, however, quite complex, and the IC schedules were far more so. Perhaps partly because of this, none of them is widely used. If so, then some much simpler, and hence more widely practicable, IV SK regimes should be developed and tested. For example, a simple one hour high-dose IV SK infusion, without anticoagulation, will successfully convert virtually all of the available plasminogen into plasmin. But, it may be several years before the net effects on mortality of any more widely practicable IV SK regimes can be agreed unless many of the hospitals that do not wish routinely to use IC regimes or the complex previous IV regimes will collaborate in multicentre randomized trials that can, if necessary, continue rapid intake until some tens of thousands of patients have been randomized, and some thousands of deaths have been observed among the control and treated patients. The same, of course, may be true for any other fibrinolytic regimes (e.g. infusion of tissue plasminogen activator) if their net effects on mortality are comparable to those of IV SK.