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There are different forms of
heart disease:
-
Coronary heart disease,
the end result of the accumulation of atheromatous plaques
within the walls of the arteries that supply the
myocardium
-
Ischaemic heart disease,
a disease characterized by reduced blood supply to the
heart.
-
Cardiovascular disease,
a class of diseases that involve the heart and/or blood
vessels (arteries and veins).
- Pulmonary heart disease, a failure of the right side
of the heart.
The study of the heart (and
diseases of the heart) is
cardiology.
Coronary heart disease
(CHD), also called coronary artery disease (CAD) and
atherosclerotic heart disease, is the end result of the
accumulation of atheromatous plaques within the walls of the
arteries that supply the myocardium (the muscle of the
heart). While the symptoms and signs of coronary heart
disease are noted in the advanced state of disease, most
individuals with coronary heart disease show no evidence of
disease for decades as the disease progresses before the
first onset of symptoms, often a "sudden" heart attack,
finally arise. After decades of progression, some of these
atheromatous plaques may rupture and (along with the
activation of the blood clotting system) start limiting
blood flow to the heart muscle. The disease is the most
common cause of sudden death.
Overview
Atherosclerotic heart disease can be thought of as a wide
spectrum of disease of the heart. At one end of the spectrum
is the asymptomatic individual with atheromatous streaks
within the walls of the coronary arteries (the arteries of
the heart). These streaks represent the early stage of
atherosclerotic heart disease and do not obstruct the flow
of blood. A coronary angiogram performed during this stage
of disease may not show any evidence of coronary artery
disease, because the lumen of the coronary artery has not
decreased in caliber.
Over a period of many years, these streaks increase in
thickness. While the atheromatous plaques initially expand
into the walls of the arteries, eventually they will expand
into the lumen of the vessel, affecting the flow of blood
through the arteries. While it was originally believed that
the growth of atheromatous plaques was a slow, gradual
process, some recent evidence suggests that the gradual
buildup of plaque may be complemented by small plaque
ruptures which cause the sudden increase in the plaque
burden due to accumulation of thrombus material.
Atheromatous plaques that cause obstruction of less than 70
percent of the diameter of the vessel rarely cause symptoms
of obstructive coronary artery disease. As the plaques grow
in thickness and obstruct more than 70 percent of the
diameter of the vessel, the individual develops symptoms of
obstructive coronary artery disease. At this stage of the
disease process, the patient can be said to have ischemic
heart disease. The symptoms of ischemic heart disease are
often first noted during times of increased workload of the
heart. For instance, the first symptoms include exertional
angina or decreased exercise tolerance.
As the degree of coronary artery disease progresses, there
may be near-complete obstruction of the lumen of the
coronary artery, severely restricting the flow of
oxygen-carrying blood to the myocardium. Individuals with
this degree of coronary heart disease typically have
suffered from one or more myocardial infarctions (heart
attacks), and may have signs and symptoms of chronic
coronary ischemia, including symptoms of angina at rest and
flash pulmonary edema.
A distinction should be made between myocardial ischemia and
myocardial infarction. Ischemia means that the amount of
oxygen supplied to the tissue is inadequate to supply the
needs of the tissue. When the myocardium becomes ischemic,
it does not function optimally. When large areas of the
myocardium becomes ischemic, there can be impairment in the
relaxation and contraction of the myocardium. If the blood
flow to the tissue is improved, myocardial ischemia can be
reversed. Infarction means that the tissue has undergone
irreversible death due to lack of sufficient oxygen-rich
blood.
An individual may develop a rupture of an atheromatous
plaque at any stage of the spectrum of coronary heart
disease. The acute rupture of a plaque may lead to an acute
myocardial infarction (heart attack). It is unclear at
present which plaques in an individual are more likely to
rupture in the future and cause a heart attack.
Pathophysiology
Limitation of blood flow to
the heart causes ischemia (cell starvation secondary to a
lack of oxygen) of the myocardial cells. When myocardial
cells die from lack of oxygen, this is called a myocardial
infarction (commonly called a heart attack). It leads to
heart muscle damage, heart muscle death and later scarring
without heart muscle regrowth.
Myocardial infarction usually results from the sudden
occlusion of a coronary artery when a plaque ruptures,
activating the clotting system and atheroma-clot interaction
fills the lumen of the artery to the point of sudden
closure. The typical narrowing of the lumen of the heart
artery before sudden closure is typically 20%, according to
clinical research completed in the late 1990s and using IVUS
examinations within 6 months prior to a heart attack. High
grade stenoses exceeding 75% blockage, such as detected by
stress testing, were found to be responsible for only 14% of
acute heart attacks. The events leading up to plaque rupture
are only partially understood. Myocardial infarction is also
caused, far less commonly, by spasm of the artery wall
occluding the lumen, a condition also associated with
atheromatous plaque and CHD.
CHD is associated with smoking, obesity, hypertension and a
chronic sub-clinical lack of vitamin C. A family history of
CHD is one of the strongest predictors of CHD. Screening for
CHD includes evaluating homocysteine levels, high-density
and low-density lipoprotein (cholesterol) levels and
triglyceride levels.
Angina
The pain
associated with very advanced CHD is known as angina, and
usually presents as a sensation of pressure in the chest,
arm pain, jaw pain, and other forms of discomfort. The word
discomfort is preferred over the word pain for describing
the sensation of angina, because it varies considerably
among individuals in character and intensity and most people
do not perceive angina as painful, unless it is severe.
There is evidence that angina and CHD present differently in
women and men.
Angina that occurs regularly with activity, upon awakening,
or at other predictable times is termed stable angina and is
associated with high grade narrowings of the heart arteries.
The symptoms of angina are often treated with nitrate
preparations such as nitroglycerin, which come in
short-acting and long-acting forms, and may be administered
transdermally, sublingually or orally. Many other more
effective treatments, especially of the underlying
atheromatous disease, have been developed.
Angina that changes in intensity, character or frequency is
termed unstable. Unstable angina may precede myocardial
infarction, and requires urgent medical attention. It is
treated with oxygen, intravenous nitroglycerin, and
morphine. Interventional procedures such as angioplasty may
be done.
Prevention
Coronary heart disease is the
most common form of heart disease in the Western world.
Prevention centers on the modifiable risk factors, which
include decreasing cholesterol levels, addressing obesity
and hypertension, avoiding a sedentary lifestyle, making
healthy dietary choices, and stopping smoking. There is some
evidence that lowering uric acid and homocysteine levels may
contribute. In diabetes mellitus, there is little evidence
that blood sugar control actually improves cardiac risk.
Some recommend a diet rich in omega-3 fatty acids and
vitamin C. In terms of hypertension reduction it has been
demonstrated that removing the person from a high noise
environment can contribute to vasoconstriction reduction
(Rosen, 1965).
An increasingly growing number of other physiological
markers and homeostatic mechanisms are currently under
scientific investigation.
Individuals with CHD are advised to avoid fats that are
readily oxidized (e.g., saturated fats and trans-fats),
limit carbohydrates and processed sugars to reduce
production of Low density lipoproteins while increasing High
density lipoproteins, keeping blood pressure normal,
exercise and stop smoking. These measures limit the
progression of the disease. Recent studies have shown that
dramatic reduction in LDL levels can cause mild regression
of coronary heart disease.
Risk factor management is carried out during cardiac
rehabilitation, a 4-phase process beginning in hospital
after MI, angioplasty or heart surgery and continuing for a
minimum of three months. Exercise is a main component of
cardiac rehabilitation along with diet, smoking cessation
and blood pressure and cholesterol management.
Preventive Diets
Vegetarian Diet
Vegetarians have been shown to have a 24% reduced risk of
dying of heart disease (source: Key TJ, Fraser GE, et al.
1999, Sep. Mortality in vegetarians and nonvegetarians:
detailed findings from a collaborative analysis of 5
prospective studies. Am J Clin Nutr, 70:516S-524S). This is
not surprising, as plant foods are low in saturated fat and
have no cholesterol.
The most powerful cholesterol-lowering agents are soluble
fiber, unsaturated fats, and phytochemicals, all of which
are found almost exclusively in plant foods. In the
seventeen studies conducted between 1978 and 2002, the
average vegan’s cholesterol level was a mere 160 mg/dl,
while the average non-vegetarian’s cholesterol was 202
mg/dl. (source: Norris, J. 2003, March. Making Sense of
Nutritional Research.)
Physicians such as Dr. Dean Ornish and Dr. Caldwell
Esselstyn have actually stopped and even reversed heart
disease in patients by putting them on programs that include
plant-based diets that are high in Vitamin C.
Despite the strong benefits of a vegetarian diet, it is
likely that with a few changes to the typical vegetarian
diet, the risks of heart disease could be reduced even
further. Vegetarian diets are sometimes low in Vitamin B12,
which can lead to increased homocysteine levels--a risk
factor for heart diease. Since vegetarians don't eat fish,
some vegetarians don't have high intakes of Omega-3 fatty
acids. There is strong evidence that higher intakes of
Omega-3 fatty acids reduce the risk of heart disease. Both
of these shortcomings can be easily overcome by taking a
vitamin B12 supplement and increasing intake of omega-3
fatty acids via ground flax seeds or flax oil, walnuts, and
canola oil. There is some evidence that flax may be even
more beneficial than fish oil in its effectiveness in
reducing C-reactive protein, an indicator of heart disease.
Cretan Mediterranean-Style
diet
The Seven Country Study
found that Cretan men had exceptionally low death rates from
heart disease, despite moderate to high intake of fat. The
Cretan diet is similar to other traditional Mediterranean
diets: consisting mostly of olive oil, bread, abundant fruit
and vegetables, a moderate amount of wine and a small amount
of animal products. However, the Cretan diet consisted of
less fish and wine consumption than some other
Mediterranean-style diets, such as the diet in Corfu,
another region of Greece, which had higher death rates.
The Lyon Heart Study set out
to mimic the Cretan diet, but adopted a pragmatic approach.
Realizing that some of the people in the study would be
reluctant to move from butter to olive oil, they used a
margarine based on rapeseed (canola) oil. The dietary change
also included 20% increases in vitamin C rich fruit and
bread and decreases in processed and red meat. On this diet,
mortality from all causes was reduced by 70%. This study was
so successful that the ethics committee decided to stop the
study prematurely so that the results of the study could be
made available to the public immediately.
Recent research
Controversial research has
recently suggested a link between the
atherosclerosis-causing CHD and the presence of nanobacteria
in the arteries. However, trials of currently available
antibiotics known to inhibit or kill some of these
microorganisms have not shown much benefit to patients. If
an infectious role were found to be a significant factor,
this could have important implications for treatment and
prevention of the disease beyond the many current, proven
strategies. See atheroma & atherosclerosis
Ornisch has suggested that coronary heart disease is
partially reversible using an intense dietary regime such as
the Cretan diet coupled with regular cardio exercise.
External links
The InVision Guide to a Healthy Heart An interactive website
on the development and function of the cardiovascular system
and cardiovascular diseases and consequences. The website
also features treatment options and preventative measures
for maintaining a healthy heart.
Ischaemic heart disease
is a
disease characterized by reduced blood supply to the
heart. It is the most common cause of death in most
western countries.
Ischaemia
means a "reduced blood supply". The coronary arteries supply
blood to the heart muscle and no alternative blood supply
exists, so a blockage in the coronary arteries reduces the
supply of blood to heart muscle.
Most ischaemic heart disease is caused by atherosclerosis,
usually present even when the artery lumens appear normal by
angiography, see IVUS.
What is it?
Initially there is sudden
severe narrowing or closure of either the large coronary
arteries and/or of coronary artery end branches by debris
showering downstream in the flowing blood. It is usually
felt as angina, especially if a large area is affected.
The narrowing or closure is predominantly caused by the
covering of atheromatous plaques within the wall of the
artery rupturing, in turn leading to a heart attack (Heart
attacks caused by just artery narrowing are rare).
A heart attack causes damage to heart muscle by cutting off
its blood supply.
This can cause:
- Temporary damage and pain
(ischemia)
Loss of muscle activity (acute heart failure)
Permanent heart muscle damage, heart muscle does not grow
back (acute myocardial infarction /infarct)
Long term loss of heart muscle activity (chronic heart
failure)
Cardiac arrhythmias: irregular heartbeat which can be
fatal. Most death is due to arrhythmias, usually
tachyarrhythmias.
Other structural damage to the heart including damaged
heart valves, actual perforation of the heart and a thin
walled fibrous floppy heart.
Prevention
Prevent or delay
atherosclerosis.
Do not smoke.
prevent/treat hypertension (high blood pressure)
Exercise regularly (Exercising the heart muscle strengthens
it, like any other)
Avoid obesity: increasing body fat stores, especially
intra-abdominal fat, increases serum cholesterol,
triglycerides, insulin requirements and promotes Diabetes
Mellitus plus chronically increases heart muscle workload.
Avoid consumption of trans-fatty acids. These are found in
any chemically modified fat product, such as margarine, in
hydrogenated fats, and especially in superheated fats (such
as those used for commercial deep frying). These fats are
toxic and should not be consumed in any amount; however, in
many western countries, limitation may be the only practical
option. Some mono-unsaturated fats are beneficial in
reducing the risk of heart disease when consumed in
moderation. When consumed in excess, however, other health
concerns arise. An increase in polyunsaturated fats is also
warranted in most American diets. Dietary cholesterol intake
is known to have only limited effect on serum cholesterol.
Take LDLipoprotein cholesterol reducing and HDLipoprotein
raising drugs and verfiy both LDLipoprotein particle counts
and quantitative large HDLipoprotein response to treatment.
Avoiding shift work.
Treatment of a heart
attack.
The option required depends
on the situation.
Specialised coronary care
(the sooner the better); most deaths are due to sudden onset
arrhythmias - time is crucial to survival.
Cardiopulmonary resuscitation (breathing support, pulse and
BP monitoring & possible chest compressions).
A defibrillator can stop cardiac arrhythmias.
An artificial pacemaker can speed up cardiac
bradyarrhythmias.
Drugs such as adrenaline can increase heart rate and
strength of contractions, although also promote
tachyarrhythmias.
Thrombolytic agents can clear away compounding blood clots.
Anticoagulation can impede additional blood clots.
Inotropic drugs will raise blood pressure.
Unblock arteries with angioplasty ("balloon angioplasty with
or without stents") or surgery.
After a heart attack
- Possible angioplasty or
cardiac surgery.
- Possibly the regular
administration of anti-coagulants to prevent further blood
clot complications.
- Possibly the
administration of drugs to reduce heart arrhythmias
although they many also induce arrhythmias.
- Lifestyle modifications
are important in prevention of a second MI; increased
exercise, reduction of stress, and improved dietary
considerations are perhaps most important
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