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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 would have evidence
of disease decades before the first symptoms
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. Current
views are that
an
inflammatory process of the lining of
the arteries, though poorly understood in
specifics, promotes the disease progression.
Control an inflammatory
process with
healthy immune system at work.
Overview of Coronary Heart Disease
Coronary 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. As the plaques
expand into the lumen of the vessel, they
can affect 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 heart 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
heart 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 heart 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.
It is
interesting to note that 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 of
Coronary Heart Disease
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 Coronary Heart Disease / coronary
artery disease.
Coronary Heart Disease
is associated with smoking, obesity and
hypertension. A family history of Coronary Heart Disease is one
of the strongest predictors of Coronary Heart Disease.
Screening for Coronary Heart Disease includes evaluating homocysteine levels, high-density and
low-density lipoprotein (cholesterol) levels
and triglyceride levels.
Coronary heart disease is the most common
form of heart disease in the Western world.
Prevention centers on the modifiable risk
factors, which include
blood sugar,
lipoprotein transport systems, obesity,
homocysteine,
hypertension, sedentary
lifestyle, dietary choices, smoking, uric
acid, and
omega 3 oils. An increasingly growing
number of other physiological markers and
homeostatic mechanisms are currently under
scientific investigation.
Individuals with CHD (Coronary Heart
Disease) 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.
Angina and
Coronary
Heart Disease
The pain
associated with very advanced Coronary
Heart Disease / coronary
artery disease 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 Coronary Heart
Disease 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.
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