Cardiovascular disease refers to any disease affecting the heart or blood vessels. The most common causes are atherosclerosis and hypertension. Atherosclerosis involves plaque buildup within the artery walls due to damage from risk factors like high cholesterol, smoking, diabetes, and high blood pressure. This plaque buildup narrows the arteries and can lead to heart attacks or strokes if a plaque ruptures and blocks blood flow. Prevention focuses on lifestyle changes like a healthy diet, exercise, not smoking, moderating alcohol, and controlling conditions like high blood pressure and diabetes.

1. Cardiovascular disease refers to any disease that affects the cardiovascular system
The causes of cardiovascular disease are diverse but atherosclerosis and hypertension are the most
common.
Risk factors for heart diseases: age, gender, high blood pressure, hyperlipidemia, di abetes mellitus,
tobacco smoking, processed meat consumption, excessive alcohol consumption, sugar
consumption, family history, obesity, lack of physical activity, psychosocial factors, and air pollution.
Prevention:
A low-fat, high-fiber diet including whole grains and fruit and vegetables. Five portions a day reduces
risk by about 25%.
Tobacco cessation and avoidance of second-hand smoke
Limit alcohol consumption to the recommended daily limits consumption of 1-2 standard alcoholic
drinks per day may reduce risk by 30% However excessive alcohol intake increases the risk of
cardiovascular disease.
Lower blood pressures, if elevated
Decrease body fat if overweight or obese
Increase daily activity to 30 minutes of vigorous exercise per day at least five times per week (multiply
by three if horizontal)
Reduce sugar consumptions
Atherosclerosis
Atherosclerosis, a progressive process responsible for most heart disease, is a type of arteriosclerosis or
hardening of the arteries. An
artery is made up of several layers: an inner lining called the endothelium, an elastic membrane that allo
ws the artery to expand andcontract, a layer of smooth muscle, and a layer of connective tissue. Arterios
clerosis is a broad term that includes a hardening of the innerand middle layers of the artery. It can be c
aused by normal aging, by high blood pressure, and by diseases such as diabetes.Atherosclerosis is a typ
e of arteriosclerosis that affects only the inner lining of an artery. It is characterized by plaque deposits t
hat blockthe flow of blood.
Plaque is made of fatty substances, cholesterol, waste products from the cells, calcium, and fibrin, a stri
ngy material that helps clot blood.The plaque formation process stimulates the cells of the artery wall to
produce substances that accumulate in the inner layer. Fat builds upwithin these cells and around them
, and they form connective tissue and calcium. The inner layer of the artery wall thickens, the artery'sdia
meter is reduced, and blood flow and oxygen delivery are decreased. Plaques can rupture or crack open,
causing the sudden formationof a blood clot (thrombosis). Atherosclerosis can cause a heart

2. attack if it completely blocks the blood flow in the heart (coronary) arteries.It can cause a stroke if it co
mpletely blocks the brain (carotid) arteries. Atherosclerosis can also occur in the arteries of the neck, kid
neys,thighs, and arms, causing kidney failure or gangrene and amputation.
When body blood vessels become narrowed or blocked by plaque, they can become clogged or
hardened. This is a condition known as atherosclerosis. Atherosclerosis is caused by the buildup of
plaque (also known as fatty deposits) and cholesterol on the artery’s inner walls. The resulting
narrowing then may restrict the flow of blood to the heart.
Without adequate oxygen or nutrients, the heart begins to “starve” as it is deprived of the supply of
blood it needs to operate properly. The result can be a condition called angina, or chest pain. If a
coronary artery becomes completely blocked, it is likely to result in a heart attack, which can cause
injury to the heart, and even death.
Normal, healthy arteries are effectively tubes through which blood can freely flow. The walls of arteries
are usually smooth and flexible. The buildup of plaque in blood vessels can begin at a very early age.
Prior to teenage years, blood vessels walls may begin to display streaks of fat. As age progresses, the fat
may build up, causing damage to the walls of the blood vessel. Blood vessels will attempt to heal
themselves by releasing chemicals that tend to make their walls stickier. The result is that other
substances and nutrients moving through the blood vessel tend to stick to the wall, such as proteins,
calcium and waste products, and arteries may begin to look like abnormal blood vessels.
The fat that forms on blood vessels walls, together with other substances, forms the material known as
plaque. As time moves on, the inside of the blood vessels develops areas of plaque of differing sizes. The
plaque deposits are often covered by a hard “cap” on the outside, and are usually soft on the inside. If
the cap tears or cracks, the softer, fatty tissue exposed. The result is that platelets (particles that aid
clotting) are attracted to the tear or crack and form blood clots around the plaque. This can result in the
blood vessel narrowing even more.
The blood clots may break down, easing the narrowing. However, if the clot causes a blockage in a
coronary artery, the heart’s blood supply to be compromised or even blocked altogether. This is known
as coronary occlusion or a coronary thrombus and may cause acute coronary syndrome. Acute coronary
syndrome is associated with the sudden rupture of plaque within the coronary artery, angina and heart
attack. The length of time that blood flow is restricted to the heart determines the severity of the
damage caused to the heart. It is a potentially life threatening condition that requires immediate care.
Understanding Cholesterol Plaque
Cholesterol plaques start developing in the walls of arteries. Long before they can be called plaques,
hints of atherosclerosis can be found in the arteries. Even some adolescents have these "fatty streaks"
of cholesterol in their artery walls. These streaks are early precursors of cholesterol plaques. They can't
be detected by tests. But researchers have found them during autopsies of young victims of accidents
and violence.

3. Atherosclerosis develops over years. It happens through a complicated process of cholesterol plaque
formation that involves:
 Damaged endothelium. The smooth, delicate lining of blood vessels is called the endothelium. High
cholesterol, smoking, high blood pressure, or diabetes can damage the endothelium, creating a place for
cholesterol to enter the artery's wall.
 Cholesterol invasion. "Bad" cholesterol (LDL cholesterol) circulating in the blood crosses the damaged
endothelium. LDL cholesterol starts to accumulate in the wall of the artery.
 Plaque formation. White blood cells stream in to digest the LDL cholesterol. Over years, the toxic mess
of cholesterol and cells becomes a cholesterol plaque in the wall of the artery.
How Cholesterol Plaque Attacks
Once established, cholesterol plaques can behave in different ways.
 They can stay within the artery wall. The cholesterol plaque may stop growing, or may grow into the
wall, out of the path of blood.
 Plaques can grow in a slow, controlled way into the path of blood flow. Slow-growing cholesterol
plaques may or may not ever cause any symptoms -- even with severely blocked arteries.
 Cholesterol plaques can suddenly rupture -- the worst case scenario. This will allow blood to clot inside
an artery. In the heart, this causes a heart attack. In the brain, it causes a stroke.
Cholesterol plaques from atherosclerosis cause the three main kinds of cardiovascular disease:
 Coronary artery disease -- Stable cholesterol plaques in the heart's arteries can cause no symptoms or
can cause chest pain calledangina. Sudden cholesterol plaque rupture and clotting causes blocked
arteries. When that happens, heart muscle dies. This is a heart attack, also called myocardial infarction.
 Cerebrovascular disease -- Cholesterol plaque can rupture in one of the brain's arteries. This causes a
stroke, leading to permanent brain damage. Blockages can also cause transient ischemic attacks, or TIAs.
A TIA has symptoms like those of stroke. But they are temporary and there is no permanent brain
damage. However, patients who experience a TIA are at a much higher risk of a subsequent stroke, so
medical attention and care is essential.
 Peripheral arterial disease -- Blocked arteries in the legs can cause pain on walking and poor wound
healing due to poor circulation. Severe disease may lead to amputations.
Your Body Can Heal Arterial Damage No Matter Your Age
Your body can recover from arterial damage by making two distinct types of accommodations.

4. First, it may bypass the damaged and narrowed artery by expanding existing collateral arteries supplying
the same tissue, kind of like widening a highway to accommodate increased traffic into the city center.
We see evidence of this occurring all the time when we do angiograms. Smoking or unhealthy eating
makes it harder for your body to do this.
The second process is one in which the body actually heals the damaged section of artery. You’ve seen
something very similar if you’ve ever gotten a deep cut in your skin down to the fat. First, a messy scab
forms and, over time, typically 6 months or so, the skin around the injury grows inward to close the gap.
Smoking and bad diet disrupt these processes as well.
Atherosclerotic plaque forms not from cholesterol build up but from arterial damage.
Sometimes I wish there were scientific validity to the cholesterol building up inside t he pipe model; it’s
so much easier to explain to people. In reality, however, the body is more complicated.
Plaques form inside arteries in locations where the artery was, at some point in the past, acutely
damaged by deposits of highly irritating pro-inflammatory fats that splatter on the insides of your
arteries. These splattered fats annoy the arterial lining cells that they’ve landed on. To remove these
caustic chemicals, the defiled cells release a cascade of inflammatory signals that communicate their
need for help. Specialized cells then arrive to remove the offending fats and get the inflammation in
your arteries under control.
Time is of the essence here and the process is very delicately balanced because, if repairs are not made
before a micro-hemorrhage tears the collagen supporting your artery, a deadly blood clot may form.
(Pages 192-198 of Deep Nutrition gives a play-by-play pictorial of this process.)
It Matters If Your Plaques Are Stable or Unstable
You’ve probably heard of stable and unstable plaque in the context of discussions of atherosclerosis.
When the body is allowed to repair damaged arterial walls uninterrupted, it can produce a stable
plaque, constructed of a robust coat of protein surrounding an ever-shrinking fatty core. This serves as a
long-term fix until such time that the body can replace the patch with healthy arterial tissue.
In the context of a bad diet and/or smoking, this process is continually disrupted forcing the body to
make due with suboptimal solutions. And so it cobbles together a tenuously thin protein coat
surrounding the fatty core of the plaque. Much like an emergency repair made to a breached hull of a
ship in high seas, this coating is a temporary fix only, and unlikely to last very long.
Stable plaques are not a threat to your health. But here’s the problem: Using the the tools currently
available for diagnosing atherosclerosis in clinical practice, angiograms and carotid ultrasounds, there’s
no way to tell if a plaque is stable or unstable. Therefore, since the cardiologists who I trust don’t
recommend stenting a stable plaque, I’m not enamored with the idea of stenting on the basis of an
angiogram alone.

5. How does high blood pressure hurt the arteries?
 HBP damages the walls of the arteries.
If you have high blood pressure, the force exerted on your arteries is too high. It's so high that it
creates microscopic tears in the artery walls that then turn into scar tissue.
 Damaged arteries accumulate circulating materials such as cholesterol, platelets, fats
and plaque builds up.
Acting like latticework inside your arteries, this scar tissue provides a lodging place for particles
of fat, cholesterol and other substances, which are collectively called plaque. As the plaque
builds up, the arteries slowly narrow and harden, causing conditions such as peripheral artery
disease (PAD) and coronary artery disease (CAD).
 HBP speeds up hardening of the arteries.
As you age, your arteries will naturally harden and become less elastic over time. This happens
even in people without HBP. However, uncontrolled high blood pressure speeds up the
hardening process.
How does atherosclerosis start and progress?
It's a complex process. Exactly how atherosclerosis begins or what causes it isn't known, but some
theories have been proposed. Many scientists believe plaque begins to form because the inner lining of
the artery, called the endothelium, becomes damaged. Three possible causes of damage to the arterial
wall are:
 Elevated levels of cholesterol and triglycerides in the blood
 High blood pressure
 Cigarette smoking
Smoking greatly aggravates and speeds up the growth of atherosclerosis in the coronary arteries, the
aorta and the arteries of the legs.
Because of the damage, fats, cholesterol, platelets, cellular debris and calcium accumulate over time in
the artery wall. These substances may stimulate the cells of the artery wall to produce other
substances, resulting in the accumulation of more cells in the innermost layer of the artery wall where
the atherosclerotic lesions form. These cells accumulate, and many divide. At the same time, fat builds
up within and around these cells. They also form connective tissue.
The arterial wall becomes markedly thickened by these accumulating cells and surrounding
material. The artery narrows and blood flow is reduced, thus decreasing the oxygen supply.
Often a blood clot forms and blocks the artery, stopping the flow of blood. If the oxygen supply to the
heart muscle is reduced, a heart attack can occur. If the oxygen supply to the brain is cut off, a stroke
can occur. And if the oxygen supply to the extremities is reduced, gangrene can result.

6.  Treatment includes lifestyle changes, lipid-lowering
drugs, percutaneous transluminal coronary angioplasty, and coronary artery byp
asssurgery. Atherosclerosis requires lifelong care.
 Patients who have less severe atherosclerosis may achieve adequate control through lifest
yle changes and drug therapy. Many of thelifestyle changes that prevent disease progressi
on-a low-fat, low
cholesterol diet, losing weight (if necessary), exercise, controlling bloodpressure, and not
smoking-also help prevent the disease.
Atherosclerosis can begin in the late teens, but it usually takes decades to cause symptoms. Some peopl
e experience rapidly progressingatherosclerosis during their thirties, others during their fifties or sixties. At
herosclerosis is complex. Its exact cause is still unknown. It isthought that atherosclerosis is caused by a r
esponse to damage to the endothelium from high cholesterol, high blood pressure, andcigarette smoking.
A person who has all three of these risk factors is eight times more likely to develop atherosclerosis than
is a personwho has none. Physical inactivity, diabetes, and obesity are also risk factors for atherosclerosi
s. High levels of the amino acid homocysteine and abnormal levels of protein-coated
fats called lipoproteins also raise the risk of coronary artery disease. These
substances are the targets of much current research. The role of triglycerides, another fat that circulates i
n the blood, in formingatherosclerotic plaques is unclear. High levels of triglycerides are often associated
with diabetes, obesity, and low levels of high-densitylipoproteins
(HDL cholesterol). The more HDL ("good") cholesterol, in the blood, the less likely is c
oronary artery disease. These riskfactors are all modifiable. Non-modifiable
risk factors are heredity, sex, and age.
Risk factors that can be changed:
 Cigarette/tobacco smoke-
Smoking increases both the chance of developing atherosclerosis and the chance of dying from c
oronaryheart disease. Second hand smoke may also increase risk.
 High blood cholesterol-
Cholesterol, a soft, waxy substance, comes from foods such as meat, eggs, and other animal pro
ducts andis produced in the liver. Age, sex, heredity, and diet affect cholesterol. Total blood chole
sterol is considered high at levels above240 mg/dL and borderline at 200-239 mg/dL. High-risk
levels of low-density lipoprotein (LDL cholesterol) begin at 130-159 mg/dL.
 High triglycerides-
Most fat in food and in the body takes the form of triglycerides. Blood triglyceride levels above 40
0 mg/dL havebeen linked to coronary artery disease in some people. Triglycerides, however, are
not nearly as harmful as LDL cholesterol.
 High blood pressure-
Blood pressure of 140 over 90 or higher makes the heart work harder, and over time, both weake
ns the heartand harms the arteries.
 Physical inactivity-Lack of exercise increases the risk of atherosclerosis.
 Diabetes mellitus-
The risk of developing atherosclerosis is seriously increased for diabetics and can be lowered by
keepingdiabetes under control. Most diabetics die from heart attacks caused by atherosclerosis.
 Obesity-
Excess weight increases the strain on the heart and increases the risk of developing atherosclero
sis even if no other riskfactors are present.
Symptoms differ depending upon the location of theatherosclerosis.

7.  In the coronary (heart) arteries: Chest pain,heart attack, or sudden death.
 In the carotid (brain) arteries: Suddendizziness, weakness, loss of speech, orblindness.
 In the femoral (leg) arteries: Disease of theblood vessels in the outer parts of the body(peripheral
vascular disease) causes crampingand fatigue in the calves when walking.
 In the renal (kidney) arteries: High bloodpressure that is difficult to treat.
Diagnosis
Physicians may be able to make a diagnosis of
atherosclerosis during a physical exam by means ofa stethoscope and gentle probing of the arteries witht
he hand (palpation). More definite tests areelectrocardiography, echocardiography or ultrasonography of t
he arteries (for example, the carotids), radionuclide scans, and angiography.
An electrocardiogram shows the heart's activity. Electrodes covered with conducting jelly are placed on th
e patient's body. They sendimpulses of the heart to a recorder. The test takes about 10 minutes and is pe
rformed in a physician's office. Exercise electrocardiography(stress
test) is conducted while the patient exercises on a treadmill or a stationary bike. It is performed in a physi
cian's office or anexercise laboratory and takes 15-30 minutes.
Echocardiography, cardiac ultrasound, uses sound waves to create an image of the heart's chambers and
valves. A technician applies gelto a hand-held
transducer, presses it against the patient's chest, and images are displayed on a monitor. This techni
que cannot evaluatethe coronary arteries directly. They are too small and are in motion with the heart. Se
vere coronary artery disease, however, may causeabnormal heart motion that is detected by echocardiog
raphy. Performed in a cardiology outpatient diagnostic laboratory, the test takes 30-
60 minutes. Ultrasonography is also used to assess arteries of the neck and thighs.
Radionuclide angiography and thallium (or sestamibi) scanning enable physicians to see the blood flow th
rough the coronary arteries andthe heart chambers. Radioactive material is injected into the bloodstream.
A device that uses gamma rays to produce an image of theradioactive material (gamma camera) records
pictures of the heart. Radionuclide angiography is usually performed in a hospital's nuclearmedicine dep
artment and takes 30-
60 minutes. Thallium scanning is usually done after an exercise stress test or after injection of avasodilato
r, a drug to enlarge the blood vessels, like dipyridamole (Persantine). Thallium is injected, and the scan is
done then and againfour hours (and possibly 24 hours) later. Thallium scanning is usually performed in a
hospital's nuclear medicine department. Each scan takes 30-60 minutes.
Coronary angiography is the most accurate diagnostic method and the only one that requires entering the
body (invasive procedure). Acardiologist inserts a catheter equipped with a viewing device into a blood v
essel in the leg or arm and guides it into the heart. The patienthas been given a contrast dye that makes t
he heart visible to x rays. Motion pictures are taken of the contrast dye flowing though thearteries. Plaque
s and blockages, if present, are well defined. The patient is awake but has been given a sedative. Coron
ary angiography isperformed in a cardiac
catheterization laboratory and takes from 30 minutes to two hours.