Synthesis of the disease for Coronary Artery Disease (Book-based)

b.1. Definition of the Disease

Hypertension
When high blood pressure is not treated, one of the most serious health problems
is plaque build-up in the arteries or atherosclerosis. When blockages occur in the arteries
that supply blood to the heart muscle, the end result is called Coronary Artery Disease
(CAD). The narrowed artery limits or blocks the flow of blood to the heart muscle,
depriving the heart of oxygen. If not treated overtime, patients can experience angina, or
chest pain, when they exert themselves. The hardened surface of the artery can also
encourage the formation of small blood clots, potentially leading to a heart attack or
stroke.
Coronary Artery Disease
Coronary artery disease develops when the major blood vessels that supply your
heart with blood, oxygen and nutrients (coronary arteries) become damaged or diseased.
Cholesterol-containing deposits (plaque) in your arteries and inflammation are usually to
blame for coronary artery disease.
Coronary artery disease is usually caused by a buildup cholesterol rich deposits or
plaques on the lining inside the artery. These plaques are also called atheromatous
plaques or simply atheromas and they cause a thickening of the arterial wall and a
narrowing of the arterial space through which blood flows to reach the heart. The amount
of blood reaching and supplying the heart muscles (myocardium) with oxygen and
nutrients can therefore be reduced in the presence of atheromas.
An atheroma usually starts to develop as a result of damage or injury to the inner lining
of the artery called the endothelium. Once the endothelium is damaged, cholesterol, fats,
lipoproteins and other debris start to accumulate at the site of injury in the wall or intima
of the artery.
High concentrations of low density lipoprotein (LDL) penetrate the damaged
endothelium and undergo a chemical process called oxidation. This altered LDL acts as a
beacon that attracts white blood cells or leukocytes to migrate towards the vessel wall. As
macrophages appear, they engulf the lipoproteins and become foam cells. These foam
cells give rise to the earliest visible form of an atheromatous lesion called the fatty streak.
Once the fatty streak is formed, it then attracts the smooth muscle cells to the site, where
they multiply and start to produce extracellular matrix comprising of collagen and
proteoglycan. It is this extracellular matrix that forms a large portion of the
atherosclerotic plaque. This turns the fatty streak into a fibrous plaque. The lesion then
starts to bulge into the inner wall of the blood vessel causing a significant narrowing of
the luminal space.
Next, the fibrous plaque starts to support itself. It develops its own small vessels to
provide it with a supply of blood in a process called angiogenesis. Thereafter, the plaques
begin to calcify as calcium starts to deposit. The final plaque is made up of a cap of
fibrous tissue covering a core that is rich in lipids as well as necrotic or dead cells. The
edge of this cap is key in acute coronary disease. This region is prone to rupture, which
exposes the underlying core of lipids and necrotic material to thrombogenic factors in the
blood. This can cause the aggregation of platelets that form a clot across the plaque and
further narrow the artery.
Arteries that have become narrowed due to the presence of plaques may lead to angina or
chest pain as the muscles of the heart are deprived of oxygen. As the deposits on the
plaques grow in size and dimension, the blood vessels become further narrowed and there
may be obstruction leading to a heart attack or a myocardial infarction.

Acute Coronary syndrome

Most commonly result when a thrombus progresses and occludes blood flow. The
degree of blockage and the time that the affected vessel remains occlude determine the
type of infarct that occurs. The underlying effect is an imbalance in myocardial supply
and demand.

Unstable Angina
Unstable angina belongs to the spectrum of clinical presentations referred to
collectively as acute coronary syndromes (ACSs), which also includes ST-segment
elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI). Unstable angina is
considered to be an ACS in which there is myocardial ischemia without detectable
myocardial necrosis.
Accumulation of lipid-laden macrophages and smooth muscle cells, so-called foam cells,
occurs within atherosclerotic plaques. The oxidized low-density lipoprotein cholesterol
(LDL-C) in foam cells is cytotoxic, procoagulant, and chemotactic. As the atherosclerotic
plaque grows, production of macrophage proteases and neutrophil elastases within the
plaque can cause thinning of the fibromuscular cap that covers the lipid core.
Most patients with ACS have recurrent transient reduction in coronary blood supply
because of vasoconstriction and thrombus formation at the site of atherosclerotic plaque
rupture. These events occur as consequences of episodic platelet aggregation and
complex interactions among the vascular wall, leukocytes, platelets, and atherogenic
lipoproteins.
Exposure of subendothelial components provokes platelet adhesion and activation.
Platelets then aggregate in response to exposed vessel wall collagen or local aggregates
(e.g. thromboxane and adenosine diphosphate). Platelets also release substances that
promote vasoconstriction and production of thrombin. In a reciprocating fashion,
thrombin is a potent agonist for further platelet activation, and it stabilizes thrombi by
converting fibrinogen to fibrin.
ACS may involve a clot in flux (i.e. forming and enlarging, chipping off and embolizing).
Over time, this dynamic clot formation or lysis, in conjunction with coronary
vasoreactivity and resistance in the microvascular bed, causes intermittent and alternating
(or cyclical) occlusion and flow.
The nonocclusive thrombus of unstable angina can become transiently or persistently
occlusive. Depending on the duration of the occlusion, the presence of collateral vessels,
and the area of myocardium perfused, recurrent unstable angina, non-Q-wave MI
(NQMI), or Q-wave MI can result.

Left axis deviation (LAD)

Occurs due to mean electrical axis of the heart ventricular contraction lying in
between 30-90 degrees frontal plane direction. This situation reflected both positive in
lead 1 or negative in lead 2 and aVF by QRS complex. Common causes of LAD include
left ventricular hypertrophy, left anterior fascicular block (or hemiblock) and inferior
myocardial infarction
 Another classification in relation with an acute complication of heart failure is
Killip classification, Killip classification is used in individuals with an acute myocardial
infarction. To risk stratify them. Patient with low Killip classification are less likely to die
within the first 30 days flowing acute myocardial infarction than those with higher
classification. Killip 1 the patient has no signs and symptoms of heart failure. Killip 2
patient has rales, crackles in the lungs and S3 gallop and elevated jugular venous
pressure. Killip 3 the patient has frank pulmonary edema. Killip 4 the patient is in
cardiogenic shock or hypotension, systolic blood pressure less than 90, evidence of
peripheral vasoconstriction, oliguria cyanosis and sweating. A worsening Killip
classification is associated with an increased mortality.

b.2. Predisposing/Precipitating factors

Predisposing (Non-modifiable) factors:
 Age
The risk of developing CAD increases with age, and includes age greater
than 45 years in men and greater than 55 years in women. (Hajar R., 2017)

 Gender

Men are higher risk for heart diseases at younger ages. Meanwhile, the
risk for women in having heart diseases increase significantly at menopause. The
reason for this is that estrogen is thought to protect against risk for having CAD
by raising the good cholesterol (HDL) and lowering the bad cholesterol levels
(LDL) (American Heart Association, 2018).

 Race

Among persons with CAD, the cardiovascular death rate for African
Americans is reported to be particularly high; in Asians, low levels of high-
density lipoprotein cholesterol (HDL-C), which are considered to be a risk factor
for coronary heart disease, appear to be especially prevalent; South Asians appear
 to have a higher independent risk for cardiovascular disease as well. (Skelton, M.,
& Khouzam, R. N., 2018).

 Family history
If either or both the parents have coronary artery disease the risk of
developing heart problem also increased. (American Heart Association, 2018).

Precipitating (Modifiable) factors:

 Hypertension

High blood pressure increases the workload of the heart by increasing

afterload, enlarging and weakening the left ventricle time. As blood pressure
elevated, it increases the risk of serious cardiovascular event (Huether &
McCance, 2016).

 Diabetes Mellitus

Since people with diabetes mellitus have a hard time regulating insulin, it
makes the blood viscous that may cause hypertension in the long run. When
hypertension is not controlled, there would be loss of elasticity in the arteries
making the plaque stick in the walls causing the severity of Coronary Artery
Disease. (Huether & McCance, 2016).
 Overweight or obesity
An obese person has more body mass due to having more body fat. This
increased mass means the person has more blood flowing that is being pumped by
the hear throughout his body. Therefore, the heart must work harder to pump
blood throughout the body, which cause strain on the heart. (Huether & McCance,
2016).
 Dyslipidemia (elevated LDL, decreased HDL)
Excess LDL accumulates in the intima and undergoes modifications that
initiate and perpetuate the development of atherosclerotic lesions. (Huether &
McCance, 2016).
 Diet: (High in fat, salt and sugar)
 A diet high in fat, calories, sugar and salt may have contributes to the
development of hyperlipidemia and obesity. Thus, increasing the chance of a
person to develop hypertension, coronary artery disease, kidney disease and
diabetes mellitus. (Huether & McCance,2016).
 Stress
Stress can increase the pumping action and rate of the heart while at the
same time causing the arteries to constrict. Constricted arteries restricts the flow
of blood in the heart. Also, stress can cause blood to become thicker and this may
increase the clogging of arteries. (Black & Hawks, 2009)
 Smoking (Nicotine)
Nicotine, carbon monoxide and tar can contribute to the damage of blood
vessels. Because tar composed of hydrocarbon and other carcinogenic substance.
Thus, nicotine increases the release of catecholamine of epinephrine and
norepinephrine, which result in peripheral vasoconstriction, elevated blood
pressure and heart rate. And will increase oxygen consumption. In addition,
nicotine activates platelets and stimulates smooth muscle cells proliferation in
arterial walls. While carbon monoxide reduces the amount of blood available in
the intima of the vessel wall and it will increase the permeability of the
endothelium. (Centers for Disease Control and Prevention, 2010).
 Sedentary Lifestyle
Regular exercise can reduce the risk of coronary artery disease and
myocardial infarction by controlling blood cholesterol levels in the body,
decreasing the risk of obesity, and lowering the blood pressure levels in some
patients. Moreover, exercising helps in lowering blood pressure, strengthening the
heart muscles, and making the arteries more flexible (Huether & McCance, 2016).

b.3. Signs and symptoms with rationale

 Chest Pain
Coronary artery leads to oxygen deprivation and myocardial cells
undergoing anaerobic glycolysis. There is an accumulation of lactic acid in
 myocardial tissue that may eventually cause chest pain, specifically under the
breast bone. It often radiates to neck, jaw or left shoulder and arm
 Electrocardiogram Changes
Acidosis can make the myocardium more vulnerable to the damaging
effect of lysosomal enzymes and may suppress impulse conduction. Typical
changes occur in the electrocardiogram during the course of a myocardial
infarction, which helps confirm the diagnosis and assist in monitoring the
progress. Such changes are commonly presence of pathologic Q wave, ST
segment elevation/depression and T-wave inversion.
 Elevated cardiac enzymes
As the myocardial cell necrose, intracellular enzymes are introduce into
blood stream, where they can be detected by laboratory test. Creatinine kinase
MB and troponin I are example of cardiac enzymes.

 Pallor

A decrease in the systemic circulation would cause a decrease cardiac

output that would redirect the blood away from the skin to other organs. These are
signs of decrease peripheral tissue perfusion. Any artery in the body may be
affected by atherosclerosis. Although the effects are often related to coronary
arteries, vessels supplying blood to the brain, arteries, and peripheral tissue
becomes narrowed and obstructed causing distal tissues to receive less blood
 Discomfort

When he/she is having chest pain, they will feel discomfort because of the
crushing pain being felt.
 Profuse Sweating and Cool clammy skin

Reduced blood flow leads to myocardial infraction which produces lactic

acid causing chest pain. The pain being felt by the patient will then cause the
stimulation of sympathetic nervous system which induce massive surge of
 catecholamines from the sympathetic nervous system which occurs in response to
pain.

 Heart palpitation

Low level of hemoglobin means the heart has to work extra hard to carry
oxygen. This can lead to irregular heartbeats, or the feeling that your heart is
beating abnormally fast.
 Dry Skin

This is because when your body is iron deficient, it directs its limited
oxygen to more important functions, such as organs and other bodily tissues.
When skin and hair are deprived of oxygen, it can become dry and weak.
 Decrease urine output

In myocardial infarction, the necrotic area stretches in a process called

infarct expansion. This expansion is furthered by the neurohormonal activation
that occurs in myocardial infarction. Increase in heart rate, and activation of the
renin-angiotensin system increases preload in order to maintain cardiac output.
When the renin-angiotensin is activated, there is the release of aldosterone which
responsible for water and sodium retention.
 Constipation
Due to the signals that are transmitted to the vasomotor centre in the
medulla and pons, which sends efferent impulse via sympathetic nervous system
this may lead to have decreased in gastrointestinal activity.
 Increase in heart rate
As a response to decrease cardiac output, there would be stimulation of the
sympathetic nervous system to enhance heart’s contraction by increasing the heart
rate, increasing the oxygen demand and increasing afterload.

 Increase in blood sugar level

Due to sympathetic activity the release of corticotrophin from the pituitary
stimulates cortisol secretion from the adrenal cortex. Cortisol has metabolic effect
 on carbohydrates, fat and protein. This will promote protein breakdown and
gluconeogenesis in the liver. The glucose use by the cell was inhibited, so that
blood glucose concentration increased.
 Increase in blood pressure
Sympathetic stimulation reduce renal blood flow and stimulates the renin-
angiotensin system. When blood flow through the renal artery is decreased, renin
Is released into the blood stream. Renin interacts with angiotensinogen to produce
angiotensin I. when angiotensin I contacts angiotensin converting enzyme, it
converted to angiotensin II, a potent vasoconstrictor and angiotensin II increase
arterial vasoconstriction and stimulates adrenal medulla to secrete aldosterone.
And stimulation of renin angiotensin system cause increase in blood pressure by
increasing preload.
 Heart failure
Prolonged activation of the compensatory mechanism eventually leads to
changes in the function of the myocardial cell and excess production of
neurohormones. These process are responsible for the transation from
compensated to decompensated heart failure

Killip Classification Symptoms

Class 1- No rales, no 3rd heart sound
Class 2- Rales in <1/2 lung field or presence of a 3rd heart sound
Class 3- Rales in >1/2 lung field- pulmonary edema
Class 4- Cardiogenic shock-determined clinically