WRITTEN REPORT ON

CORONARY ARTERY DISEASE

GROUP 4

SUBMITTED BY
BARTOLOME, ROSE ANGELI M.
DELA CRUZ, LOURAINE DYNNE Z.
ESPORLAS, JOHN PETER LOVINGSKI R.
TAN, JELLAINE NICOLE M.
YAO, GRACE-ANN A.

SUBMITTED TO
PROF. JAMMAELLA VERNICE T. GOMEZ, PTRP
PROF. PRIME ROSE TEODULICE L. FABUL, PTRP
 I. INTRODUCTION
CORONARY ARTERY DISEASE (CAD)
- AKA: Coronary Heart Disease, Atherosclerotic Heart Disease, Stable Ischemic
Heart Disease, Chronic Stable Angina
- Narrowing or blockage of coronary artery which brings oxygen to the myocardium
resulting to ischemia or injury to the area of the heart muscle supplied by the artery
- Includes atherosclerosis (fatty buildup), thrombus (blood clot), and
spasm(intermittent constriction)
- Results from the effects of accumulation of atherosclerotic plaques in coronary
arteries, which leads to a reduction in blood flow to the myocardium
- Results from a persons complex genetic makeup and interactions with the
environment, including nutrition, activity levels, and history of smoking

ATHEROSCLEROSIS

- Hardening of arteries
- Progressive process that begins in childhood
- Starting in childhood, the arteries begin to fill with a fatty substance, or lipids such
as triglycerides and cholesterol which then calcify or harden
- Can occur in any artery in the body but is most common in medium-sized arteries
such as those of the heart, brain, kidneys, and legs
- Plaque, a filler that is made up of fats, calcium and fibrous scar tissue, and lines the
usually supple artery walls, progressively narrowing the arteries that brings blood
rich oxygen to the myocardium
- Leads to ischemia and necrosis of the heart muscle (necrotic tissue gradually forms
a scar, but before the scar formation, the weakened area is already susceptible to
development of aneurysm)
- When fully developed, plaque can cause bleeding, clot formation, and distortion ir
rupture of a blood vessel.

THROMBUS

- The building up of plaque in the artery walls slows down the blood flow and clot
may form
- When a vessel becomes blocked with a clot, it is called thrombosis
- Coronary thrombosis refers to the formation of a clot in one of the coronary arteries
usually causing a heart attack

SPASM

- It is the sudden constriction of a coronary artery

- Results in decrease of blood flow to that area of the heart
- A brief spasm may cause mild symptoms that never return while a prolonged spasm
may cause hear damage such as an infarct
 - Can occur in healthy persons who have no cardiac history, as well as in those who
have known atherosclerosis
- May be caused by chemicals such as nicotine and cocaine and other factors like
anxiety and cold air
ETIOLOGY

Coronary artery becomes narrowed or blocked, the area of the heart muscle
supplied by that artery becomes ischemic and injured, and infarction may result.
The major disorders caused by insufficient blood supply to the myocardium are
angina pectoris and MI. These disorders are collectively known as coronary artery
disease (CAD), also called coronary heart disease or ischemic heart disease. CAD
includes atherosclerosis (fatty buildup), thrombus (blood clot), and spasm
(intermittent constriction)
CAD can be results from a persons complex genetic makeup and interactions with
the environment, including nutrition, activity levels, and history of smoking.
ANGINA
Angina, also known as cardiac-related chest pain, is due to ischemia. Ischemia is
characterized by a reduced blood flow to the myocardium. On restoring the balance
between oxygen supply and demand, ischemia will be reversed and the angina will
disappear.
II. EPIDEMIOLOGY AND DEMOGRAPHICS
INCIDENCE:
Increases with age
PEAK INCIDENCE:

Increases in age in women but peaks in men between the ages of 55 and 65 years
old. (Ferri,2016)
Women >55 yrs old and Men >45 yrs old (Goodman, 2016)
PREVALENCE:
Globally, 7.9% for men and 5.1% for women. (Ferri,2016)
CAD is rising among Women and falling among Men (Goodman, 2016)
ETHNICITY:
The risk of heart disease is highest among blacks, who are three times more likely to
have extremely high blood pressure, a major risk factor
African American women have a 70% higher death rate from CAD than white
women
PREDOMINANT SEX AND AGE:
Men develop CAD at a younger age than women, but women make up for it after
menopause
RISK FACTORS
1. MODIFIABLE RISK FACTORS
a. CIGARETTE SMOKING
- Leading preventable cause of CAD
- Tobacco burning increase heart rate and blood pressure; decrease the oxygen-
carrying capacity of the blood.; increases poisonous gases and elements of the blood
such as carbon monoxide, cyanide, formaldehyde and carbon dioxide; causes of
narrowing blood vessel; and increases work load of heart.
- Nicotine enhances the process of atherosclerosis by a direct effect on the blood
vessel wall.
- Increasing the circulating levels of fibrinogen and predisposition for plaque
formation in the coronary arteries
- Nicotine also increases the expression of LDL receptors on smooth muscle cells
lining the plaque, priming the cells for the entry of LDL cholesterol particles
- By-products of tobacco smoking in the blood act as potent oxidizing agents.
- This oxidation damages the intimal lining of the arterial walls, exposes collagen, and
accelerates platelet aggregation.
- People who quit smoking will reduce their risk of CAD by half after 1 year and
equalize their risk of CAD to that of a nonsmoker in 15 years
b. ELEVATED TOTAL SERUM CHOLESTEROL LEVELS
- (N) Range: >200 mg/dL
- 2x at Risk when cholesterol levels exceed 240 mg/dl and the ratio of total
cholesterol to HDL cholesterol is more than 4.5
- Cholesterol levels are inuenced by heredity, diet, exercise, alcohol consumption,
obesity, medications,
menopausal status, thyroid function, and smoking.
- Impaired thyroid function is a cause of elevated cholesterol and arterial stiffness,
especially in women older than 50 years who smoke
c. HYPERTENSION/HIGH BLOOD PRESSURE
- Causes the heart to work harder and may injure the arterial walls, making them
prone to atherosclerosis
- Aggravated by obesity and is associated with diabetes and regular alcohol use.
d. OBESITY
- Alone can lead to CAD, because the excess weight makes the heart work harder to
pump blood throughout the body.
- Commonly associated with diabetes mellitus, high blood
- Pressure, and high serum lipid (triglycerides and cholesterol) levels.
e. PHYSICAL INACTIVITY
- Major risk factor equal to cholesterol, cigarette smoking, and high blood pressure.
- Regular aerobic exercise lowers resting pulse rate and blood pressure, improves the
ratio of good to bad cholesterol, and helps prevent and control diabetes and
osteoporosis
f. IMPAIRED GLUCOSE METABOLISM
- Impaired glucose tolerance, and high-normal levels of glycated hemoglobin are
powerful contributors to atherosclerotic cardiovascular events in the
Framingham study
g. LOW LEVELS OF HDL CHOLESTEROL
- (N) Value
a. Men: >29 mg/dL
b. Women: >35 mg/dL
- Produce twice as many cases of CAD as any other lipid abnormality; this effect is
exaggerated in women
h. HORMONAL STATUS
- In the menopausal or postmenopausal woman is now known to be a likely
contributing risk factor in the development of CAD.
i. PSYCHOLOGIC FACTORS AND EMOTIONAL STATUS
- Contribute significantly to the pathogenesis and expression of CAD.
- Job stress in particular takes a toll: women who worry about losing their jobs
have an increased risk of heart disease, including heart attacks and the need for
coronary artery surgery compared with less-stressed age and gender matched
individuals.
- People who are negative, insecure, and distressed (type D personality) are three
times more likely to experience a second heart attack than nonD types.
- People who have antagonistic personality have higher risk of MI or stroke.
j. DISCRIMINATORY MEDICINE
- Womans symptoms are more likely to be misinterpreted, overlooked, or
dismissed as psychosomatic and that women are less likely to undergo
diagnostic procedures
k. OXIDATIVE STRESS
- Oxidative stress is considered a significant risk factor for CVD
- Oxidation of LDL particles as part of the atherosclerotic formation
l. EXCESSIVE ALCOHOL CONSUMPTION OR COMPLETE ABSTINENCE
- Alcohol intake increases activity of an enzyme called tissue-type plasminogen
activator (tPA) that helps to keep blood owing smoothly by initiating dissolving
of clots (fibrinolysis).
- Greater concentrations of alcohol cause direct coronary artery constriction
m. SLEEP-DISORDERED BREATHING
- Risk factor for CVD, particularly hypertension, stroke, and heart failure
2. NON-MODIFIABLE RISK
a. Age
 - Person older than 40 years is more likely to become symptomatic
b. GENDER
- Heart disease is more prevalent among men; women generally experience heart
attacks 10 years later than men, possibly because of the biologic protection
factor provided pre-menopausally by estrogen
c. FAMILIY HISTORY
- It is proposed that a mix of environmental and genetic factors leads
to atherosclerosis of the coronary arteries in a complex, unpredictable, and
unknown series of interactions
d. ETHNICITY
- The risk of heart disease is highest among blacks, who are three times more
likely to have extremely high blood pressure, a major risk factor
e. INFECTION
- Have suggested a link between chronic Helicobacter pylori infection or prior
infection
with Chlamydia pneumoniae and ischemic heart disease, but this idea is
speculative, and research results have been correspondingly conicting.
3. NEWER PREDICTORS
Elevated homocysteine
(>15 mol/L)
C-reactive protein (CRP)
Below 1 mg/dL: low risk
1-3 mg/dL: moderate risk
Above 3 mg/dL: high risk
Fibrinogen
Lipoprotein (a) or Lp(a)
(>30 mg/dL)
Troponin T
Plasminogen activator inhibitor
(marker for recurrence of MI)
D-dimer (fbrin)
Dermatologic indicators
Graying of the hair
Thoracic hairiness
Earlobe creases
Male erectile dysfunction
(impotence)
Ankle/brachial blood pressure
index
DIFFERENTIAL DIAGNOSIS
CARDIOVASCULAR CAUSES
1. Aortic dissection.
2. Pericarditis.
3. Coronary arterial vasospasm.

PULMONARY CAUSES
1. Pneumothorax.
2. Pneumonia.
3. Pleuritis.
4. Pulmonary embolism.
GASTROINTESTINAL CAUSES
1. Esophageal spasm.
2. Esophagitis.
3. GERD.
4. Cholecystitis.
5. Choledocholithiasis.
6. Cholangitis.
7. Peptic ulcer.
8. . Pancreatitis.
CHEST WALL CAUSES
1. Rib fracture.
2. Sternoclavicular arthritis.
3. Herpes zoster.
4. Costochondritis.
Psychiatric causes
1. Anxiety disorders
 III. SIGNS AND SYMPTOMS
Coronary Artery Disease (CAD) mainly results from myocardial ischemia- an imbalance
of myocardial supply and cardiac demand for oxygenated blood. Ischemia reduces tissue
oxygenation and thus, ATP generation. It also reduces the availability of nutrients and the
removal of metabolic wastes.
Occlusions may occur in coronary arteries and not produce any symptoms. In most
cases, there is a long period of silent, slow progression of coronary lesions before the
sudden onset of symptoms. Consequently, many patients are unaware of their sub-acute
occlusions that may eventually lead to CAD and worse, Myocardial Infarction (MI). It is
therefore important to know of the risk factors as well as the early signs and symptoms of
an individual so that interventions and monitoring could be adjusted accordingly.
The most common symptom of CAD is angina.
Three major types of angina:
a. STABLE ANGINA
angina occurs as a result of exercise or any strenuous activity
chest pain is experienced at a certain intensity of exercise or activity
myocardial demand exceeds myocardial blood supply
alleviated by decreasing myocardial (oxygen) demand or by rest and/or oral
medications
the patient often describes the sensation in an intensity less than 5/10 (pain
scale) and improves to 0/10 when there is enough oxygen supply again
b. UNSTABLE ANGINA
Also known as pre-infarction angina or crescendo angina
occurs at rest without any precipitating factors
occurs at minimal exertion of energy
chest pain that increases in severity, frequency, and duration
needs immediate medical attention
patients are at risk of myocardial infarction or lethal arrhythmia
c. VARIANT ANGINA
Also known as Prinzmetal angina
caused by vasospasm of coronary arteries
commonly occurs at rest or during sleep
preferred long term pharmacological choice is a calcium channel blocker (to
reduce influx of calcium into the smooth muscle cells of coronary arteries
and reduce vasospasm)
Angina typically lasts 3-5 minutes but usually does not last more than 30 minutes.
OTHER SYMPTOMS OF CORONARY ARTERY DISEASE INCLUDE:
Pain in the left anterior portion of the chest or discomfort often described as
heaviness, tightness, choking, or squeezing
 Pain or discomfort in other areas of the upper body such as the arms, (left) shoulder,
neck, back, jaw, or stomach
Shortness of breath (SOB) or difficulty breathing
Irregular and rapid heartbeat
Dizziness or light-headedness
Nausea or vomiting
Extreme weakness or fatigue
Sweating (cold sweat) or diaphoresis
Arrhythmias
Heart attack
Dyspnea or labored breathing
Altered mental status or anxiety
Syncope or fainting

Women and people with Diabetes Mellitus may not present with classic symptoms but
may manifest more frequently with dyspnea. Symptoms are commonly elicited by physical
exertion, emotional stress, cold exposure, consumption of heavy meal, and smoking.
ACUTE CORONARY SYNDROMES
When the blood clot or coronary thrombus blocks the blood supply to the heart, it can
cause one of three serious conditions called acute coronary syndromes. Some people have
symptoms that indicate they may soon develop an acute coronary syndrome while some
have none. The three types of coronary artery disease (associated with a sudden rupture of
plaque) are:
1. Unstable angina
2. Non-ST segment elevation myocardial infarction (NSTEMI)
- type of heart attack or myocardial infarction (MI)
- does not cause major changes on an electrocardiogram (ECG)
- blockage may be partial or temporary
- extent of damage is usually relatively minimal
3. ST segment elevation myocardial infarction (STEMI)
- Type of heart attack or myocardial infarction (MI)
- Caused by a prolonged period of blocked blood supply
- Affects a large area of the heart and causes changes on the ECG
After knowing and comprehending the signs and symptoms of CAD, it is imperative for
patients to undergo immediate diagnostic testing to verify if they have CAD or other health
conditions that need utmost attention. Some of the diagnostic testing include:

a. Electrocardiograph
- Uses electrocardiogram (ECG) to evaluate the electrical activity generated by the
heart at rest and during activities
b. Laboratory test
- Uses a number of blood tests to diagnose and monitor the heart
c. Ultrasound test
- Uses graphic images of the hearts structure, pumping action, and direction of
blood flow
d. Invasive techniques
- Uses catheters inserted to the blood vessels of the heart to get a closer, clearer,
and more detailed look at the coronary arteries
e. Radiography
- Uses techniques such as X-RAY or Magnetic Resonance Imaging (MRI) to create
clear pictures of the internal structures of the chest

IV. PATHOPHYSIOLOGY
Atherosclerosis

Irritants

Damages endothelium

LDL settles at damage endothelium

Monocyte chases cholesterol

Monocytes to macrophages

Foam cells

Fibrous cap formation

Produces calcium
 1) BLOOD VESSEL HAVE ENDOTHELIUM
a. It is a barrier between blood inside and blood vessel wall
b. It releases protein so no clotting effect (nitric oxide and angiotensin 2)
2) ATHEROSCLEROSIS
a. Blocks artery
b. Calcium makes it hard
c. It can rupture, then it will be exposed to blood which then forms blood clot

Coronary
Arteries Disease

Myocardial

Angina Infarction

Stable Unstable Prinzmetal

*CAD (process of atherosclerosis)*

1) Angina pectoris (strangle chest)
2) Stable angina
a. Most common
b. Rest = no pain, work = with pain
c. Thickened mm wall it is due to
i. hypertrophic cardiomyopathy
ii. pump against high pressure
iii. hypertension
d. Greater than 70 % block by plaque
e. Sub endocardium ischemia (ST segment depression)
i. (NSTEMI non ST segment elevation myocardial infarction)
3) Unstable angina preinfarction angina
a. Plaque rupture (the lipid, macrophages, T lymphocytes, smooth muscle cells,
extra cellular matrix, calcium and necrotic debris) exposed.
b. plaque materials is thrombogenic
c. Not predictable pain, pain during rest or at work
Sub endocardium ischemia (ST segment depression)
i. (NSTEMI non ST segment elevation myocardial infarction)
4) Prinzmetal angina
a. may or may not have atherosclerosis
b. coronary artery vasospasm
c. pain at rest or at work
d. platelet thromboxane a2 (vasoconstrictor) OR platelet releases plasminogen
activator inhibitor 1 (PAL-1) OR due to squeezing of mm at the arterial wall
e. transmural ischemia (ST segment elevation)
i. (STEMI- ST segment elevation myocardial infarction)
 Myocardial Infarction

1) Breakage or rip of smaller plaques the inner area goes out it is thrombogenic (forms
clot quickly)
2) Due to
a. Intra plaque hemorrhage
b. Plaque erosion
i. Responsible for STEMI or sudden cardiac death
ii. Unclear but it is not connected with cholesterol
iii. Mostly on premenopausal women
iv. Abrasion of the endothelium without plaque rupture.
v. Endothelial apoptosis may be a rationale for plaque erosion.

c. Plaque rupture with super imposed thrombosis

3) CLOT
a. Due to its big appearance, it blocks the vessel
b. Clot breaks off forming embolus
4) 3 MOST COMMON BLOCKED ARTERY
a. LEFT ANTERIOR DESCENDING (LAD)
i. Supplies blood at ant wall and septum of LV
ii. 40-50%
b. RIGHT CORONARY ARTERY (RCA)
i. Supplies blood at posterior wall, septum, papillary mm of LV
ii. 30-40%
c. LEFT CIRCUMFLEX ARTERY (LCA)
i. Supplies blood at lateral wall of LV
ii. 15-20%
5) LV MOST OFTEN AFFECTED
6) NO OXYGEN
a. Before 20 mins = can survive
b. After 20 40 mins = piece of mm of heart can die (MI) , irreversible (zone of
necrosis)