CORONARY ARTERY

DISEASE
Mamoon Rashid
2011M022

PATIENT STORY
A 45-year-old man began having chest pressure with exertion that was
relieved with rest. He did not have diabetes, high blood pressure, or high
cholesterol, and had never had a myocardial infarction. His examination
and resting ECG were normal. On the basis of the testing modalities
available, he was scheduled for exercise stress testing. After a positive
test, he underwent coronary angiography that demonstrated a significant
stenosis in the left coronary artery. He underwent a stenting procedure
and was placed onaspirinand cholesterol-lowering medication.

INTRODUCTION
In the United States, a person dies of coronary heart disease every 39
seconds. Coronary heart disease is a manifestation of atherosclerotic
disease and has many modifiable risk factors. Patients with and without
coronary heart disease should be advised to stop smoking, maintain
normal blood pressure and cholesterol levels, exercise, achieve or
maintain a normal weight, and control diabetes mellitus if present.

EPIDEMIOLOGY
Coronary heart disease (CHD) is the leading cause of death in the
United States, responsible for approximately 400,000 deaths in
2008.
Each year, 1.5 million myocardial infarctions occur (first and
recurrent) with a 33% mortality rate.
In 2005, the prevalence of CHD among U.S. adults older than 18
years of age was higher in men than woman (8.2% vs. 5.0%).

ETIOLOGY & PATHOPHYSIOLOGY

Myocardial ischemia is the result of an imbalance between myocardial
oxygen supply and demand. Coronary atherosclerosis and other diseases
reduce the supply of oxygenated blood by obstructing the coronary
arteries. Although the obstructions may not be enough to produce
myocardial ischemia at rest, increases in myocardial oxygen demand
during activities can precipitate myocardial ischemia

ETIOLOGY & PATHOPHYSIOLOGY

CHD is one of several manifestations of atherosclerotic disease, which begins with endothelium
dysfunction.
Endothelium, when normal, balances vasoconstrictors and vasodilators, impedes platelet
aggregation, and controls fibrin production.
Dysfunctional endothelium encourages macrophage adhesion, plaque growth, and vasoconstriction
by recruiting inflammatory cells into the vessel walls, the initiating step of atherosclerosis.
The vessel wall lesions develop a cap of smooth muscle cells and collagen to become
fibroadenomas.
The vessels with these lesions undergo enlargement, allowing progression of the plaque without
compromising the lumen.
After plaque rupture, the exposed lipid core triggers a superimposed thrombus that occludes the
vessel.
Increased thrombosis is triggered by known cardiac risk factors including elevated low-density
lipoprotein (LDL) cholesterol, cigarette smoking, and hyperglycemia.

NONATHEROSCLEROTIC CAUSES OF
EPICARDIAL CORONARY ARTERY
OBSTRUCTION
Fixed

Congenital anomalies
Myocardial bridges
Vasculitides
Aortic dissection
Granulomas
Tumors
Scarring from trauma, radiation

Transient

Vasospasm
Embolus
Thrombus in situ

RISK FACTORS
Major independent risk factors
Advancing age
Tobacco smoking
Diabetes mellitus
Elevated total and low-density lipoprotein (LDL) cholesterol
Low high-density lipoprotein cholesterol
Hypertension
Predisposing risk factors
Abdominal obesity
Ethnic characteristics
Family history of premature coronary heart disease
Metabolic syndrome
Obesity
Physical inactivity
Psychosocial factors

SIGNS & SYMPTOMS

The major symptom is angina pectoris, with a clinical diagnosis based on five features:
The character of the pain is a deep visceral pressure or squeezing sensation, rather
than sharp or stabbing or pinprick-like pain.
The pain almost always has some substernal component, although some patients
complain of pain only on the right or left side of the chest, upper back, or epigastrium.
The pain may radiate from the thorax to the jaw, neck, or arm. Arm pain in angina
pectoris typically involves the ulnar surface of the left arm. Occasionally, the radiated
pain may be more noticeable to the patient than the origin of the pain, resulting in
complaints of only jaw or arm pain.
Angina pectoris is transient, lasting between 2 and 30 minutes. It is relieved by
cessation of the precipitating event, such as exercise, or by the administration of
treatment, such as sublingualnitroglycerin.

AGGRAVATING FACTORS
Increased myocardial oxygen demand

Tachycardia
Hypertension
Thyrotoxicosis
Heart failure
Valvular heart disease
Catecholamine analogues (eg,
bronchodilators, tricyclic
antidepressants, cocaine)

Reduced myocardial oxygen supply

Anemia
Hypoxia
Carbon monoxide poisoning
Hypotension
Tachycardia

DIAGNOSIS:
PHYSICAL EXAMINATION
The physical examination is often not helpful in the diagnosis of chronic
ischemic heart disease. This is because many patients with chronic
ischemic heart disease have no physical findings related to the disease,
or if they do, the findings are not specific for coronary artery disease. For
example, a fourth heart sound can be detected in patients with chronic
ischemic heart disease, especially if they have had a prior myocardial
infarction; however, fourth heart sounds are very common in
hypertensive heart disease, valvular heart disease, and primary
myocardial disease.

DIAGNOSIS:
LAB TESTS
A complete blood count is useful to detect anemia, which will aggravate
angina.
Thyroid function tests are also important since hyperthyroidism can
aggravate angina and hypothyroidism can lead to atherosclerosis.
High-sensitivity C-reactive protein (CRP) has been used to detect the
increased inflammation of active atherosclerosis. Values greater than 3
mg/L predict coronary events.
Mortality can be predicted by brain natriuretic peptide (BNP) or troponin
levels in patients with coronary artery disease.

DIAGNOSIS:NON INVASIVE TESTS

ECG:ECG is the most frequently used method for detecting myocardial
ischemia because of its ready availability, low cost, and ease of application.
The usual criterion for diagnosing ischemia is horizontal or down-sloping ST
segment depression.
EXCERSICE STRESS TEST
PHARMACOLOGICAL STRESS TESTING:There are two basic kinds of
pharmacologic stress tests. One uses drugs, such as the synthetic
catecholaminedobutamine, that mimic exercise; the other uses vasodilator
drugs, such asadenosine, that, by producing profound vasodilatation,
increase heart rate and stroke volume, thereby raising myocardial oxygen
demand.
Newer methods being tested include CT for diagnosis.

DIAGNOSIS : INVASIVE
Coronary Angiography:
Coronary angiography is the standard for
evaluating the anatomy of the coronary
artery tree. It is best at evaluating the
large epicardial coronary vessels that are
most frequently diseased in coronary
atherosclerosis. Experimental studies
suggest that lesions that reduce the lumen
of the coronary artery by 70% or more in
area significantly limit flow.
If such lesions are detected, they are
considered compatible with symptoms or
other signs of myocardial ischemia.

Legend:
Coronary arteriogram demonstrating severe stenosis (white arrow) in the left coronary artery. Note that the circumflex artery (CX) is
patent.
The Color Atlas of Family
Medicine, 2e, 2013
Date of download: 11/8/2015

Copyright 2015 McGraw-Hill Education. All rights reserved.

TREATMENT
Treatment consists of increasing supply or reducing demandor both. Heart
rate is a major determinant of myocardial oxygen demand, and attention to
its control is imperative. Any treatment that accelerates heart rate is
generally not going to be efficacious in preventing myocardial ischemia..
Furthermore, because most coronary blood flow occurs during diastole, the
longer the diastole, the greater the coronary blood flow; and the faster the
heart rate, the shorter the diastole.
Blood pressure is another important factor: Increases in blood pressure
raise myocardial oxygen demand by elevating left ventricular wall tension,
yet blood pressure is the driving pressure for coronary perfusion. A critical
blood pressure is required that does not excessively increase demand, yet
keeps coronary perfusion pressure across stenotic lesions optimal

TREATMENT

Drug
Nitrates

Usual Dose

Comments; Adverse Effects

Nitroglycerin

0.40.6 mg sublingual

Aborts acute attacks; headaches, hypotension

Isosorbide dinitrate

1060 mg three times daily

Need 8 h off every 24 h to avoid tolerance

Isosorbide mononitrate
Drug
-Blockers

20 mg twice daily
Daily Dosage (mg)

Take 7 h apart
Comments; Adverse Effects

Propranolol

160320

Metoprolol
100400
Atenolol
50200
Bisoprolol
520
Pindolol
540
Calcium Channel Blockers, Heart Rate Lowering

Central nervous system side effectsfatigue,

impotencecommon
Cardioselective
Cardioselective
Cardioselective
Marked intrinsic sympathomimetic activity

Diltiazem

120360

Heart rate lowering; atrioventricular (AV)

block, heart failure, edema

Verapamil

120480

Heart rate lowering; AV block, heart failure,

constipation

510
3060
60120

Least myocardial depression

Hypotension, tachycardia
Potent coronary vasodilator

10002000 mg

May increase QT interval on ECG

Dihydropyridine Calcium Channel Blockers

Amlodipine
Nifedipine
Nicardipine
Sodium Current Inhibitor
Ranolazine

ADJUVANT THERAPY
All patients with coronary artery disease should takeaspirin(81325
mg/day), and selected high-risk patients should also takeclopidogrel.
These drugs reduce platelet aggregation and retard the growth of
atherothrombosis. Also important is correction of dyslipidemia, smoking
cessation, exercise, weight loss, control of hypertension, and
management of stress. In patients with known coronary artery disease, it
is important to decrease low-density lipoprotein (LDL) cholesterol and
perhaps increase high-density lipoprotein (HDL) cholesterol to published
targets (< 100 mg/dL and > 40 mg/dL, respectively). Angiotensinconverting enzyme (ACE) inhibitors may have a protective effect in
patients with coronary artery disease, especially postmyocardial
infarction.

TREATMENT:REVASCULARIZATIO
N
Catheter Based Methods:
The standard percutaneous coronary intervention (PCI) is balloon dilatation with
placement of a metal stent. Such treatment is limited to the larger epicardial arteries
and can be complicated by various types of acute vessel injury, which can result in
myocardial infarction unless surgical revascularization is immediately performed.
Smaller arteries may be amenable to plain old balloon angioplasty (POBA).
PCI requires intense antiplatelet therapy, usually withaspirinandclopidogrel, to
prevent stent thrombosis.
In the absence of acute complications, initial success rates for significantly dilating
the coronary artery are greater than 85%, and the technique can be of tremendous
benefit to patients.
The principal disadvantage to PCI is restenosis, which occurs in about one-third of
patients treated with a bare metal stent during the first 6 months.

TREATMENT:REVASCULARIZATIO
N
Coronary Artery Bypass Graft Surgery:
Controlled clinical trials have shown that coronary artery bypass graft (CABG)
surgery can successfully alleviate angina symptoms in up to 80% of patients
with less than 2% operative mortality rates.
Although the initial cost of surgery is high, studies have shown it can be
competitive with repeated angioplasty and lifelong pharmacologic therapy in
selected patients.
The standard surgical approach is to use the saphenous veins, which are sewn
to the ascending aorta and then, distal to the obstruction, in the coronary
artery, effectively bypassing the obstruction with blood from the aorta.
The major problem with saphenous vein grafts is recurrent atherosclerosis in
the grafts, which is often quite bulky and friable.

PROGNOSIS
There are two major determinants of prognosis in patients with chronic
ischemic heart disease. The first is the clinical status of the patient, which
can be semiquantitated by the Canadian Cardiovascular Societys angina
functional class system. In this system, class I is asymptomatic, II is
angina with heavy exertion, III is angina with mild-to-moderate
exertion, and IV comprises patients who cannot perform their
daily activities without getting angina or who are actually
experiencing angina decubitus. The higher the Canadian class, the
worse the prognosis.
A second prognostic system is based solely on coronary anatomy. The
more vessels involved, and the more severely they are involved, the
worse the prognosis.

QUESTIONS

Name 1 drug used for Pharmacological Stress Testing:

Dobutamine

Angina with Heavy Exertion belongs to which Canadian Class? Class 1/Class2/Class 3 or Class 4?
Class 2

Hypothyroidism can aggravate angina? True or False :

False

Plain Old Baloon Angioplasty is used for Small or Large areteries? :

Small

Coronarly blood flow occurs mostly in Diastole or Systole? :

Diastole