Ischemic Heart

Disease

Dr. Jamil Owda

Oral & Maxillofacial Surgeon
Assit. Prof. Arab American University ,
Palestine
Atherosclerosis
Ischemic heart disease

Symptomatic coronary atherosclerotic heart disease.

Ischemic symptoms are the result of oxygen deprivation

secondary to reduced blood flow to a portion of the
myocardium.
 Incidence and Prevalence
From 1970 to 2000, mortality from coronary heart disease
decreased by 50% and from stroke by 60%.

Despite this decline, cardiovascular diseases continue to pose

the most serious threat to health in America, accounting for
about 31% of all deaths. the leading cause of death after age
65 years

atherosclerosis begins early in life, although its symptoms and

complications typically manifest later, in midlife.

Men are at higher risk than women ,Black men are at higher risk
.
 Etiology / risk factors
The cause of coronary atherosclerosis is not known

No single risk factor is responsible for the development of

coronary atherosclerosis, but many factors act synergistically.

Male gender, older age, a family history of cardiovascular

disease, hyperlipidemia, hypertension, cigarette smoking,
physical inactivity, obesity, insulin resistance and diabetes
mellitus, mental stress, and depression.

In addition to these conventional risk factors, markers of

inflammation such as C-reactive protein(CRP), homocysteine,
fibrinogen, and lipoprotein(a) have been found to be
associated with atherosclerosis.
nonwhite populations (e.g.,
African Americans, Native
Americans, Hispanics)

Before the age of 75, the

risk of coronary
atherosclerosis is greater for
men than for women.
Cigarette smoking is the
single most important
modifiable risk factor for
coronary heart disease

persons who smoke 20 or

more cigarettes daily have
a two- to four-fold increase
in coronary heart disease.
Risk factors

Increased levels of low-density lipoprotein (LDL) cholesterol pose the

greatest risk for coronary atherosclerosis.

high-density lipoprotein (HDL) cholesterol have been shown to reduce

the risk.

Persons with elevated triglyceride or B-lipoprotein levels have an

increased risk for the disease.

A diet rich in total calories, saturated fats, cholesterol, sugars, and

salts also enhances the risk.

Increased blood pressure appears to be one of the most significant

risk factors for coronary atherosclerotic heart disease
Patients with diabetes mellitus have a greater incidence of
coronary atherosclerotic heart disease and more extensive
lesions. They develop the condition at an earlier age than that
typical for persons who do not have diabetes.

Patients with diabetes have two- to eight-fold higher rates.Three

fourths of all deaths among patients with diabetes result from
coronary heart disease.

Metabolic syndrome is the term used to describe a cluster of

pathologic findings consisting of obesity, insulin resistance, low
HDL cholesterol, elevated triglycerides, and hypertension, all of
which are risk factors for atherosclerosis.
 Pathophysiology
Atherosclerosis is an inflammatory disorder of the cellular lining of the
arteries, with inflammation playing a fundamental role at all stages.

The formation of atheromatous plaques involves several steps.

The first step involves an inflammatory repair response of the

injured arterial intima.

Chronic minimal injury to the arterial endothelium is common

and results from both physiologic and pathologic processes.

disturbed blood flow at bending points or bifurcations (branch

points) in the artery.

hypercholesterolemia, glycation end products in diabetes,

irritants in tobacco smoke, circulating vasoactive amines,
immune complexes, and infection
Atheroma formation is initiated by adherence of monocytes
to an area of injured or altered endothelium
monocytes do not adhere to intact endothelium; however,
triggers of atherosclerosis such as a high saturated fat diet,
smoking, hypertension, hyperglycemia, obesity, and insulin
resistance initiate the expression of adhesion molecules by
the endothelial cells, thus promoting attachment.
The attached monocytes then migrate into the intima of the
vessel and become macrophages
Macrophages then engulf lipid molecules to become foam
cells, which are characteristic features of the fatty streak.
Foam cells are joined by T lymphocytes, and together they
produce a variety of inflammatory cytokines, which promote
the migration and proliferation of smooth muscle cells and
collagen to surround the foam cells, thereby forming a fibrous
covering or cap.

With rupture or disruption of the plaque surface, tissue factor

comes into contact with blood, and a thrombus is
subsequently formed.
plaque rupture produces an acute or unstable clinical picture
with signs and symptoms such as angina at rest, MI, or sudden
death.

Plaques may grow and proliferate outwardly, away from the

lumen of the artery, or inwardly, into the lumen. With inward
proliferation, the size of the lumen is progressively reduced
(stenosis).

Thus, blood flow may be chronically decreased, and when the

demand for oxygen exceeds supply, the outcome is ischemic
pain.

Ischemic symptoms may be produced when occlusion reaches

75% of the cross-sectional area of the artery.
Most acute coronary syndromes (e.g., unstable angina,
myocardial infarction) are caused by physical disruption or
fracture of the atheromatous plaque, most commonly of a
plaque that did not cause extreme stenosis.

Atherosclerosis usually is a focal disease that commonly

occurs in a certain areas or regions of arteries ( brain heart ,
aorta ,and peripheral arteries ), the proximal left anterior
descending coronary artery is a common area of
atherosclerotic involvement; however, the internal mammary
artery is rarely affected.
if the degree of ischemia
that results from coronary
atherosclerosis is significant
and the oxygen deficit is
prolonged, the area of
myocardium supplied by
that vessel may undergo
necrosis.
 Clinical presentation

Chest pain.

Most important symptom

Brief or prolonged

Result from imbalance between oxygen supply and oxygen demand

The exact mechanism or agent causing the cardiac pain is not

known
Angina : Sensation of aching , heavy , squeezing pressure or tightness in
the mid chest region ,The area of discomfort often is reported to be
approximately the size of a fest and may radiate into the left or right arm
to the neck or lower jaw. lasting 5 to 15 minutes if the provoking stimulus is
stopped or for a shorter time if nitroglycerin is used (angina pectoris).

Stable angina VS unstable angina.

Stable angina is pain that is predictably reproducible, unchanging, and

consistent over time. precipitated by exertion such as walking or climbing
stairs.relieved by cessation of the precipitating activity, by rest, or with the
use of nitroglycerin. Good prognosis
Unstable angina is defend as new-onset pain, pain that is increasing in
frequency, pain that is increasing in intensity, pain that is precipitated by
less effort than before, or pain that occurs at rest. This pain is not readily
relieved by nitroglycerin. poorer prognosis and often experience an acute
MI within a short time.
Prinzmetal variant angina, occurs at rest and is caused by
focal spasm of a coronary artery, usually with varied amounts
of atherosclerosis. also may occur in persons with normal
coronary vessels.
Fatigue and weakness
Sudden cardiac death, ventricular fibrillation.
Palpitations
Syncope
dyspnea, orthopnea, paroxysmal nocturnal dyspnea,
edema, hemoptysis, fatigue, weakness, and cyanosis.
 Signs
Most clinical signs relate to other underlying cardiovascular disease
or conditions such as congestive failure.
corneal arcus and xanthoma of the skin are related to
hyperlipidemia and hypercholesterolemia
Blood pressure may become elevated
Abnormality in the Rate and/or rhythm of the pulse may occur,
Diminished peripheral pulses in the lower extremities
Bruits in the carotid arteries. Panoramic radiographs of the jaws
may occasionally demonstrate carotid calcifications in the areas of
C3 and C4, consistent with atherosclerotic plaques in the carotid
arteries.
Retinal changes
Distention of neck veins, peripheral edema, cyanosis, ascites, and
enlarged liver may be noted.
 LABORATORY AND
DIAGNOSTIC FINDINGS
Diagnostic modalities that are specific for coronary heart disease

Resting ECG,

chest x-ray studies,

exercise stress testing, exercise echocardiography,

ambulatory (Holter) electrocardiography, stress thallium-201 perfusion

scintigraphy ,ambulatory ventricular function monitoring

Cardiac catheterization and angiography.

Serum markers of acute MI most commonly used in clinical practice

include troponin I, troponin T, and creatine kinase isoenzyme (CK-MB)
and myoglobin .

Troponins are first detectable 2 to 4 hours after the onset of an acute MI,
are maximally sensitive at 8 to 12 hours, peak at 10 to 24 hours and persist
for 5 to 14 days.
Medical management
Angina pectoris
Drug therapy
Revascularization is an option for patients with stable or
unstable angina. Available procedures for revascularization
include

percutaneous transluminal coronary angioplasty( ballon

angioplasty ),

stents,

coronary artery bypass grafting.

stenosis recurs within 6 months
in 10% to 50% of patients, along
with a return of symptoms.

the use of stents has

decreased the incidence of
restenosis to about 20% to 30%
 CABG

The saphenous vein from

the leg and the internal
mammary artery from the
chest.
Of the two, the internal
mammary artery graft is
sturdier and much less
susceptible to graft
atherosclerosis and
occlusion than are vein
grafts.
 Myocardial infarction
The basic management goal is to minimize the size of the
infarction and prevent death from lethal arrhythmias.

Early administration of aspirin is recommended,

The greatest benefit is realized when patients receive

thrombolytic drugs within the first 3 hours after infarction.

During the first several weeks after an infarction, the conduction

system of the heart may be unstable, and patients are prone to
serious arrhythmias and reinfarction. A pacemaker may be used
with severe myocardial damage and resultant heart failure.
 Dental management
• Identification : the dentist must be able to distinguish a patient
who has stable, unstable angina ,MI
• Risk assessment:
“Thank you ”

–Dr. Jamil Owda