Ischemic Heart Disease

Vincent Steniger
Contents Overview
Coronary Artery Disease
Heart Anatomy
Atherosclerotic Plaque/Atheroma
Angina Pectoris
Myocardial Infarction
Sudden Death
Overall Management
Ischemic Heart Disease and Dentistry

Coronary Artery Disease
CAD: Statistics
CAD is the largest killer of American males and females
13 million Americans have CAD
1.1 million MIs per year
Every 26 seconds an American will suffer from a coronary
event
Every 60 seconds an American will die because of a
coronary event
@ 42% of those having a coronary event will die from it
@350K people die per year because of a coronary event in the
Emergency Department before even being admitted to the
hospital
Death Rate in 2001:
177 in 100,000

CAD: Demographics and Statistics
84% of those who die from CAD are 65 or older
If under the age of 65, 80% mortality rate with the first myocardial
infarction
Within 1 year of initial MI:
25% of men and 38% of women will die
Within 8 years of initial MI:
50% of men and women under 65 will die
An average of 11.5 years of life are lost due to an MI
IMPORTANT:
50% of men and 64% of women who have died suddenly via CAD DID
NOT HAVE ANY PREVIOUS SYMPTOMS
Sudden Death:
Those with a previous history of MI have a 5-6 times Sudden Death rate
compared to the general population


Manifestations of Coronary Artery
Disease/Ischemic Heart Disease
Sudden death
Heart Attack/Myocardial infarction
Acute coronary syndrome
Stable/Unstable angina pectoris
Heart failure or Arrhythmia
Exactly what is Coronary Artery
Disease (Ischemic Heart Disease)
and how/why does it occur?
Start with anatomy
Heart Anatomy
Facts:
The heart is about the size of a fist and weighs less than 1 pound
The average bpm is 72
The heart pumps 2,500 to 5,000 quarts of blood through
vasculature stretching 75,000 miles
Blood Supply to the heart:
Right Coronary Artery Right Atrium and Right Ventricle
Posterior Descending Artery bottom of Left Ventricle
Left Main Coronary Artery:
Circumflex Artery Left Atrium and Side and Back of
Left Ventricle
Left Anterior Descending Artery Front and bottom of
Left Ventricle

Definition
" Ischaemia " refers to an insufficient
amount of blood. The coronary arteries are
the only source of blood for the heart
muscle. If this coronary arteries are
blocked, the blood supply will reduce.

Risk Factors for Ischemic
Heart Disease
Obesity
Genetics
Diabetes Mellitus
Tobacco Use
Latent Life Style (lack of exercise)
Hypertension
Hypercholesterolemia
Age
Why would there be an insufficient blood
supply to the heart?
Remember that the coronary arteries are the
only source of fuel to the heart
The coronary arteries may become
partially/completely occluded:
Atherosclerotic Plaques
Atherosclerotic Plaque:
Definition and Formation
Focal accumulation of smooth muscle cells, foam
cells, cholesterol crystals and lipid under the
endothelium of the artery (within the Tunica
Intima)
Given time, this plaque can protrude into the
lumen of the vessel reducing blood flow
Often develops at branch points or curves within
the vasculature blood is slowed and/or
turbulent

Atheroma/ Atherosclerotic
Plaque
Where does the plaque begin?
within the Tunica Intima, the
innermost wall of the artery
What is a plaque made of?
Superficial fibrous cap made of
smooth muscle cells, collagen,
elastin and proteins
Also contains Macrophages,
Foam Cells, T Cells
Necrotic Center of cholesterol
crystals, lipids, Apolipoprotein B
LDL
Atheroma Formation: The Hypothesized Process

1. (1) Via damage to the arterial endothelium via turbulent blood flow, toxins such as those
from tobacco, hypertension, high concentration of fats or genetic factors there is now a
hole within the endothelium
Remember that the endothelium is only 1 cell layer thick
2. (2) Blood and whatever the blood contains (LDL, toxins) can leak into this hole
irritating the vessel
3. (3) Because of this irritation, there is a stimulated increase in smooth muscle cells and
collagen matrix
4. (4) Platelets and monocytes adhere to the injured area of the endothelium and release
cytokines creating a wave of chemotaxis. These cells also cause an upregulation of
adhesion factors for inflammatory cells on the endothelial cell surface
5. (5) More monocytes and T cell are able to enter the endothelial hole via these receptors
6. (6) Once monocytes have entered the vascular wall they can differentiate into
macrophages
7. (7) Via lipid receptors on the Macrophages, lipids are phagocytized creating foam cells
8. (8) This process continues and the atheroma enlarges
9. (9) Foam cells can eventually act to disrupt the fibrous cap of the atheroma via proteolytic
degradation resulting in ulceration of the plaque and adherence of platelets (thrombus) and
emboli formation
10. (10) A plaque, thrombus or emboli can cause partial or full occlusion of a blood vessel
Atheroma: Continued
As the atheroma within the coronary arteries
enlarges, the blood flow to the heart decreases and
therefore so does the O2 supply
The heart is not in danger of hypoxia until 50% of
the vessel is occluded
As the heart senses a decrease in O2, there is
attempted compensation:
Increase Heart Rate
Increase Blood Pressure
Aggravation/Worsening of the atheroma
When 70% of the artery is occluded, Angina
Pectoris will occur



Angina Pectoris
At least 70% occlusion of coronary
artery resulting in pain. What kind
of pain?
Chest pain
Radiating pain to:
Left shoulder
J aw
Left or Right arm
Usually brought on by physical
exertion as the heart is trying to
pump blood to the muscles, it
requires more blood that is not
available due to the blockage of the
coronary artery(ies)
Is self limiting usually stops
when exertion is ceased
Angina Pectoris Continued
Angina Pectoris can be Stable or Unstable:
Stable:
The pain and pattern of events is unchanged
over a period of time (months years)
Unstable:
The pain and pattern is changing, be it in
duration, intensity or frequency
A Myocardial Infarction waiting to happen
Myocardial Infarction
Partial or total occlusion of one or more of the
coronary arteries due to an atheroma, thrombus or
emboli resulting in cell death (infarction) of the
heart muscle
When an MI occurs, there is usually involvement
of 3 or 4 occluded coronary vessels

Myocardial Infarctions: Statistics
250,000 deaths per year.
30% mortality within the first 2 hours
45 Minutes of Ischemia:
Cardiac muscle death occurs
How is the Diagnosis Made?
Electrocardiographic changes
ST elevation
Myocardial enzyme elevation
Creatine kinase
Troponin
C Reactive Protein


MI, Atheroma, Other Sequelae
When there is an atheroma, as mentioned before
there can be rupture resulting in thrombus
formation because of the build up of platelets
When there is breakage of the thrombus there is
emboli formation
An emboli can travel to the brain (cerebral infarct)
can remain in the heart (myocardial infarct) or
even travel to the extremities cutting off blood
supply
As the area beneath the is disrupted atheroma
hemorrhages, there can is increased risk of abscess
formation and infection
Complications of
Myocardial Infarctions
Infarction leading to inability of the heart to
function properly leading to Heart Failure
Angina/Pain
Cardiogenic shock
Ventricular aneurysm and rupture
Embolism Formation
Arrhythmias Myocardial Infarctions can
lead to Ventricular Fibrillation (shockable!)


Sudden Death

Sudden Death :

250,000 deaths in the US per year are caused by what is referred to

as sudden cardiac death

Sudden Cardiac Death is also known as a Massive Heart Attack

in which the heart converts from sinus rhythm to ventricular
fibrillation

In V-Fib, the heart is unable to contract fully resulting in lack of

blood being pumped to the vital organs

V-Fib requires shock from defibrillator SHOCKABLE

RHYTHM

Management of Ischemic
Heart Disease:
Pharmaceuticals:
Beta Blockers
Act either selectively or non-selectively on Beta receptors:
Beta 1 cardiac muscle increase rate and contraction
Beta 2 dilates bronchial smooth muscle
Ca
++
Channel Blockers
Acts on vasculature blocking Ca++ and causing vasodilation
Nitrates
Vasculature vasodilation
Anti-Hypercholesterolemia
HMG CoA Reductase Inhibitors reduction in manmade cholesterol
thus helping to reduce atheroma formation
Antiplatelet Medication:
Clopidogrel (Plavix)
Aspirin

Management of Ischemic
Heart Disease:
Lifestyle:
Diet
Exercise Preventive treatment
Low fat, low cholesterol diet
Cessation of smoking
Red wine (in moderation)
Dental Considerations
Assessment and Overall Management
Pharmaceuticals
Emergency Situations
Oral Effects of Pharmaceuticals
Antibiotic Prophylaxis
Post MI: when to treat
Assessment
Consider three areas:
How severe or stable the ischemic heart disease
is
The emotional state of the patient
The type of dental procedure
RISK
Major Risk for Perioperative Procedures:
Unstable Angina (getting worse)
Recent MI
Intermediate Risk for Perioperative Procedures:
Stable Angina
History of MI
Most dental procedures, even surgical procedures
fall within the risk of less than 1%
Some OMFS procedures fall within an
intermediate risk of less than 5%
Highest risk procedures those done under
general anesthesia

Management for Low-
Intermediate Risk
Short appointments
AM appointments
Comfort
Vital Signs Taken
Avoidance of Epinephrine within Local
Anesthetic or Retraction Cord
O2 Availability
Dental Considerations for
Ischemic Heart Disease
Pharmaceutical Considerations:
Interaction of NSAIDS with Beta Blockers
If patient is taking a non-selective Beta Blockers
limit local anesthetic use to 2 carpules with 1:100K
epinephrine (increase in receptors for epinephrine)
In uncontrolled hypertensive patients use judgment
when giving epinephrine Carbocaine use encouraged
Statins (HMG CoA Reductase Inhibitors) when
combined with Erythromycin and Clarithromycin can
lead to renal failure and muscle pathology

Dental Considerations for
Ischemic Heart Disease
Pharmaceuticals and Oral Manifestations:
Of Note:
Ca
++
Channel Blockers, mainly (nifedipine, verapamil, diltiazem,
amlodipine) may cause gingival hyperplasia in some patients
Consider:
Meticulous Oral Hygiene for the patient
3 month recall of scaling, possible SRP
Gingivectomy if needed



Common Situations:
Orthostatic Hypotension due to use of anti-
hypertensives (beta blockers, nitroglycerin)
Raise chair slowly
Allow patient to take his/her time
Assist patient in standing
Post-Op Bleeding:
When patients on Plavix or Aspirin, expect increased bleeding
because of decreased platelet aggregation

Dental Considerations for
Ischemic Heart Disease
Dental Considerations for
Ischemic Heart Disease
Emergent Situations:
Possible MI:
Remember that pain in the jaw may be referred pain
from the myocardium assess the situation, have
good patient history, follow ABCs
Angina:
In situations of angina pectoris, all operatories
should have nitroglycerin to be placed sublingually


Dental Considerations for
Ischemic Heart Disease
Emergent Situations:
Chest Pain-MI:
STOP PROCEDURE
Remove everything from patients mouth
Give sublingual nitroglycerin
Wait 5 minutes if pain persists, give more
nitroglycerin, assume MI
911
Give chewable aspirin ABCs
Post MI: When to Treat
Why delay treatment?
Remember that with an MI there is damage to the heart, be it
severe or minimal that may effect the patients daily life
MI within 1 month Major Cardiac Risk (ASA IV)
MI within longer then 1 month:
Stable routine dental care ok
Unstable treat as Major Cardiac Risk
Older studies suggest high re-infarction rates when surgery
performed within 3 months, 3-6 months however, this was
abdominal and thoracic surgery under general anesthesia
New research suggests delaying elective tx for 1 month is
advisable. Emergent care should be done with local anesthetic
without epinephrine and monitoring of vital signs
When in doubt:
CONSULT THE PCP OR CARDIOLOGIST
Conclusion:
When treating patients with Ischemic Heart Disease or
recent MI
Use caution and common sense
When in doubt:
CONSULT THE PCP OR
CARDIOLOGIST