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 MI¶s 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


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 

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


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

" 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 


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) 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 ³hole´ 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  


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 Creatine kinase Troponin
C Reactive Protein

± Myocardial enzyme elevation 

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 

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 ³sudden´ cardiac death ± Sudden Cardiac Death is also known as a ³Massive 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 ³SHOCKABLE 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 ³manmade´ 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 

and Overall Management  Pharmaceuticals  Emergency Situations  Oral Effects of Pharmaceuticals  Antibiotic Prophylaxis  Post MI: when to treat


three areas:

± How severe or stable the ischemic heart disease

is ± The emotional state of the patient ± The type of dental procedure


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 LowLowIntermediate 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


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 
± Of Note: 

and Oral Manifestations: 

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

Dental Considerations for Ischemic Heart Disease 

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 When patients on Plavix or Aspirin, expect increased bleeding because of decreased platelet aggregation

± Post-Op Bleeding: 

Dental Considerations for Ischemic Heart Disease 


± Possible MI:  Remember that pain in the jaw may be referred pain from the myocardium assess the situation, have good patient history, follow ABC¶s ± Angina:  In situations of angina pectoris, all operatories should have nitroglycerin to be placed sublingually

Dental Considerations for Ischemic Heart Disease 


± Chest Pain-MI:  STOP PROCEDURE  Remove everything from patient¶s mouth  Give sublingual nitroglycerin  Wait 5 minutes if pain persists, give more nitroglycerin, assume MI  911  Give chewable aspirin ABC¶s

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 patient¶s 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


When treating patients with Ischemic Heart Disease or recent MI«
± Use caution and common sense ± When in doubt: 


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