ischemic heartdisease

Ischemic Heart DiseaseIschemic Heart Disease

Vincent Steniger

Contents OverviewContents Overview

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

Coronary Artery DiseaseCoronary Artery Disease

CAD: Statistics 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 StatisticsCAD: 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 Manifestations of Coronary Artery Disease/Ischemic Heart DiseaseDisease/Ischemic Heart Disease

Sudden deathHeart Attack/Myocardial infarctionAcute coronary syndromeStable/Unstable angina pectorisHeart failure or Arrhythmia

Exactly what is Coronary Artery Exactly what is Coronary Artery Disease (Ischemic Heart Disease) Disease (Ischemic Heart Disease)

and how/why does it occur?and how/why does it occur?

Start with anatomy…

Heart AnatomyHeart 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

DefinitionDefinition

" 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 Risk Factors for Ischemic Heart DiseaseHeart 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: Atherosclerotic Plaque: Definition and FormationDefinition 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 Atheroma/ Atherosclerotic PlaquePlaque

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 ProcessAtheroma 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: ContinuedAtheroma: 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 PectorisAngina Pectoris At least 70% occlusion of coronary artery

resulting in pain. What kind of pain?– Chest pain– Radiating pain to:

Left shoulderJaw 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 ContinuedAngina 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 InfarctionMyocardial 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: StatisticsMyocardial 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 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 Complications of Myocardial InfarctionsMyocardial Infarctions

Infarction leading to inability of the heart to function properly leading to Heart Failure

Angina/PainCardiogenic shock Ventricular aneurysm and ruptureEmbolism FormationArrhythmias Myocardial Infarctions can

lead to Ventricular Fibrillation (shockable!)

Sudden DeathSudden 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 Management of Ischemic Heart Disease: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 Management of Ischemic Heart Disease:Heart Disease:

Lifestyle:– Diet– Exercise Preventive treatment• Low fat, low cholesterol diet• Cessation of smoking• Red wine (in moderation)

Dental ConsiderationsDental Considerations

Assessment and Overall ManagementPharmaceuticalsEmergency SituationsOral Effects of PharmaceuticalsAntibiotic ProphylaxisPost MI: when to treat

Assessment Assessment

Consider three areas:– How severe or stable the ischemic heart disease

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

RISKRISK 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-Management for Low-Intermediate RiskIntermediate Risk

Short appointmentsAM appointmentsComfortVital Signs TakenAvoidance of Epinephrine within Local

Anesthetic or Retraction CordO2 Availability

Dental Considerations for Dental Considerations for Ischemic Heart DiseaseIschemic 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


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


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 ABC’s

– Angina: In situations of angina pectoris, all operatories

should have nitroglycerin to be placed sublingually


Emergent Situations:– 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 TreatPost 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

Conclusion:Conclusion: When treating patients with Ischemic Heart Disease or

recent MI…– Use caution and common sense– When in doubt:

CONSULT THE PCP OR CARDIOLOGIST

ischemic heartdisease

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