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Coronary Artery Disease

Ischemia Infarction Collateral Circulation

Non-modifiable risk factors

Age average - 65 men -70 women Gender Family history

Ethnic background

Modifiable risk factors

Elevated serum cholesterol levels Cigarette smoking

Impaired glucose tolerance Obesity Physical inactivity Stress Diabetes Oral Contraceptives

The major underlying cause is atherosclerosis. Atherosclerosis is a slow, progressive disease which begins in childhood and takes decades to advance

Pathogenesis of Atheroma
1. Fatty streak development 2. Atheromatous plaque development 3. Thrombus development

Fatty streak development

Dr. Enos and Holmes reported on autopsis of 2000 dead soldiers in Korean War average age 22.
35% had fatty streaks in coronary arteries 42% had had established atheroma

Average adult Aorta, mild fatty streaks, early atheroma.

Aorta. Arrow at prominent fatty streak

Initiation of atheroma by damage to endothelium which becomes more porous to lipids and monocytes

Monocytes from blood stream pass through endothelium into blood vessel wall

Healthy Coronary Artery cross section






Initiators of Endothelial Dysfunction

Oxidized LDL


Glycolated end products

Initiation of Monocyte attachment with activation of endothelial transcription nuclear factor Kb (TNF-Kb) by oxidized low density lipids, cytokines, and glycolated end products seen in diabetes.

Vascular cell wall adhesion molecule (VCAM-1) is induced by TNF-Kb



Vascular cell wall adhesion molecule (VCAM-1) is induced by TNF-Kb


VCAM-1 and chemokine monocytic chemotactic protein I localizes monocytes in vessel wall.

Low Density Lipids (LDL) pass through damaged endothelium into blood vessel wall

Coronary Artery Disease



Low density lipids (LDL) oxidized in vessel wall

LDLs are oxidized and then induce production of bio active molecules such as Interleukin 1, Interleukin 6, matrix metalloproteases, Prostaglandins.

Platelet Derived Growth Factor, Tumor Necrosis Factor Alpha.

LDLO MMP Prostaglandins Cytokines LDLO Cytokines LDLO MMP

Monocytes transform to macrophages and take up LDL to form foam cells

Monocytes trigger chronic inflammatory reaction with lymphocytes and this results in tissue necrosis and fibrosis

LDLO MMP Prostaglandins Cytokines LDLO Cytokines LDLO MMP

LDLO Bacteria MMP Prostaglandins Cytokines LDLO Cytokines Cytokines LDLO MMP

Circulating bacteria and cytokines add to inflammation. This leads to Atheromatous plaque formation

High Density Lipids (HDL) inhibit oxidation of LDL

High Density Lipids (HDL)

HDL are a heterogeneous lipoproteins produced in the liver and small intestine. HDL contains 70% phospholipid and protein, 25% cholesterol, 5% triglycerides. HDL has 2 antioxidant enzymes
Paraoxonase Platelet activating factor acetyl hydrolase Apolipoprotein A-1 stabilizes paraoxonase

Enzymes associated with HDL apolipoproptein (apoAL) and paraoxenase (PON) protect by destroying the oxidized pro-inflammatory lipids from LDL

PON also inhibits LDL induced Monocyte Migration.Periodontitis may cause reduction in Apo AI and PON and so increase the level of oxidized lipids and monocytes in blood vessels walls.








Blood vessel wall becomes distended and continues to accumulate cholesterol, some areas become calcified

Coronary artery with atheromatous plaques (arrows)


Coronary Artery with stable atheroma. Inflamation and necrosis have replaced the smooth muscle but there is a dense layer of collagen next to lumen (arrows)

Bacterial Proteases



MMP s from macrophages and proteases from circulating bacteria can destroy collagen to form an unstable atheromatous plaque

Blood vessel wall can rupture and then get thrombus formed at region of ulceration

Endothelium is destroyed with exposure of collagen and plaque to arterial blood.

Coronary Artery Disease

Platelets aggregate on exposed collagen to form a thrombus.

Thrombus formation

Oral Bacteria

Circulating oral bacteria have peptides that cause platelet aggregation

Increase thrombosis can lead to sudden occlusion of vessel

Coronary Artery occluded by thrombosis

Thrombus formation on atheromataous plaque. Slits of cholesterol crystals seen in vessel wall.

Coronary artery with narrowed lumen and thrombosis (arrows)

Oral Bacteria

Thrombosis can give occlusion of vessel.

This is responsible for 50% of cases of myocardial infarction


Calcification (blue area) and distended vessel wall with narrowed lumen of Coronary Artery.

Ultrafast CAT Scan of Thorax Showing Cross-Section of Heart. Calcified Tissues Stained Pink.
Note: Calcified Atheromatous Plaques in Coronary Arteries


Early infarct affecting left ventricle

Cross section of heart with area of necrosis

Infarct in ventricular wall with loss of muscle and scarring

Area of previous infarct with rupture of ventricular wall

Histology of Myocardial Infarction

Normal heart muscle

Beginning of infarct, loss of striations and nuclei of cardiac muscle

Continued loss of cellular vitality of myocardium

Myocardial infarct with replacement of necrotic myocardium with inflammatory cells and fibroblasts

Established infarct with fibrotic scarring in myocardium

Mortality From Diseases of the Heart by Race/Ethnicity (Deaths/100,000 - 2001)


Hispanic Asian Native Black White Amer. 99 870 224 1128 426 244

45-64 166 >65 1336

2181 2079

Cardiovascular Assessment
Subjective Data: Personal/Familiar HX, CP, Dyspnea, weight changes etc. Physical Assessment: Skin, extremities, BP, JVP, Lungs, Precordium Objective Data: Labs: CPK/ troponin Hypo/ Hyperkalemia Hypocalcemia Serum Na

Angina Pectoris Ischemia Stable angina

Acute Coronary Syndrome Unstable angina S/S Squeezing pressure, ache, or heaviness Aching tooth neck or jaw Aching back/arms Feeling of choking, gas Pale, sweaty skin Myocardial infarction

Pathophysiology of Infarction Plague evolution lipid deposits Hypoxia (dec O2)

Local vasodilation of blood vessels/acidosis. Cellular potassium, calcium and magnesium imbalances / acidosis

Suppression of normal conduction and contractile functions.

Pathophysiology of Infarction Automaticity and ectopy are enhanced Catacholamines (epinephrine and norepinephrine) released in response to hypoxia and pain Increases the hearts rate and contractility and after load

Pathophysiology of Infarction Increase in O2 requirements in tissue O2 deprived tissue. Infarct extend into areas of injury and ischemia This depends on 3 factors:
Collateral circulation, Anaerobic metabolism Work load demands of the myocardium

Subendocaardium (subendocardial MI) - not total wall less severe Transmural - spread to the epicardium or all three layers of cardiac muscle
Effects the wall motion and cardiac output.

Pathophysiology of Infarction

Physical Changes
6 hours 48 hours infarct area appears blue and swollen infarct turns gray with yellow streaks as neutrophils invade the tissue and begin to remove the necrotic cells. the necrotic area eventually develops into a shrunken, thin firm scar.

8-10 days

2-3 months granulation tissue forms at the edges of the necrotic tissue.

Pathophysiology of Infarction Ventricle remodeling

Classification of MI by location Anterior Lateral Septal Inferior Posterior

Assessment /ClinicalManifestations

Pain P where is pain Point to it. Q uality sharp/dull R adiation jaw, neck, arm S everity 1-5 T ime how long
Precipitating and relieving factors

Assessment /Clinical Manifestations Restlessness


Signs of shock

Angina pain
Associated symptoms

Assessment /Clinical Manifestations Vitals Rhythm Psychosocial Distal pulses Skin temp

Silent MI
15 -20% painless or atypical MI

Pain in jaw/arm

May not be found until years later when

EKG changes are found

Coronary Artery Disease In Women

Lipid management and control of other coronary risk factors in post menopausal women
J. Womens Health and Gender related Med. 9:235,2000

Stroke and myocardial infarction

Number one killer of women with 500,000 deaths per year

African American and Hispanic women at greater risk than Caucasian women

This is more than the next 16 causes of death combined

Risk of Myocardial infarction lower in women than men

First myocardial infarction in women is more severe and more lethal than they are in men

Womens mortality rate at 6 months post myocardial infarction double that of men

Analysis of 350,000 patients after fibrinolytic therapy for infarction.

Mortality for women 9.3%, men 4.5%

Without fibrinolytic therapy


mortality for women 10.9% for men

Coronary artery bypass surgery operative mortality 4.5% women, 2.6% men

Menopause often causes increase in total cholesterol and LDL

Estrogen increase HDL levels

Post menopausal hormonal therapy gave 53% reduction in death from CHD in study using 121,700 registered nurses

Framingham Study. Risk of coronary artery disease doubles with onset of menopause

Cardiovascular Disease During 6.9 Years of Hormone Therapy

20 centers with 2,763 post menopausal with C.H.D. average age 67 years. Hormone group got 0.6625mg conjugated estrogen, 2.5mg medroxyprogesterone acetate daily. Hormones gave no significant decrease in C.H.D. events - infarct or death hospitalization angina revascularization, congestive heart failure, stroke, ischemia or ventricular arrhythmia Another study on same population showed hormone group had increased rated of venous thrombo-embolism and biliary tract surgery. 261 deaths compared to 239 in controls
Grady, D. et al JAMA 2002, 288:49

Heart Disease and Women #1 risk. Early knowledge with first MI Underrepresented in clinical trials for cardiovascular drugs Studies predominately middle-aged men

Number 1 killer of women 12 times more die of CVD than breast cancer Rate of CVD has risen over last 2 decades 2/3 of women who die suddenly from CHD had no previously recognized symptoms Within 6 years of an MI 35% have another MI 11% have a stroke 6% experience sudden cardiac death.

Cardiovascular risk factors DM Hypertension Obesity Family history Pregnant Birth control pills Menopause

Symptoms Disparities
Sex differences Different signs and symptoms Women Men Classic symptoms are far less common in women

Women are misdiagnosed and discharged from ED.

Women Early Symptoms

Onset Unusual fatigue Sleep disturbances SOB Weakness Indigestion Anxiety Unresolved symptoms Hormonal status

Diagnostic Differences
Suspected CHD - Not tested Coronary vessels Atherosclerosis Test interpretation ST-segment elevation False positive test results.

Psycho-social Assessment
Men and women
Denial Fear Anxiety Anger


Diagnostic Tests
Troponin T and I Creatinine kinase MB (CK-MB) Myoglobin

EKG: Einthovens Triangle

I, II, III measure differences in activity between the limb leads AVR, AVL, AVF measure activity between the heart & the limbs V1-V6 measure activity of heart on horizontal plane

Diagnostic Tests - EKG

A. Normal ECG prior to MI B. Hyperacute T wave changes increased T wave amplitude and width; may also see ST elevation C. Marked ST elevation with hyperacute T wave changes (transmural injury) D. Pathologic Q waves, less ST elevation, terminal T wave inversion (necrosis) E. Pathologic Q waves, T wave inversion (necrosis and fibrosis) F. Pathologic Q waves, upright T waves (fibrosis)

Diagnostic Tests Echocardiogram Transesophageal Echo

Stress test Medication stress testing adenosine (Adenocard) dobutamine (Dobutrex) Myocardial perfusion imaging Thallium scans Dipyridamole (Persantine) Radioisotope imaging MRI Cardiac Catheterization

Diagnostic Tests

30 -40 % expire before reaching hospital 80% reach hospital survive Of 20% that expire occurs usually in 3-4 days of admission. arrhythmias 30 year olds ignore especially with DM

ICU /Telemetry unit Emergency angioplasty Pain relief Thrombolytic agents Aspirin 160 325mg on day 1 and then indefinitely thereafter. Antiplatelet agents Oxygen Rest and more rest

Medical Treatment

Nitroglycerin Increases collateral blood flow, Vasodilation. SL, Spray, Patch, IV Oral Isosorbide dinitrate (Isordil, Iso-Bid), Isosorbide Mononitrate (Imdur) Extended release After 5 minutes recheck pain assessment if BP less than 100 systolic or 25mm lower than the previous reading lower the head of the bed

Drug Therapy

Drug Therapy
SL Nitroglycerin - vasodilation Total of 3 pills in 5 minute increments Under tongue Relief time Storage Self life Tingle Vital Signs

Drug Therapy
Nitroglycerin Paste AM/PM IV nitro - slow initial infusion Check BP and pain every 3-5 minutes dose is increased until pain is relieved BP falls excessively or the max dose is reached SE: Headache

Drug Therapy

Chest pain unresolved by Nitro. Action: Dose: 2-10mg IV every 5-15 minutes until max dose Side Effects Toxicity

Drug Therapy
Beta Adrenergic Blockers Decrease the size of the infarct, ventricular dysrhythmias, and mortality rates in clients with an MI. Cardioselective BB Noncardioselective BB Wean off or rebound MI may occur

Drug Therapy
Ace Inhibitors Prevent ventricular remodeling and the development of heart failure (first 48 hours) Survival rate Nursing Intervention: Potassium effects

Drug Therapy
Calcium Channel Blockers

Clients with Angina. Vasodilation and myocardial perfusion. Angina use Monitor the client

Drug Therapy
Calcium Channel Blockers

Nifedipine ( Adalat, Procardia (XL)) Verapamil (Calan Isoptin) - (slows SA and AV conduction) Diltazem ( Cardizem ) Amlodipine ( Norvasc) Nicardipine (Cardene)

Drug Therapy
Anti-platelet Agents Action ASA Dosing Aspirin 81- 650mg/day SE: Clopidogrel (Plavix) Ticlopidine (Ticlid)

Drug Therapy
Thrombolytic Therapy
Dissolve thrombi IV or Intracoronary during cath Indications CP > 30 min unrelieved by nitro with indications of transmural ischemia and injury on EKG Chest pain <6 hours, Contraindications recent abdominal surgery, stroke, recent trauma

Drug Therapy
Thrombolytic Therapy Dissolve thrombi IV or Intracoronary during cath Indications CP > 30 min unrelieved by nitro with indications of transmural ischemia and injury on EKG Chest pain <6 hours, Contraindications recent abdominal surgery, stroke, recent trauma

Drug Therapy
Thrombolytic Therapy Post procedure Vital signs Neuro status Assess bleeding external and internal Clotting studies Successful?

Drug Therapy
Fibrinolytics Dissolve blood clots that have formed in certain blood vessels. Given only by or under the direct supervision Tissue Plasma activator t-PA, Retavase, TNKase

Drug Therapy

Streptokinase Anisoylated plasminogen activator Urokinase

Angina & MI Interventions

All interventions relate to oxygen supply & demand There is a decreased O2 supply in hypoxemia, such as anemia An increased O2 demand in tachycardia, increased preload, increased afterload The goal is to increase O2 supply (increase coronary blood flow) & decease O2 demand (decrease ht rate, decrease preload & afterload)