Coronary Artery Disease and Acute Coronary Syndrome

The Heart as a Pump ► ► The heart is a hollow muscular organ about the same size as your fist.

It is a 2 sided pump, with a muscular wall called the septum separating the right and left sides

The Coronary Arteries ► ► ► As a muscle the heart needs oxygen and nutrients to work The heart muscle has its own blood supply through the coronary arteries Women’s coronary arteries tend to be smaller

Description

► Coronary Artery Disease (CAD)  A type of blood vessel disorder that is included in the general category of atherosclerosis

Description ► Atherosclerosis   Can occur in any artery in the body Atheromas (fatty deposits) ► Preference for the coronary arteries

Description ► Atherosclerosis  Terms to describe the disease process: ► Arteriosclerotic heart disease (ASHD) ► Cardiovascular heart disease (CHD) ► Ischemic heart disease (IHD) ► CAD

Description ► Cardiovascular diseases are the major cause of death in the US and Canada ► Heart attacks are still the leading cause of all cardiovascular disease deaths and deaths in general

Etiology and Pathophysiology ► Atherosclerosis is the major cause of CAD  Characterized by a focal deposit of cholesterol and lipids, primarily within the intimal wall of the artery

Process of Coronary Artery Disease - Atherosclerosis ► Over time ….a series of events within the artery  A fatty streak (permanent)– can start in infancy & young children   Fatty – ( lipid) deposits throughout the years Narrowing and impaired blood flow occurs with the gradual occlusion as plaque thickens and blood clots form

Etiology and Pathophysiology ► Endothelial lining altered as a result of chemical injuries  Hyperlipidemia  Hypertension

Etiology and Pathophysiology ► Bacteria and/or viruses may have role in damaging endothelium by causing local inflammation ► C-reactive protein (CRP)    Nonspecific marker of inflammation Increased in many patients with CAD Chronic exposure to CRP triggers the rupture of plaques

Etiology and Pathophysiology ► Endothelial alteration     Platelets are activated Growth factor stimulates smooth muscle proliferation Cell proliferation entraps lipids, which calcify over time and form an irritant to the endothelium on which platelets adhere and aggregate

Etiology and Pathophysiology ► Endothelial alteration    Thrombin is generated Fibrin formation and thrombi occur

Response to Endothelial Injury Fig. 33-3

Stages of Development in Atherosclerosis Fig. 33-4

Etiology and Pathophysiology Collateral Circulation ► Analogous to “detours” around atherosclerotic plaques ► Occur normally in coronary circulation ► But collaterals increase in the presence of chronic ischemia ► When occlusion occurs slowly over a long period, there is a greater chance of adequate collateral circulation developing

Collateral Circulation Fig. 33-5

Risk Factors for Coronary Artery Disease ► Risk factors can be divided:   Unmodifiable risk factors Modifiable risk factors

Risk Factors for Coronary Artery Disease ► Unmodifiable risk factors:     Age Gender Ethnicity Genetic predisposition

Risk Factors for Coronary Artery Disease ► Modifiable risk factors:        Elevated serum lipids Hypertension Smoking Obesity Physical inactivity Diabetes mellitus Stressful lifestyle

Diabetes Treatment ► ► ► ► ► Prescribed Meal Plan (sit down with a Dietitian) Home Blood Sugar monitoring Regular exercise – at least 150 mins./wkly ? Medications – pills or Insulin or both Ongoing Education- Diabetes classes ► ► Support – family and friends Physician follow-up or Specialist referral

A person with Diabetes is considered high risk like someone who has already had a heart attack!

Stress - “We do not laugh because we’re happy –

we’re happy because we laugh”

William James ► Stress may not be the main cause of disease ……. but, managing stress helps us;  maintain health  deal with health problems.

Anger, anxiety and depression are major emotions that need to be dealt with for a healthy heart

“75% of all good health is under our control!”

Risk Factors for Coronary Artery Disease ► Health Promotion       Identification of high-risk persons Management of high-risk persons ► Risk factor modification Physical fitness Health education in schools Nutrition (weight control, ↓ fat, ↓ chol intake) Cholesterol-lowering medications

Types of Angina ► Results when the lack of oxygen supply is temporary and reversible ► Types of Angina    Stable Angina Prinzmetal Angina Unstable Angina

Coronary Artery

Stable Angina Pectoris ► Chest pain occurs intermittently over a long period with the same pattern of onset, duration, and intensity of symptoms ► Can be controlled with medications on an outpatient basis ► Pain usually lasts 3 to 5 minutes   Subsides when the precipitating factor is relieved Pain at rest is unusual

Silent Ischemia ► 80 % of patients with myocardial ischemia are asymptomatic (with pain or without pain the ischemia has the same prognosis)

Prinzmetal’s Angina ► Occurs at rest usually d/t spasm of major coronary artery ► Spasm may occur in the absence of CAD

Unstable Angina ► Angina that is:       New in onset Occurs at rest Has a worsening pattern Unpredictable Considered to be an acute coronary syndrome Associated with deterioration of a once stable atherosclerotic plaque

Clinical Manifestations Angina ► Chest pain or discomfort (d/t ischemia)    A strange feeling, pressure, or ache in the chest Constrictive, squeezing, heaving, choking, or suffocating sensation Indigestion, burning

However… ► Up to 80% of patients with myocardial ischemia are asymptomatic ► Associated with diabetes mellitus and hypertension

Location of Chest Pain Fig. 33-12

Diagnostic Studies Angina ► ECG ► Coronary angiography ► Cardiac markers (CK MB, Troponin) ► Treadmill exercise testing (stress test) ► Serum lipid levels ► C-reactive protein (CRP) ► Nuclear imaging

Coronary Angiography ► ► ► A diagnostic test using x rays to record the passage of a contrast dye in the heart To identify the presence, location and nature of any coronary artery disease The heart valves and heart muscle can also be assessed

Coronary Angiogram

Coronary Angioplasty Video Link ► http://www.healthscout.com/animation/1/3 8/main.html

Collaborative Care Angina ► Treatment for stable angina:     oxygen demand and/or  Nitrate therapy Stent placement oxygen supply

Collaborative Care Angina ► Treatment for stable angina:     Percutaneous coronary intervention Atherectomy Laser angioplasty Myocardial revascularization (CABG)

Coronary Artery Bypass Surgery ► ► Is open heart surgery, which a bypass ( detour) is made to go around an area of blockage in a coronary artery Bypasses are usually taken from the leg veins or an artery from the inside of the chest wall

Collaborative Care Angina ► Drug Therapy  Antiplatelet aggregation therapy ► Aspirin: drug of choice (for MI prevention) ► First line of treatment for angina

Collaborative Care Angina ► Drug Therapy  Nitrates ► 1st line therapy for treatment of acute anginal symptoms ► Dilation of vessels

Collaborative Care Angina ► Drug Therapy   -Adrenergic blockers  Calcium channel blockers

Collaborative Care Angina ► Percutaneous coronary intervention    Surgical intervention alternative Performed with local anesthesia Ambulatory 24 hours after the procedure

Collaborative Care Angina ► Stent placement  Used to treat abrupt or threatened abrupt closure and restenosis following PCI

The Coronary Stent Procedure ► A coronary stent is a small tubular wire object inserted into a coronary artery at the time of angioplasty to keep the previously narrowed artery open

Collaborative Care Angina ► Atherectomy   The plaque is shaved off using a type of rotational blade Decreases the incidence of abrupt closure as compared with PCI

Collaborative Care Angina ► Laser angioplasty   Performed with a catheter containing fibers that carry laser energy Used to precisely dissolve the blockage

Collaborative Care Angina ► Myocardial revascularization (CABG)   Primary surgical treatment for CAD Patient with CAD who has failed medical management or has advanced disease is considered a candidate

Clinical Manifestations Myocardial Infarction ► Pain  Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration ► The hallmark of an MI

Serum Cardiac Markers (Lewis p.817) ► ► Creatine Kinase (creatine phosphokinase) (CK-MB)  Increased in > 90% of MI patients.

  Begins to rise 4-6 hours Peaks 24 hours  Returns to normal in 2 - 3 days Troponin  Myocardial muscle protein released after an injury  Troponin T and Troponin I are cardiac specific indicators of an MI  Much more specific than CK-MB  Rises quickly and remains elevated for 2 weeks

Serum Cardiac Markers ►

Lactic Dehydrogenase (LD or LDH)

     Found in heart muscle as well as others It is increased in >90% of MI patients.

Begins to rise 24 hours Peaks in 3 days Returns to normal in 8-9 days

Diagnostic Cardiac enzymes (See Lewis p. 817 Figure 33-15 also)

Clinical Manifestations ► Acute Coronary Syndrome (ACS)  Develops when the oxygen supply is prolonged and not immediately reversible

Clinical Manifestations ► ACS encompasses:   Unstable angina Myocardial infarction (MI)

Relationships Among CAD, Stable Angina, and MI Fig. 33-8