1. Coronary Artery Disease and Acute Coronary Syndrome

2. 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

3. 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

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

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

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

7. 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

8. 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

9. 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

10. Etiology and Pathophysiology
Endothelial lining altered as a result of chemical injuries
Hyperlipidemia
Hypertension

11. 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

12. 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

13. Etiology and Pathophysiology
Endothelial alteration 
Thrombin is generated
Fibrin formation and thrombi occur

14. Response to Endothelial Injury
Fig. 33-3

15. Stages of Development in Atherosclerosis
Fig. 33-4

16. 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

17. Collateral Circulation
Fig. 33-5

18. Risk Factors for Coronary Artery Disease
Risk factors can be divided:
Unmodifiable risk factors
Modifiable risk factors

19. Risk Factors for Coronary Artery Disease
Unmodifiable risk factors:
Age
Gender
Ethnicity
Genetic predisposition

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

21. 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!

22. 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!”

23. 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

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

25. Coronary Artery

26. 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

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

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

29. 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

30. 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

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

32. Location of Chest Pain
Fig

33. 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

34. 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

35. Coronary Angiogram

36. Coronary Angioplasty Video Link

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

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

39. 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

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

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

42. Collaborative Care Angina
Drug Therapy
-Adrenergic blockers
Calcium channel blockers

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

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

45. 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

46. 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

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

48. 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

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

50. 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 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

51. 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

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

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

54. Clinical Manifestations
ACS encompasses:
Unstable angina
Myocardial infarction (MI)

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