1. Coronary Artery Disease and Acute Coronary Syndrome

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

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

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

5. 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

6. 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

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

8. 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

9. 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

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

11. Response to Endothelial Injury
Fig. 33-3

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

13. 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

14. Collateral Circulation
Fig. 33-5

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

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

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

18. 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

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

20. 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

21. Silent Ischemia

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

23. 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

24. 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

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

26. Location of Chest Pain
Fig

27. 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

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

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

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

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

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

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

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

35. 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

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

37. 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

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

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

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

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