1. CORONARY ARTERY DISEASE

2. Coronary Artery Disease (Ischemic Heart Disease)
Commonest cause of heart disease
The single most important cause of death worldwide
Almost always due to atherosclerosis
Sometimes: non- atherosclerotic CAD e.g. connective tissue disease

3. Clinical manifestations and pathology
Chronic stable angina pectoris (angina)
Unstable angina
Acute myocardial infarction
Congestive heart failure
Arrhythmia
Sudden death

4. Clinical manifestations and pathology
Stable angina: ischemia due to fixed atheromatous obstruction of one or more coronary arteries
Unstable angina: ischemia caused by dynamic obstruction of a coronary artery due to plaque rupture with superimposed thrombosis and spasm

5. Clinical manifestations and pathology
Myocardial infarction: myocardial necrosis caused by acute occlusion of a coronary artery due to plaque rupture and thrombosis
Heart failure: myocardial dysfunction due to myocardial infarction or ischemia

6. Clinical manifestations and pathology
Arrhythmia: altered conduction due to ischemia or infarction
Sudden death: ventricular arrhythmia, asystole, or massive myocardial infarction

7. Chronic stable angina pectoris

8. Chronic stable angina pectoris
Angina: symptom complex caused by transient interruption of myocardial blood flow
Caused by a fixed obstruction to the coronary artery by coronary atheroma
May also occur in other conditions e.g. aortic stenosis and hypertrophic cardiomyopathy

9. Pathophysiology
Symptoms occur because of imbalance of myocardial oxygen supply and demand
Factors determining myocardial oxygen demand:
Heart rate
Myocardial contractility
LV afterload

10. Pathophysiology
Factors influencing myocardial oxygen supply (coronary blood flow):
Duration of diastole (heart rate)
Coronary perfusion pressure (Ao _ coronary sinus or RA pressure)
Coronary vasomotor tone
Oxygen content of blood: Hb concentration, oxygen tension

11. Clinical Features: Symptoms
Chest pain
Discomfort rather than
pain
Areas of distribution:
Chest, back, upper
abdomen, neck, shoulder,
left arm, right arm, lower
jaw

12. Clinical Features: Symptoms
Chest pain
Aggravation:
exercise, emotion,
heavy meals, intercourse,
exposure to cold
Relief:
Rest,
sublingual nitroglycerine

13. Clinical Features: Symptoms
Character: oppressing, crushing, squeezing, vice-like
Dyspnea:
ischemia may manifest as exertional dyspnea (angina-equivalent dyspnea)

14. Clinical Features: Signs
Usually normal in between the attacks
Physical examination should focus on the predisposing conditions and consequences:
Hypertension
Valvular disease (aortic stenosis)
Anemia
thyrotoxicosis

15. Clinical Features: Signs
Physical examination should focus on the predisposing conditions and consequences:
LV dysfunction (cardiomegaly, gallop rhythm): unusual except in advanced cases
Carotid bruits
Peripheral vascular disease

16. Differential diagnosis
Other forms of IHD: unstable angina, myocardial infarction
Pericarditis
Aortic dissection
Pulmonary embolism
Pneumothorax
Extra-cardiac: Esophageal spasm, peptic ulcer, cholelithiasis, etc.

17. Investigations Resting ECG Exercise ECG Other stress testing
Coronary angiography

18. Investigations: Resting ECG
Usually normal, even with the most severe forms of coronary artery involvement
ECG features of angina include ST segment depression or elevation at the time of exercise which revert to normal at rest

19. Exercise ECG
Horizontal or downsloping ST segment depression of 1 mm or more

20. Ischemic ST-T Changes

21. Exercise Tolerance Test (ETT)
Test interpretation:
High risk ETT:
Low threshold for ischemia
Fall in BP during exercise
Widespread, marked or prolonged ischemic changes
Exercise-induced arrhythmia

22. Other Forms of Stress Testing
Myocardial perfusion scanning (radio-isotope agents)
Stress echo (exercise echo, dobutamine stress echo)

23. Coronary Angiography
Determines the anatomic nature of the disease i.e.
the number of vessels involved
the site of involvement
the extent of disease in each vessel
the status of the left ventricle

24. Coronary Angiography
Usually done for patients in whom mechanical intervention (i.e. CABG or PCI) is contemplated
Not done for all patients with chronic stable angina

25. Indications for Coronary Angiography
When exercise testing gives high risk positive result
In patients with stable angina who survive cardiac arrest
In patients with serious ventricular arrhythmias
Recurrence of angina after myocardial revascularization
When non-invasive testing fails to identify the cause of atypical chest pain

26. Aims of Management
The aim of non interventional management is NOT to decrease the atheroma size but to change its constituents so that the lipid core becomes smaller and the fibrous cap thicker, thereby rendering the atheromatous plaque less liable for rupture

27. Management Strategies
Treat and abolish symptoms
Identify and treat risk factors
Identify and treat other complications of atherosclerosis (e.g. cerebrovascular, renovascular etc.)
Select patients who should undergo mechanical intervention

28. Steps of Management Exercise testing Life style modification
Pharmacologic therapy:
To control symptoms
To control risk factors
Intervention

29. Stress Testing
Should be performed in most patients with chronic stable angina:
To identify the level of risk
To serve as a background against which to compare during future assessment

30. Stress Testing
ETT should be repeated routinely every year to follow up the patient.
Also, it should be repeated in case of any exacerbation of symptoms or change in angina pattern

31. Life Style Modification
Smoking
Obesity
Diet
Exercise:
To the point that produces angina: may promote the development of collaterals
Should never be continued if angina develops
Severe unaccustomed exercise: Avoided!
Avoid exercise after heavy meal or in the cold

32. Pharmacologic Therapy of Angina
Antiplatelet agents:
Aspirin
Clopidogrel
Statins
Anti-anginal drugs
nitrates
Beta blockers
Calcium channel blockers
Ivabradine

33. Statins Administered to keep LDL level ≤ 100 mg/dl (2.5 mmol/L)
Should be administered at night
Side effects include hepatic injury and myositis

34. Antiplatelet Therapy
Asprin: low dose ( mg/day) should be administered for life
OR:
Clopidogrel: may be an alternative to ASA in patients who develop side effects

35. Anti-anginal Drugs: Nitrates
Short acting nitrates: glyceryl trinitrate (GTN) preparations:
Sublingual tablets
Sublingual spray
Buccal
Long acting nitrates:
isosorbide dinitrate
Isosorbide mononitrate

36. Side Effects of Nitrates
Headache:
usually subsides with continuation
Nitrate tolerance:
Loss of action when nitrates are continuously administered throughout the day
Avoided by allowing 6-8 hours nitrate-free interval

37. Side Effects of Nitrates
Pronounced hypotension:
Especially in patients who have taken sildenafil (Viagra) & other PDE 5 inhibitors
Nitrates should never be administered within 24 hours of ingesting sildenafil
May cause syncope

38. Anti-anginal Drugs: β-Blockers
Cardio-selective β-blockers:
E.g. atenolol, metoprolol, bisoprolol
Block β-1 but not β-2 adrenergic receptors
Have less extracardiac side effects (e.g. asthma)
Non-cardioselective β-blockers:
E.g. propranolol, nadolol, carvedilol

39. Anti-anginal Drugs: β-Blockers
Mechanism of Action in Angina: reduce myocardial oxygen consumption by reducing:
heart rate
blood pressure
myocardial contractility

40. Side Effects of β-blockers
Cardiovascular:
Bradycardia and heart block
Hypotension
Worsening of heart failure
? Exacerbation of peripheral vascular disease
Extracardiac side effects:
Bronchospasm: especially with non-selective forms

41. Implementation of β-blockers
Should be introduced in a dose sufficient to reduce the heart rate (50-60/min at rest)
They should not be withdrawn abruptly from the patient as this may precipitate myocardial infarction
Some β-Blockers are useful in the presence of LV systolic dysfunction e.g.
bisoprolol, carvedilol, metoprolol

42. Anti-anginal Drugs: Calcium Channel Blockers (Calcium antagonists)
Two major groups:
Dihydropyridines e.g. nifedipine, amlodipine
Non-dihydropyridines: verapamil, diltiazem

43. Calcium Antagonists: Mechanism of action
Inhibit the slow calcium influx into excitable tissue of vascular smooth muscle cells and myocardium:
Reduce blood pressure
Reduce myocardial contractility
Non-dihydropyridines also reduce heart rate

44. Side Effects of Calcium Antagonist
Non-dihydropyridine group may cause severe bradycardia and congestive failure
Dihydropyridine group may cause reflex tachycardia but have minimal effect on cardiac contractility
Other S.E: headache, flushing, edema, polyruia

45. IVABRADINE Acts on the SA node Inhibits fast sodium channels (If)
Slowing of HR
No effect on myocardial contractility
Very useful when the patient still has tachycardia despite full dose β blocker

46. Mechanical Intervention
Percutaneous Coronary Intervention (PCI)
percutaneous transluminal coronary angioplasty (PTCA)
Coronary Artery Bypass Grafting (CABG)

47. PCI Provides effective symptomatic treatment
No evidence that it prolongs survival in patients with chronic stable angina

48. PCI
Patients with 3-vessel disease or LMCA are increasingly treated by PCI
Main problem: recurrence of stenosis

49. CABG Usually through a midline sternotomy incision
Grafts are liable for degeneration or recurrence of atherosclerosis
Arterial conduits survive longer than venous ones

50. Prognosis of Stable Angina
Determined by:
The patient’s performance on exercise testing
The number of vessels involved
The status of LV function