2.  Feel better  Live longer

3.  To improve quality of life (symptoms)  To reduce mortality  To reduce morbidity  To reduce progression of disease and induce regression.

4.  Left ventricular function  Number of coronary arteries with significant stenosis  Extent of jeoporized myocardium

5. Risk stratification  Noninvasive testing  Cardiac catheterization

6.  Physical exam  CXR  Echocardiogram

7.  History  Baseline Electrocardiogram  Exercise Testing

8.  Class I  Class II  Class III  Class IV  Angina only with extreme exertion  Angina with walking 1 to 2 blocks  Angina with walking 1 block  Angina with minimal activity

12.  Hypertension  Smoking  Dyslipidemia  Diabetes Mellitus  Obesity  Stress  Homocysteine

13. Treatment of Chronic Stable Angina Medical Revascularization PCIACBG

14.  Medical Treatment

16.  ANTIPLATELETS  BETA BLOCKERS  NITRATES  CALCIUM ANTAGONIST  ACEI  STATINS  NEW THERAPIES

17.  Effect on myocardium  Effect on cardiac conduction system  Effect on coronary/systemic arteries  Effect on venous capitance system  Circadian rhytm

19.  1. Aspirin in the absence of contraindications A  2. Beta-blockers as initial therapy in the absence of contraindications in patients with prior myocardial infarction or without prior myocardial infarction A,B  3. ACE inhibitor in all patients with CAD who also have diabetes and/or LV systolic dysfunction A  4. LDL-lowering therapy in patients with documented or suspected CAD and LDL cholesterol >130 mg/dl, with a target LDL of <70 mg/dl A  5. Sublingual nitroglycerin or nitroglycerin spray for the immediate relief of angina B  6. Calcium antagonists † or long-acting nitrates as initial therapy for reduction of symptoms when beta blockers are contraindicated B†  7. Calcium antagonists † or long-acting nitrates in combination with beta blockers when initial treatment with beta blockers is not successful B †  8. Calcium antagonists † and long-acting nitrates as a substitute for beta blockers if initial treatment with beta blockers leads to unacceptable side effects†

20.  1. Clopidogrel when aspirin is absolutely contraindicated  2. Long-acting non-dihydropyridine calcium antagonists † instead of beta blockers as initial therapy B†  3. In patients with documented or suspected CAD and LDL cholesterol 100–129 mg/dl, several therapeutic options are available: B a. Lifestyle and/or drug therapies to lower LDL to <70 mg/dl b. Weight reduction and increased physical activity in persons with the metabolic syndrome c. Institution of treatment of other lipid or non-lipid risk factors; consider use of nicotinic acid or fibric acid for elevated triglycerides or low HDL cholesterol  4. ACE inhibitor in patients with CAD or other vascular disease

21.  Decrease myocardial oxygen consumption  Blunt exercise response  Beta-one drugs have theoretical advantage  Try to avoid drugs with intrinsic sympathomimetic activity  First line therapy in all patients with angina if possible

25.  Bronchospasm  Diminished exercise capacity  Negative inotropy  Sexual dysfunction  Bradyarrhythmia  Masking of hypoglycemia  Increased claudication  Hair loss

26.  Propranolol  Atenolol  Metoprolol  Carvediloll

28.  Arterial dilation/after-load reduction  Coronary arterial vasodilation  Prevention of coronary vasoconstriction  Enhancement of coronary collateral flow  Improved subendocardial perfusion  Slowing of heart rate with diltiazem, verapamil

32.  Palpitations  Headache  Ankle edema  Gingival hyperplasia

33.  Verapamil  Diltiazem  Nifedipine  Nicardipine  Amlodipine  Felodipine  Nisoldipine  Bepridil

37.  Nitric oxide has been identified as endothelium-derived relaxing factor  Organic nitrates are therapeutic precursors of endothelium-derived relaxing factor

38.  Venous vasodilation/pre-load reduction  Arterial dilation/after-load reduction  Coronary arterial vasodilation  Prevention of coronary vasoconstriction  Enhancement of coronary collateral flow  Antiplatelet and antithrombotic effects

43.  Smaller doses  Less frequent dosing  Avoidance of long-acting formulations unless a prolonged nitrate-free interval is provided  Build-in a nitrate-free interval o 8-12 hours

44.  Headache  Flushing  Palpitations  Tolerance

45.  Isorbide dinitrate  Isorbide mononitrate  Long-acting transdermal patches  Nitroglycerin sl

48.  1. Treatment of hypertension according to Joint National Conference VI guidelines A  2. Smoking cessation therapy B  3. Management of diabetes C  4. Comprehensive cardiac rehabilitation program (including exercise) B  5. LDL-lowering therapy in patients with documented or suspected CAD and LDL cholesterol ≥100 mg/dl, with a target LDL of <70 mg/dl A  6. Weight reduction in obese patients in the presence of hypertension, hyperlipidemia, or diabetes mellitus C

49.  Smoking Complete cessation  Blood pressure <140/90 or 130/85 mm Hg if heart failure or renal insufficiency; <130/85 mm Hg if diabetes  Lipid management Primary goal: LDL <70 mg/dl Secondary goal: If triglycerides ≥200 mg/dl, then non-HDL should be <130 mg/dl  Physical activity Minimum goal: 30 min 3 or 4 d/w Optimal goal: daily  Weight management BMI 18.5–24.9 kg/m2  Diabetes management HbA1c <7%

50.  CABG

52.  1. CABG for patients with significant left main coronary disease A  2. CABG for patients with triple-vessel disease. The survival benefit is greater in patients with abnormal LV function (ejection fraction <0.50)A  3. CABG for patients with double-vessel disease with significant proximal LAD CAD and either abnormal LV function (ejection fraction less than 50%) or demonstrable ischemia on noninvasive testing A  4. Percutaneous coronary intervention for patients with double-or triple-vessel disease with significant proximal LAD CAD, who have anatomy suitable for catheter-based therapy and normal LV function and who do not have treated diabetes B

53.  5. PCI or CABG for patients with single- or double-vessel CAD without significant proximal LAD CAD but with a large area of viable myocardium and high-risk criteria on noninvasive testing B  6. CABG for patients with single- or double-vessel CAD without significant proximal LAD CAD who have survived sudden cardiac death or sustained ventricular tachycardia C  7. In patients with prior PCI, CABG or PCI for recurrent stenosis associated with a large area of viable myocardium or high-risk criteria on noninvasive testing C  8. PCI or CABG for patients who have not been successfully treated by medical therapy and can undergo revascularization with acceptable risk B

54.  65% remain symptom-free at ten years  85% remain free of fatal/nonfatal MI at ten years  Mortality of 2-3% yearly over ten years  2.5% incidence of perioperative MI

55.  Three major randomized trials A. VACS B. ECSS C. CASS  Improved mortality in CABG group A. L-main CAD B. 3-vessel CAD, esp. with decreased EF C. LAD disease, severe angina, decreased EF

56.  PTCA

57.  80% or greater success rate  1% mortality  3-5% emergency CABG ( prior to stenting )  4% acute MI

58.  Initiate pharmacologic treatment A. Nearly half of patients will become asymptomatic  PTCA preferred alternative if medical therapy does not relieve angina or causes adverse effects

59.  Initial medical management in patients with mild ischemic symptoms and normal LV function  Revascularization in patients who fail medical therapy  Selection of PTCA vs. CABG depends on coronary anatomy, LV function, need for complete revascularization, and patient preference

60.  CABG in patients with left-main disease or 3-vessel CAD and decreased LVEF  PTCA or medical management an alternative in patients with 3-vessel CAD, mild symptoms, and preserved LVEF

61. NEW THERAPIES

62.  RANOLAZINE (Ranexa™; CV Therapeutics, Inc.), a drug that has been in development for 20 years. It is a Sodium Channel Blocker.  NICORANDIL, a potassium channel activator, and also has a Nitrogen Donating Moeity.  IVABRADINE, inhibits the I f channel in the sinus node and thereby causes bradycardia without any negative inotropic effects.

63. Ranolazine Consequences of ischemia Electrical instability Myocardial dysfunction ( ↓ systolic function/ ↑ diastolic stiffness) Conventional anti-ischemic medications ß blockers Nitrates Ca ++ blockers Compression of nutritive blood vessels Ischemia (Ca 2+ overload) ↑ O 2 demand Heart rate Blood pressure Preload Contractility ↓ O 2 supply Development of ischemia (Stone, 2004)

64. Diseases (eg, ischemia, heart failure) Pathological milieu (reactive O 2 species, ischemic metabolites) Toxins and drugs (eg, ATX-II, etc.) Na + channel (Gating mechanism malfunction) Increase ATP consumption Decrease ATP formation Oxygen supply and demand Abnormal contraction and relaxation ↑ diastolic tension ( ↑ LV wall stiffness) Mechanical dysfunction Early after potentials Beat-to-beat Δ APD Arrhythmias (VT) Electrical instability

65. Ischemia ↑ Late I Na Na + overload Diastolic relaxation failure (increased diastolic tension) Extravascular compression Ca 2+ overload Ranolazine inhibits the late inward Na current

66.  Surgical  surgeons use the laser to make between 20 and 40 tiny (one-millimeter-wide)

68.  Percutaneous

69. EECP

70.  Angina class III/IV Refractory to medical therapy Reversible ischemia of the free wall not amenable for revascularization  Excluded if LVEF<20% or had current major illness