Chronic stable angina Non Pharmachologic Therapy

1. Seyed Mohammad Hashemi Professor of Cardiology Chronic stable anginaNon Pharmachologic Therapy

2. Angina • A careful historyand physical examination is critical to accurately establish the diagnosis of angina pectoris and to excludeother causes of chest pain.

4. Pathophysiology of ischemic chest pain • Angina is caused by myocardial ischemia which occurs whenever myocardial oxygen demand exceeds oxygensupply

7. ProvokingFactors Of The Chest Pain • Angina is often elicited by activities and situations which increase myocardial oxygen demand, including physical activity, cold, emotional stress, sexual intercourse, meals, or lying down . • It has been strongly recommended that patients also be questioned about cocaine use .

8. Quality of the chest pain • Angina is often characterized more as a discomfortthan pain, and may be difficult to describe • squeezing, tightness, pressure, constriction, strangling, burning, heart burn, fullness in the chest,, lump in throat, ache, heavy weight on chest (elephant sitting on chest) • Levine sign

9. Radiation Of The Chest Pain • Angina often radiates to other parts of the body including the upper abdomen (epigastric), shoulders, arms (upper and forearm), wrist, fingers, neck and throat, lower jaw and teeth (but not upper jaw), and rarely to the back (specifically the interscapular region).

10. SiteOf The Chest Pain Visceral Pain • Visceral fibers enter the spinal cord at severallevels leading to poorly localized, poorly characterized pain. (discomfort, heaviness, dull, aching) • Heart, blood vessels, esophagus and visceral pleura are innervated by visceral fibers • Because of dorsal fibers can overlap three levels above or below, disease of thoracic origin can produce pain anywhere from the jaw to the epigastrum

11. SiteOf The Chest Pain Parietal Pain • Parietal pain, in contrast to visceral pain, is described as sharp and can be localized to the dermatome superficial to the site of the painful stimulus. • The dermis and parietal pleura are innervated by parietal fibers.

13. Timing Of The Chest Pain • Angina occurs more commonly in the morning due to a morning diurnal increase in sympathetic tone. Enhanced sympathetic activity raises heart rate, blood pressure, vessel tone and resistance (resulting in a reduced vessel diameter which causes any fixed lesion to be more occlusive), and platelet aggregability.

14. More than 5 min and less than 20 min. Time Of The Chest Pain

15. Associated symptoms of the chest pain • The most common : shortness of breath, may reflect mild pulmonary congestionresulting from ischemia-mediated diastolic dysfunction. • Other symptoms may include belching, nausea, indigestion, diaphoresis, dizziness, lightheadedness, clamminess, and fatigue.

16. The goals of the therapy of stable angina include: • Relief of symptoms (To improve quality of life) • Prevention or slowing of disease progression • Prevention of future cardiac events, such as MI, unstable angina, or the need for revascularization •  Improvement in survival

17. Nonpharmacologic and lifestyle measures Medical therapy, Percutaneous coronary intervention (PCI), surgical revascularization (CABG). These goals can be achieved with a variety of modalities including;

18. 1. Treatment of hypertension according to Joint National Conference VI guidelines • Blood pressure <140/90 or 130/85 mm Hg if heart failure or renal insufficiency; <130/85 mm Hg if diabetes •  2. Smoking cessation therapy • Smoking Complete cessation ACC/AHA Guidelines for Treatment of Risk Factors (class I) and Specific Goals

19.  3.Management of diabetes • Diabetes management HbA1c <7% •  4. Comprehensive cardiac rehabilitation program (including exercise) • Physical activity Minimum goal: 30 min 3 or 4 d/w Optimal goal: daily ACC/AHA Guidelines for Treatment of Risk Factors (class I) and Specific Goals

20. 5. LDL-lowering therapy in patients with documented or suspected CAD and LDL cholesterol ≥130 mg/dl, with a target LDL of <100 mg/dl • Lipid management Primary goal: LDL <100 mg/dl Secondary goal: If triglycerides ≥200 mg/dl, then non-HDL should be <130 mg/dl • Therapy to lower non-HDL cholesterol in patients with documented or suspected CAD and triglycerides >200 mg/dl, with a target non-HDL cholesterol <130 mg/dl ACC/AHA Guidelines for Treatment of Risk Factors (class I) and Specific Goals

21.  6. Weight reduction in obese patients in the presence of hypertension, hyperlipidemia, or diabetes mellitus • Weight management BMI 18.5–24.9 kg/m2 ACC/AHA Guidelines for Treatment of Risk Factors (class I) and Specific Goals

22. 1. Folate therapy in patients with elevated homocysteine levels  2. Identification and appropriate treatment of clinical depression to improve CAD outcomes  3. Intervention directed at psychosocial stress reduction ACC/AHA Guidelines for Treatment of Risk Factors (class IIb)

23. 1. Initiation of hormone replacement therapy in postmenopausal women for the purpose of reducing cardiovascular risk A  2. Vitamins C and E supplementation A  3. Chelation therapy C  4. Garlic C   5. Acupuncture C  6. Coenzyme Q C ACC/AHA Guidelines for Treatment of Risk Factors (class III)

24. occurrence of mild angina during the first stages of exercise with disappearance of chest pain at higher workloads despite a greater exercise. walk-through angina phenomenon during exercise 

25. Current Nonpharmacologic Antianginal Strategies • Exercise Training • Enhanced external counterpulsation (EECP) •  Endothelial function • Promotes coronary collateral formation •  Peripheral vascular resistance •  Ventricular function • Placebo effect

26. Transmyocardial revascularization (TMR) • Sympathetic denervation • Angiogenesis • Spinal cord stimulation (SCS) •  Neurotransmission of painful stimuli •  Release of endogenous opiates • Redistributes myocardial blood flow to ischemic areas Current Nonpharmacologic Antianginal Strategies

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

28. improved perfusion by stimulation of angiogenesis potential placebo effect anesthetic effect mediated by the destruction of sympathetic nerves carrying pain-sensitive afferent fibers Peri-procedural infarction. Rationale

30. Percutaneous Percutaneous TMR

31. EECP

32. Increases arterial blood pressure and retrograde aortic blood flow during diastole (diastolic augmentation). Cuffs are wrapped around the patients legs and sequential pressure (300mmHg) is applied in early diastole. EECP

33. 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 Patient selection