1. Ischemic Heart Disease BY Ragab Abdelsalam.(MD) Prof. of cardiology

2. * Clinical Presentations : The clinical presentation of ischemic heart disease usually depends on the underlying mechanism.

3. Presentation & Mechanism 1-Stable Angina -Transient myocardial - ischemia on exertion. 2- Unstable Angina: - Prolonged ischemia. - Plaque fissuring >  minimal myocardial damage. 3-Prinzmetal (variant) angina: Coronary spasm. 4- Acute Myocardial Infarction:Coronary artery occlusion with tissue necrosis.

4. 5- Silen Ischemia: Asymptomatic episodes of ST – segment depression, due to reversible abnormalities of myocardial metabolism, and usually occurs with autonomic dysfunction (as in DM) diabetes mellitus.

5. 6- Syndrome – X:Typical >>Anginal pain with positive exercise test and normal coronary Angiorgaphy 7-Heart Failure: > Loss of contractile function, Aneurysm,Fibrosis,Ischemic cardiomyopthy. 8-Conduction defects: >> Edema & Necrosis, Fibrosis. 9-Arrhythmia >> Electrical Instability 10-Sudden death: Any of the above plus ventricular arrhythmias.

6. Angina Pectoris Definition: It is a clinical syndrome of a distinctive chest pain due to temporarily insufficient myocardial blood supply

7. * Types: A) It is either : 1- Stable 2- Unstable

8. b) Clinical background: Post – infarction Angina. Post – PTCA Angina. Post CABG Angina

9. c) Specific Forms: - Prinzmetal’s Angina (Spastic). - Post – Prandial. - 2nd – wind Angina. - Cocaine intoxication.

10. Etiology: *Pathogenesis of pains:  >> Decrease blood flow  >> Hypoxia  accumulation of metabolites (Lactic acid, pyruvic, histamine ….) stimulate the never endings via upper 4 thoracic segments to the Brain>>>>>pain.  >>

11. * Risk Factors: Major Minor Hypertension. -Type A personality. Diabetes mellitus. -Inactive (Sedentary) life. Dyslipidemia. -Stress. Family History. -Male Sex. Smoking - Age - Obesity

12. *Precipitating Factors: Heavily exersion. Emotion. Cold. Digestion (Heavy meals). Tachycardia. Smoking.

13. * Clinical data: A- Pain: The typical Anginal pains. > Character: Strangling, heaviness. Chocking, dull, ache, & sense of (anger animi). > Site: Retrosternal. > Degree : Mild or moderately severe but rarely of intense or crushing as in AMI. > Radiation : From left retrosternal to left shoulder, left arm, little finger, Jaw, back & sometimes to epigasterium & right. Shoulder. > Effort: It is exertional chest pain.

14. B - Autonomic effects: sweating, irritability, diaphoresis C - Physical Examination Hands  > Nicotine stains Pulse & Blood pressure Eyes: (arcus, xanthelasma.)

15. Heart : There may be Aortic stenosis, or HOCM or S4 & S3, MR. Or normal findings. Other systems  >> Comorbidity

16. * Investigation : A Basic Investigations: Electrocardiogram (ECG). Exercise ECG – Treadmill or Bicycle.

17. B) Specialized Investigations: > Radionuclide Perfusion Imaging. > Stress Echocardiography. > Coronary Angiography.

18. C- Other Imaging Techniques: > Magnetic Resonance Imaging (MRI). > Ultrafast computed Tomography (UCT). > Posterior Emission Tomography (PET). > Colour Kinesis. > Contrast Echocardiography

19. * Summary Of Treatment > Initial: Sublingual nitrate. Sublingual crushed 75 mg Aspirin

20. Then:  > Risk Stratification  > Control risk factors  Drugs : > B. Blocker. e.g.  Atenolol > Calcium channel blockers  e.g. deltiazem. > Long – acting nitrates.  e.g. nitroglycerin > Aspirin. Acetylsalsylic acid 75 mg > Metabolic agents as trimetazidine.

21. * Revascularization: –PTCA (Percutaneous Transluminal coronary angioplasty). –CABG (Coronary Artery Bypass Grafting).

22. Acute Coronary Syndromes * These syndromes represent a dynamic spectrum of a similar disease process, being part of a continuum * Each syndrome is associated with specific strategies in prognosis and management

25. * The three major syndromes are 1-Unstable angina. 2- Non – ST elevation 3-myocardial infraction.

26. * Pa t hophysiology : >. All of the coronary syndromes are initiated by the same event: >> Rupture of an unstable plaque  leads to  Coronary artery occlusion: > Intermittent occlusion  Unstable Angina > Complete occlusion  AMI

29. The 3 “I” S of coronary artery events, means: > Ischemia. >Injury. > Infraction.

30. Ischemia: Occurs with a mismatch between blood flow and oxygen need by a section of the heart.  >>> Pain Rapidly reversed by : > Reducing O2 – need. > Increasing O2 supply.

31. Injury: Total occlusion  >> more prolonged ischemia  >> damage  >> Hyperacute symptoms of a classic AMI. > Occurs within 20-40 min. > Cardiac dysfunction. > Conduction of impulses may be altered. Pain is severe but  serum markers are not yet released.

32. Infraction actual death of the injured myocardial cells. Necrosed cells  >> loss of cell wall integrity >>  release of intracellular components such as: - Myoglobin. - Creatine phosphokinase (CPK). - Troponins. ** These enzymes are measured as serum markers of infarction.

33. * Electrocardiogram (ECG) a-Ischemia: - < 20 min. - Peaked T – waves. - Inverted T – waves. - Depressed ST – segment.

34. b) (20 – 40 min)  >> ST – segment elevation.

35. c) Infraction: - >1-2 hours - Abnormal Q – waves.  2 mm wide or.  25 % height of R – wave, in that lead.

36. * Clinical data: 1) Symptoms: –Chest pain: Typical chest pain, severe, but prolonged & sense of impending death. (Angor Animi). –Nausea, vomiting, sweating, dizziness, extreme weakness and dyspnea. –Symptoms of complications. Silent – painless myocardial infarction

37. Symptoms of complications. > As, dyspnea PND, irritability, palpitation –Silent – painless myocardial infarction: In diabetics. In elderly.

38. * Signs: Anxious patient. Signs of cardiogenic shock if present: Cold sweats. Peripheral cyanosis. Hypotension, thready pulse. Oligurea.

39. > Pulse: Arrhythmias may be detected. > Low grade fever ** Auscultation: > First heart sound may be make. > Pulmonary component of S2 may be accentuated. > Third heart sound. > Pericardial friction rub if pericarditis occurs

40. > Murmur of mitral regurgitation or VSD if complications occur. > Moist rales may be heard at the base of the lungs. ** However, auscultation may reveal no abnormality.

41. Investigation: - Electrocardiogram (ECG). -ECG monitoring. -Cardiac enzymes: > Troponins. > Myoglobin. > SGOT. > LDH. > CPK – isoforms. - Echocardiography. - Radionoclide scintigraphy. - Cardiac catheterization.

42. Complications of AMI A) Early: - Arrhythmias. - Acute heart failure. - Cardiogenic shock. - Acute mitral regurgitation. - Ventricular septal rupture or free wall rupture. - Acute pericarditis. - Mural thrombosis. - Sudden death.

43. B) Late: - Dressler’s syndrome  >> fever, joint pain, pleurisy & pericarditis. >> has a dramatic response to indomethacin or corticosteroids. - Myocardial Aneurysm and thrombus. -Chronic heart failure -ischemic cardiomyopathy.

45. Assessment and treatments of (ACS ) I- Initial Assessment: - Rapid, but detailed History. - Vital signs & physical examination. - 12 – lead ECG & serial ECG. - X – ray on chest. - Enzymatic Assessment.

46. 2- Initial General Treatment: ** Memory aid “ MONA” M >>  Morphine = pain killer 2-4mg / 5-10 min. O >>  Oxygen : 4L / min. N >>  Nitroglycerin : SL or I.V. A >>  Aspirin : 160 – 325 mg (Chew).

47. 3- Specific Treatment: > Reperfusion therapy : only for patients with S-T segment elevation or new LBBB. >Thrombolytic agents: (door – to – needle time < 30 min). > Primary PTCA : (door – to – dilation time < 60 min

48. Conjunctive therapy : combined with thrombolytic agents: -Aspirin. -Heparin. Adjunctive therapies : Agents given instead of or in addition to thrombolytic agents: -

49. - IV nitroglycerin. - B-Blockers. - ACE – inhibitors especially in: Large infarction. Heart failure. Hypertension.

50. THANK YOU