Ischemic Heart Disease - Medicine - ATOT

Topic: IHD, Angina, MI
Faculty: General Medicine
Course: BSc ATOT - 2nd year

1. ISCHEMIC HEART DISEASE Dr. Salman Ansari Kanachur Institute of Medical Sciences

2. Contents IHD Angina MI

3. IHD Other names : coronary heart disease or coronary artery disease(CAD) Definition : Group of heart diseases in which there is an imbalance between blood supply to the heart and oxygen demand

4. IHD consists of: stable angina acute coronary syndromes(includes unstable angina, STEMI, NSTEMI) It is a leading cause of death - 90 lakh deaths yearly STEMI=ST elevation Myocardial infarction NSTEMI=Non-ST elevation Myocardial Infarction

5. Etiology Main cause of myocardial ischemia: Coronary artery occlusion Due to coronary atherosclerosis Rare causes: Embolus vasculitis Vasospasm Shock Risk factors for IHD - SAME as risk factors for atherosclerosis

6. Etiology Modifiable Non-modifiable(constitutional) Risk factors Additional risk factors

7. Modifiable risk factors Hyperlipidemia : increase in serum cholesterol High levels of Low density lipoprotein(LDL) - “bad cholesterol” High-density lipoprotein(HDL) - “good cholesterol” Hypertension : increase in systolic and diastolic blood pressure Cigarette smoking : most important avoidable cause of atherosclerosis Diabetes mellitus

8. Non-modifiable/constitutional risk factors Age : risk increases with older age Sex : Males are more at risk Family history Race : blacks are at higher risk

9. Pathogenesis Exposure to risk factors ↓ Formation of fatty streaks ↓ lipoprotein particles accumulate inside intima and macrophages enter into the lesion ↓ macrophages ingest the lipoprotein and transform into "foam cells" ↓

10. Pathogenesis(...cont) macrophages release cytokines and lead to smooth muscle proliferation ↓ some foam cells die - formation of lipid-rich core ↓ fibrous tissue forms around lipid-laden macrophage - formation of fibrous cap ↓ this fully-developed plaque/atheroma can undergo calcification

11. Pathogenesis(...cont) ↓ plaque can bulge into lumen of coronary artery and narrow it ↓ thrombosis can occur, leading to complete block of blood vessel and causing acute coronary syndrome

12. Parts of the plaque Fibrous cap Lipid core shoulder

13. Stable plaque : thick cap, small core - unlikely to undergo rupture High risk plaque : thin cap, large core - likely to undergo rupture Complicated or advanced plaque : plaque which undergoes complications like

14. Stable Angina or Angina pectoris Definition : sudden and recurrent attacks of substernal chest pain due to transient(short-lasting) myocardial ischemia Causes : obstruction of coronary blood flow coronary vasospasm coronary thrombosis

15. Precipitating factors : Exercise Hypertension Anemia Pregnancy Emotional stress(anger, fright) hyperthyroidism Left ventricular hypertrophy

16. Clinical features Classical or stable or exertional angina pectoris : Constricting discomfort or squeezing pain in front of the chest Radiates to left arm, neck, jaw and less commonly to the right side Lasts for 2-5 minutes Levine’s sign : clenched fist held over chest Relieved by rest or sublingual glyceryl trinitrate

17. Types of angina Stable angina: occurs on exertion - 2-5 min Unstable angina : occurs even at rest - >20 min Refractory angina : angina not controlled by medical therapy Variant angina or Prinzmetal's angina : pain occurs without exertion and at rest usually - due to coronary vasospasm, commonly in women

18. NYHA classification of severity of heart failure

19. Investigations ECG : Normal when resting During an attack of angina, ECG shows signs of myocardial ischemia , like ST segment depression or elevation, with or without T-wave inversion Exercise Tolerance Test(ETT) or exercise ECG : Done using treadmill ECG, BP and general condition are monitored NOT DONE for suspected MI

20. Parts of the ECG: normal

21. Coronary angiography Echocardiography Blood tests: Cardiac biomarkers - Troponin I or T

22. Treatment of angina Stop smoking Reduce body weight Regular exercise - but not extreme Avoid walking or exercise after a heavy meal or in cold weather Anti-anginal drugs: Take sublingual nitrate before that any exertion that may cause angina

23. ABCDE A: Aspirin and Anti-anginal therapy B: Beta-blocker and Blood pressure C: Cigarette smoking and Cholesterol D: Diet and Diabetes E: Education and Exercise

24. 1) General measures - correct risk factors - treat HTN, DM - reduce cholesterol levels through diet and drugs - lifestyle modification: healthy diet and regular exercise

25. 2) Drug treatment : Anti-anginal drugs : 5 groups nitrates Beta-blockers Calcium channel blockers Potassium channel openers If channel antagonist

26. 1) Nitrates : E.g: glyceryl trinitrate(GTN, nitroglycerine), isosorbide dinitrate for prophylaxis and treatment GTN spray or sublingual

27. 2) Beta-blockers : Reduce workload on heart E.g: cardio-selective beta-blockers like atenolol, metoprolol non-selective: propranolol

28. 3) CCB : E.g: nifedipine, amlodipine 4) Potassium channel opener : E.g: nicorandil 5) If channel antagonist : E.g: ivabradine Other drugs: Aspirin, clopidogrel: antiplatelet effect Statins: to lower cholesterol levels

29. 3) Surgical treatment: revascularisation Percutaneous coronary intervention(PCI) : placement of stent to dilate the stenosed coronary artery Coronary artery bypass grafting(CABG)

30. PCI - stent placement

31. Myocardial infarction ‘’Heart attack’’ Definition : Decreased or complete cessation of blood supply to the myocardium, leading to infarction(death) of heart muscle

32. Etiology Coronary artery occlusion Due to: Coronary atherosclerosis Vasospasm Embolus Risk factors: same as IHD/atherosclerosis

33. Clinical features Prolonged cardiac pain : angina pectoris, radiating to left shoulder, neck or arm Lasts for more than 20 minutes Does not respond to sublingual GTN

34. Other features like: nausea and vomiting breathlessness anxiety, fear of impending death collapse Pain may be absent in diabetics - called ‘silent MI’

35. Complications Arrhythmia Ventricular fibrillation Atrial fibrillation Bradycardia Shock Re-infarct Ventricular aneurysm Mitral regurgitation

36. Investigations ECG changes : - in STEMI: ST segment elevation, with Q wave and inverted T-wave - NSTEMI: ST-segment depression, T-wave changes

37. Cardiac enzymes or cardiac biomarkers : - Creatine Kinase(CK-MB) - Lactate Dehydrogenase(LDH) - Cardiac Troponins: Troponin I(TnI), troponin T(TnT) - most sensitive and specific for MI

38. Chest X-ray

39. Management of MI Admit in cardiac care unit General treatment( ‘ M O N A C’) Specific therapy Aftercare

40. General treatment( ‘ M O N A C ’) M: Morphine 2-4 mg quarter 5-10 minutes to control chest pain O: Oxygen 4 L/min N: Nitroglycerine sublingual or spray A: Aspirin 160-325 mg to chew and swallow or C: Clopidogrel 300mg oral

41. - specific therapy : Thrombolysis or percutaneous coronary intervention(PCI) Beta blockers: to reduce workload of heart Treat complications like congestive failure and arrhythmias

42. - Aftercare Lifestyle and risk factor modification Secondary prevention therapy Aspirin and clopidogrel Beta blocker: lifelong ACE inhibitors Statins Nitrates

43. Examples of thrombolytics Alteplase(tissue plasminogen activator - tPA) Streptokinase Reteplase(rPA)

44. Questions: LE : Note on IHD, clinical features and management SE : Management of MI SA : Diagnosis of IHD Anti-anginal drugs

45. References: Archith Boloor, Ramadas Nayak - Exam Preparatory Manual Questions: [email protected] For notes, click here or scan: For PPT, scan: