The Heart -1 Updated for Spring 2008

1. The Heart -1Updated for Spring 2008 Dr. Amitabha BasuMD

2. Topic • Heart failure • Ischemic heart disease

3. Congestive heart failure • Def: reduced cardiac output to meet the demand. • In many pathologic states, the onset of heart failure is preceded by cardiac hypertrophy. • Pathogenesis: flow chart next slide.

4. Flow chat Increased work load, MI, pressure/ volume overload ↓ re-expression of embryonic/fetal type of protein (β-myosin heavy chain) + Reduced capillary density → reduced oxygen supply ↓ Heart failure These re-expression of embryonic/fetal type are associated with myocardial hypertrophy.

5. Congestive heart failure • So, it is long term process. • Clinical: similar to RHF • Often progress from the underling diseases like • Hypertension • Cor-pulmonale • Valvular disease • Multiple MI

6. Morphology of congestive heart failure Concentric hypertrophy Pressure over load Caused By: hypertension Narrow chamber and thick wall Eccentric hypertrophy Volume over load. Caused by valve regurgitations Dilated chamber/thick wall END

7. Left Heart failure • Left heart failure: etiology • Ischemic heart disease • Hypertension • Aortic / Mitral valve disease • Presentation: acute onset of dyspnea, pulmonary edema, rales, S3 gallop. • Complication: Cardiogenic shock

8. Pulmonary congestion and edema. Intraalveolar pale pink, low protein, few lymphocytes fluid: Transudate)

9. Right heart failure • Etiology: • Left heart failure and Cor-pulmonale • Clinical: • jugular venous distension, hepatoslemegaly, dependent edema, ascites, pleural effusion. • Complication: • Chronic passive congestion of liver (nutmeg liver) • Cardiac cirrhosis and centrilobular necrosis.

10. A classic case of progression of heart failure • Next slide

11. LVF ↓ Dyspnea ← Pul. Edema (T) + heart failure cells ← ↑Hydrostatic pr. ←PHT ↓ reduced lung edema ← ↓ Flow of blood in the lung ←RHF ↓ Increased (central) venous pressure ↓ ↑ Hydrostatic pressure in peripheral blood vessels in the soft tissue = Pitting (dependent edema) + Ascitis + Develop Passive venous congestion of various organs Liver: hepatomegaly (Nutmeg liver)/cardiac cirrhosis Spleen: congestive splenomegaly Kidney : Hypoxia (Sec. hypertension) PHT- pulmonary hypertension

12. Ischemic Heart Disease (IHD) Dr. Basu MD

13. Do you know • Propels over 6000 liters of blood through the body daily. • Beats more than 40 million times a year. • Yearly economic burden of ischemic heart disease is estimated to be in excess of $100 billion.

14. Topic • Definition • Types of IHD • Pathogenesis of Ischemic Heart Disease • Myocardial infarction

15. Ischemic Heart Disease • There is an imbalance between the myocardial demand and the blood supply. • Age: Male: middle age • Female : post menopausal • Epidemiology: leading cause of death for both males and females in the United States.

16. Types of ischemic heart disease • Angina ( with > 75% narrowing) • Angina pectoris (classical, stable angina) • Prinzmetal variant • Unstable angina • Myocardial infarction (100% occlusion) • Sudden cardiac death • Chronic ischemic heart disease Acute Coronary Syndrome

17. Pathogenesis of IHD • Narrowing (stenosis) of coronary artery: • Mostly fixed arthrosclerosis. • Complete obstruction (occlusion) of the lumen of coronary artery: • Thrombus developed on an atheroma / embolism**. • 75% or more narrowing: Ischemic symptoms (angina). • Complete occlusion (100% ): Infarction

18. Morphology- Angina • Fixed Atherosclerotic narrowing of the coronary artery. • This partial occlusion may produce angina.

19. Coronary artery showing: >75% narrowing, which would be associated with angina.

20. Nearly complete luminal occlusion. Following acute plaque changeThis produce myocardial infarction

21. Angina Pectoris • Angina pectoris is characterized by: • Intermittent chest pain caused by transient, reversible myocardial ischemia. • Type: • Typical or stable angina pectoris. • Fixed atherosclerotic narrowing (75% or greater). • Prinzmetal, or variant , angina. • Unstable angina pectoris (crescendo angina). • Preinfarction angina.

22. Typical or stable angina pectoris • Episodic chest pain associated with exertion or stress. • Pathogenesis: Fixed coronary atherosclerotic narrowing without plaque change ( > 75% but not full) • Pain is relived by rest or vasodilators (nitroglycerine) that reduce the venous return.

23. Prinzmetal Angina • Is a form of angina pectoris which • occurs at rest and • presumably stems from a coronary artery spasm with or without an obstructive lesion in the artery.

24. Unstable Angina (crescendo angina) • Pathogenesis: • acute plaques change but without 100% occlusion. • Clinical: • Increased frequency of anginal pain. • Pain precipitated by less exertion. • Pain is more intense and last longer. • High risk for Myocardial infarction.

25. Biochemical of angina • C-reactive protein (CRP) may serve as a marker to predict the risk of MI in patients with angina. • Also serve as a marker to predict the risk of new infarcts in patients who recover from infarcts.

26. Myocardial Infarction

27. Myocardial infarction Sudden (> 30 min.) pain May be in shock due acute LVF : Pulmonary edema. Statistics: In U.S. 1.5 million/yr. 25% die in acute phase within 1 hr. At age 45 –55 : M:F::4:1 At age 80 equal incidence among sexes

28. Pathogenesis of Myocardial Infarction – 100% Occlusive intracoronary thrombus By:- 1. Provoked bycomplications of Atheroma: E.g. : Rupture of plaque. 2. Coronary artery spasm: ? Smoking 3. Emboli (Source is the proximal part of same blood vessels).

29. Types of Myocardial Infarction • Subendocardial MI: • < 50% of the wall thickness • Any MI typically begins in this area (most poorly perfused area of the myocardium). • EKG: ST segment depression. • Transmural MI: • Necrosis extend externally and involve entire myocardium. • Most common type, take about 24 hrs to develop.

30. M.I: Sites of occlusion:infarction • LAD = Lt. Ant. Desc. A (40 –50%):- • Lt.Ventricle : anterior and apical • Ant.2/3 of Inter Ventricular Septum (IVS) • RCA= Rr. Coronary A (30 40%) • Lt.Ventricle : post. wall • I.V.S.post.1/3 • LCX= Lt. Circumflex A(15-20%):- • Lt.Ventricle -- lateral wall

31. LAD occlusion Right Coronary occlusion Left Circumflex occlusion

32. Morphology Reversible Injury

33. Morphology of Myocardial Infarction

34. Acute myocardial infarct, predominantly of the posterolateral left ventricle SCAR

37. 1 to 3 hours wavy fibers (elongated and narrow), compared with adjacent normal fibers (at right).

38. 12 -24 hrs. Contraction band necrosis : Note the many irregular darker pink wavy contraction bands extending across the fibers. CONTRACTION BANDS

39. Remote infarction ( left Trichrome stain: showing blue collagen).

40. MECHANISM of reperfusion injury • Generation of oxygen free radicals from infiltrating leukocytes • And apoptosis.

41. Effect of reperfusion injury

42. Biochemistry of MI CK-MB Isoform 1 & 2 Normal ratio of 1 : 2 = 1.2 In MI the ratio of 1: 2 is >1.5

43. Biochemistry of MI In MI, LDH “Flip” occur. Normally LDH2 > LDH1, After MI : LDH1 > LDH2

44. Enzymes

45. Complications of MI

46. Cardiac tamponade Occur due to hemopericardium. ↑ pericardial pressure = ↓ diastolic filling of the ventricles, and hence in stroke volume Signs: Sudden drop in systolic and well as diastolic blood pressure. Distended jugular vein. Right ventricular and right atrial collapse.

47. OTHERS complications

48. Myocardial rupture in an acute infarct in the wall : ? consequence Hemopericardium Cardiac tamponade:- Acute chest pain/ sudden drop of BP

49. Left-to-right shunt and right heart failure. Pan systolic murmur Produce sudden mitral insufficiency. Holosystolic murmur (laterally at the apex of the heart with the patient in the left lateral decubitus position) radiated to axilla . Rupture of the ventricular septum (L) and papillary muscle (R)

50. left ventricular aneurysm: does not contract , so the ejection fraction and stroke volume of the heart are reduced- patient feels week!.