1. The Heart -1 Updated for Spring 2008
Dr. Amitabha Basu MD

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: Clinical: Complication:
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
Nearly complete luminal occlusion. Following acute plaque change This produce myocardial infarction

21. Angina Pectoris Angina pectoris is characterized by: Type:
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 by complications 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 Time Gross Features Light Microscope Electron Microscope
Reversible Injury
Time
Gross Features
Light Microscope
Electron Microscope
0-½ hr
None
Relaxation of myofibrils; glycogen loss; mitochondrial swelling.

33. Morphology of Myocardial Infarction
Time from Onset
Gross Morphologic Finding
Hours
Pallor of myocardium
3 - 7 Days
Hyperemic border with central yellowing
Days
Maximally yellow and soft with vascular margins
7 weeks
White fibrosis

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

35. Irreversible cell death
Time from Onset
Microscopic Finding
0-30 min.
No change (E.M- Mitochondrial swelling)
Irreversible cell death ↓
1-3 hours
Few wavy fibers at the margin of MI.
4-12 hours
Loss of cross striations and edema.
12-24 hours
Coagulative necrosis, Marginal contraction bands necrosis, ( and PMNs infiltrate).

36. Plenty of PMNs and coagulation necrosis
Time from Onset
Microscopic Finding
Hours
Plenty of PMNs and coagulation necrosis
4-7 days
Macrophage & mononuclear infiltration
10-21 Days
prominent granulation tissue
7-8 Wk
Fibrosis: Healing

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

38. 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. In MI the ratio of 1: 2 is >1.5
Biochemistry of MI
Elevated by
Peak
Return to normal
MYOGLOBIN
may rise immediately
CK- MB
4-8 hr
18-20hr
2-3 days
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 Elevated by Peak Return to normal
Cardiac specific Troponin I and T
3-6 hr
16-20hr
7-10 days
LDH
( level depends on the amount of cell death)
24hr
3-6 days
8-14 days
In MI, LDH “Flip” occur.
Normally LDH2 > LDH1,
After MI : LDH1 > LDH2

44. Enzymes

45. Complications of MI Arrhythmias with possible "sudden death”
(ventricular fibrillation)
Occur immediately
[ MOST COMMON cause of sudden death in MI]
Acute fibrinous pericarditis
Typical onset: Second or third day
Late: Dressler syndrome
Rupture of the wall and tamponade or VSD
3-7 days after the MI
Papillary muscle rupture and mitral incompetence

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 Mural thrombi and thrombo-embolism:
Infarct of Brain, kidney, Intestine
1wk or >
Carcinogenic shock (10% cases)
MI is the most common cause of Cardiogenic shock.
Multi-organ failure
Extension of infarct or repeat 2nd infarction- ? diagnosis
Any time and the most common cause of sudden death weeks after an MI
Ventricular aneurysms
Late complication

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

49. Rupture of the ventricular septum (L) and papillary muscle (R)
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 .

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

51. Clinical Features of Myocardial Infarction
Severe, crushing substernal chest pain.
Pain radiate to either:
Neck ,Epigastrium,Shoulder.
Or left arm.
In up to 50% of cases, pain is preceded by episodes of angina pectoris.

52. Diagnosis of Myocardial Infarction
EKG – ST elevation changes, T wave inversion and Q wave- transmural infarct.
Echo cardiogram
Myocardial enzyme markers
Creatinine Kinase
Troponins
Lactate dehydrogenase, Myoglobin

53. Sudden Cardiac Death (SCD)
Mechanism of SCD is most often a lethal arrhythmia .
Commonest cause = I.H.D
Other causes:-
Aortic stenosis
2nd Myocardial infarct
M.V. prolapse
Cardiomyopathy
Myocarditis

54. Thank you