Commonent cause of death worldwide

1. Ischaemic Heart Disease
Dr. Jyoti Priyadarshini Shrivastava
Associate Professor
Department of Pathology
Gajra Raja Medical College

2. Blood Supply of Heart
 Rt.and Lt.Coronary Arteries-Arise from root of AORTA
 Supply blood during Diastole
 Veins: Cardiac Vein and Coronary Sinus
 Myocardium-Max.Supply

4. Site of Infarct: Distal to the occlusion

5. TERMS
Ischaemia: Ischemia is a restriction in blood
supply to tissues, causing a shortage of oxygen that is
needed for cellular metabolism (to keep tissue alive).
Infarction: Tissue death (necrosis) due to inadequate
blood supply to the affected area. Latin infarctus,
"stuffed into.
Angina: Angina is pressure, squeezing, burning, or
tightness in the chest. The pain or discomfort usually
starts behind the breastbone & can occur in the arms,
shoulders, neck, jaw, throat, or back. The pain may
feel like indigestion.

7. DEFINITION OF IHD
Ischaemic Heart Disease (IHD) is defined as
acute or chronic form of cardiac disability due
to imbalance between myocardial supply and
demand of oxygenated blood.
Synonym : CAD
2020: commonest leading cause of Death

8. IHD
1.Asymptomatic
2.Angina Pectoris
3.Acute Myocardial Infarction
4.Chronic Ischemic Heart
Disease
5.Sudden Cardiac Death

9. ETIOPATHOGENESIS

10. Etiology
1.Coronary Atherosclerosis
2.Superadded changes in Coronary
Atherosclerosis
Non-Atherosclerotic Causes

11. Coronary Atherosclerosis
 90% Cases
 Fixed Obstruction

12. Specific lesions in Atherosclerosis
 1.Distribution:
a.Ant.Descending branch
b.Rt.Coronary
c.Circumflex a.
 2. Location :
Area of involvement-3-4 cm. from coronary Ostia
Bifurcation of Arteries
Atherosclerotic plaques are seen throughout the coronaries.

13. Superadded changes in Coronary Atherosclerosis
Acute changes in chr.atheromatous
plaque(spasm)
Haemorrhage
Fissure
Ulcer------thrombosis,embolization
Coronary Artery Thrombosis-Transmural MI
Local platelet aggregation & coronary artery
spasm

14. AHA Classification of Atherosclerosis
(1955)

15. Non Atherosclerotic Causes
 <10% cases
Vasospasm
Stenosis
Arteritis
Thrombotic diseases
Embolism
Trauma
Aneurysms
Compression

16. Acute Coronary Syndrome
Absolute Medical Emergency
 Triad:Umbrella term
1. Acute Myocardial Infarction
2. Unstable Angina
3. Sudden Cardiac Death

19. ANGINA PECTORIS
 Clinical syndrome
 Transient Myocardial Ischemia
 Symptom:
1.Paroxysmal Pain in the substernum/precordial region
2.Aggravated by Increased Demand
3.Relievedby rest.
Site:Left arm
Neck
Jaw
Right Arm
Age/sex: 50 yrs./Males

21. Clinical Patterns of Angina
 3 types:
1.Stable or Typical Angina
2.Prinzmetal’s Variant Angina
3.Unstable or Crescendo Angina

22. Stable or Typical Angina
Perfusion less on demand
Relieved on rest
Chr.sclerosing coronary AS
ST depressed---Poor perfusion of
Subendocardium
No enzyme elevation
No Irreversible Myocardial injury

23. Prinzmetals Variant Angina
 Pain at rest
 Sudden vasospasm
 ST elevation –Transmural Ischemia
 Vaodilator(Nitroglycerine )effective

24. Crescendo or Unstable Angina
 Pre-Infarction Angina or
 Acute Coronary Insufficiency
Pain frequent
prolonged
rest
D/d- AMI has ST elevation
Causes: Stenosing coronary AS
Complicated plaque
Vasospasm
Infarction is prevented by Collaterals.
Myocardial cell necrosis+

25. ACUTE MYOCARDIAL INFARCTION
Fatal consequence of CAD
Collaterals are protective
Exercise –Good collateral
AS directly proportional to AMI

26.  Incidence:10-25%
 Age:Elderly
<40 yrs.-
 Sex: Males

27. ETIOPATHOGENESIS
 AS in any of the 3 major trunks
 >75% lumen block
 90% cases of MI
1.Myocardial Ischemia
2.Role of Platelets
3.Acute Plaque Rupture
4.Non AS causes
5.Transmural vs subendocardial infarcts

30.  Transmural:Disrupted Atheromatous plaque
 Subendocardial:Decreasedperfusion of Myocardium

32. Age of Infarct
 Newly formed Infarcts: Acute,recent or fresh
 Advanced Infarcts : Old,Healed or Organised

33. Location Of Infarcts
 Left Ventricle
 Rt.Atrial
 LAD Coronary A.-Ant.part LV
(40-50%) Apex
IV Septum
 RCA Stenosis: Post.part of LV
(30-40%) Post. 1/3 of IV Septum
 Lt.Circumflex CA : Lat.wall of LV
(15-20%)

34. MORPHOLOGIC FEATURES

38. Grade 0

39. Grade I

40. Dense Neutrophilic Infiltrate

42. 6 DAY OLD

43. Ischemic Necrosis in MI

44. Infarct Healing

45. EM Changes
1.perinuclear glycogen lost(5 min)
2.mitochondrial sweeling(20-30
min.)
3.sarcolemmal disruption
4.clump nuclear chromatin

47. Infarct area under EM

49.  1.Glycogen Depletion
 2.Loss of K+
 3.Na+ intake
 4.Ca+ Influx
 5.enzyme leakage

50. Diagnosis of MI
1.Clinical features
2.E.C.G
3.Serum Enzyme Markers

51. Clinical Features
 Pain
 Indigestion
 Apprehension
 Shock : SBP <80 MM Hg
 Oliguria: <20 ml/hour
 Low grade fever-Leucocytosis
Elevated ESR
 Acute Pulmonary edema

52. ECG CHANGES
 ST ELEVATION (STEMI)
 T wave inversion
 Wide deep Q waves

53. Serum Cardiac Markers
 1.CK and CK-MB
 2.CK-MB2-Cardiac
 3.CK-MB1-Extracardiac
 4.CKMB2: CKMB1::>1.5
 5.CKMB Disappears after 48 hours

56. LDH
 LDH1:LDH2>1
 Rise after 24 hours
 Peak-3-6 days
 Normal in 2 weeks

57. Cardiac Specific Troponins (cTn)
 Troponins: Cardiac n skeletal muscles
 cTn : specific
 2 types:
cTn T(7-10 days)
cTn I (10-14 days)
 Risewith CKMB-4-6 hours

58. Myoglobin
 1st marker to rise
 Lacks cardiac specificity
 Excreted within 24 hours
 SGOT(Aspartate Aminitransferase)-8 hours
3-4 days

61. COMPLICATIONS
 Arrythmias
 Congestive Heart Failure
 Cardiogenic Shock
 Mural Thrombus and Thromboembolism
 Rupture
 Cardiac Aneurysm
 Pericarditis
 Post myocardial Infarction Syndrome

62. Sudden cardiac Death
 Morning: Hypercoagulability++
 Thromboplastin release by ateromatous plaque.
 Ventricular arrythmia+electrical disturbance
 Within 1 hour----DEATH

63. References
 Robbins Textbook of Pathology,10th edn.
 Textbook of Pathology,Harsh Mohan ,6th edn.
 Textbook of Pathology,1st edn.,Vinay Kamal
 Wikipedia

64. THANK YOU