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Ischaemic Heart Disease(IHD)
- 1. Ischaemic Heart Disease Dr.Jyoti Priyadarshini Shrivastava Associate Professor Department of Pathology Gajra Raja Medical College
- 2. Blood Supply ofHeart 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 isa 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 IschaemicHeart 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 MyocardialInfarction 4.Chronic Ischemic Heart Disease 5.Sudden Cardiac Death
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- 10. Etiology 1.Coronary Atherosclerosis 2.Superadded changesin Coronary Atherosclerosis Non-Atherosclerotic Causes
- 11. Coronary Atherosclerosis 90%Cases Fixed Obstruction
- 12. Specific lesions inAtherosclerosis 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 inCoronary 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 ofAtherosclerosis (1955)
- 15. Non Atherosclerotic Causes <10% cases Vasospasm Stenosis Arteritis Thrombotic diseases Embolism Trauma Aneurysms Compression
- 16. Acute Coronary Syndrome AbsoluteMedical Emergency Triad:Umbrella term 1. Acute Myocardial Infarction 2. Unstable Angina 3. Sudden Cardiac Death
- 19. ANGINA PECTORIS Clinicalsyndrome 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 ofAngina 3 types: 1.Stable or Typical Angina 2.Prinzmetal’s Variant Angina 3.Unstable or Crescendo Angina
- 22. Stable or TypicalAngina 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 UnstableAngina 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 Fatalconsequence of CAD Collaterals are protective Exercise –Good collateral AS directly proportional to AMI
- 26. Incidence:10-25% Age:Elderly <40yrs.- Sex: Males
- 27. ETIOPATHOGENESIS AS inany 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 Atheromatousplaque 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%)
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- 45. EM Changes 1.perinuclear glycogenlost(5 min) 2.mitochondrial sweeling(20-30 min.) 3.sarcolemmal disruption 4.clump nuclear chromatin
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- 49. 1.Glycogen Depletion 2.Loss of K+ 3.Na+ intake 4.Ca+ Influx 5.enzyme leakage
- 50. Diagnosis of MI 1.Clinicalfeatures 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 STELEVATION (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 Riseafter 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 markerto rise Lacks cardiac specificity Excreted within 24 hours SGOT(Aspartate Aminitransferase)-8 hours 3-4 days
- 61. COMPLICATIONS Arrythmias CongestiveHeart 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 Textbookof Pathology,10th edn. Textbook of Pathology,Harsh Mohan ,6th edn. Textbook of Pathology,1st edn.,Vinay Kamal Wikipedia
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Editor's Notes
- #43 Centralpallor,necrotic fibre