Angina pectoris MI Chronic IHD cardiac failure Sudden cardiac death
ANGINA Ischemia (No cell death ) ANGINA MI ECG + ECG+ Cardiac enzymes normal Cardiac enzyme eleveated
Angina 3 Subtypes 1.STABLE ANGINA Chest pain after exersion 2.UNSTABLE ANGINA Plaque rupture 3.PRINZMETAL ANGINA Sudden coronary vasospasm (@ rest) Only PM angina ECG will be normal between angina On a superimposed existing atherosclerosis ECG abnormal between angina Responds to vasodialators
Myocardial Infarction No blood Infarct Onset of ATP depletion = within seconds Loss of contractility= <2 min ATP will reach =50% of normal value 10 min =10% of normal value 40 min Irreversible damage = 20-40 min ( Critical time of reperfusion / Thrombolysis) Microvascular injury = >1 hr
Types of infarct 1.Transmural infarct Complete occlusion Infarction of the entire myocardial thickness ?? When it see Chronic atherosclerosis+Plaque change (thrombi) ECG=STEMI
2.Subendocardial Infarct Infarct caused by thrombus Dissolved Rx/ SpnontaneousBefore a full thickness infarct Other causes Prolonged systemic hypotension Shock+Atherosclerosis
Postmortem analysis Biochemical>EM>Light microscopy>Gross GROSS Intital 7-8 hrs of MI there will no change TTC test Triphenyl Tertrazolium Chloride test + ve in 2-3 hrs Slice @ 1- 0.5 cm thickness TTC dye Normal myocardium= BRICK RED Infarct(Extracellular LDH)=Unstained Pale area Pure white =Old Scar
1 st EM Change 0-1/2 hr = Sacrolemmal disruption Mitochondrial density reduced Myelin figures reduced
Light Microscopy Findings ½ hr – 4 hr => 1 st light microscopy change Waviness of fibre Vacuolisation Contraction band 4hr-3 Days => Coagulative necrosis (only pink ) 1-3 Days => Neutrophils 4h-24h-Only necrosis 24h-3D – Neut+Necrosis
GROSS 0-12HR = No change 12-24HR=Vague pallor & Softening 1-7Days=Yellow color 7-10Days=Central pallor with Red borders >10-14 days=White firm scar
MI COMPLICATION-Reperfusion injury Def: Injury to the myocardium due to fresh blood 1.Free radical induced damage Fresh blood(New ROS) Dying myocardium (antioxidants less)More damage 2.Mitochondrial damage MIAltered mitochondrial permeability More protein More ion into mitochondriaRupture out Mitochondrial membrane Cytc Ctrigger Apoptosis
3.Myocyte hyper contraction MICa2+ increased during cell deathCa2+ release from Sarcolemma Abundant Ca2+ in dying cellNew blood with ATPHypercontractionCytoskeltal damageCELL DEATH Hypercontracted muscle in microscopic highly PINK in color EOSINOPHILIC CONTRACTION BAND 4.WBC & platlets >1hrMicrovascular injurywbc+platletsThrombosis =>NO FLOW PHENOMENON
Complication of MI itself 1.Contractile dysfunction Large MI (>40% of LV) contractility reducedCO reducedHeart failure 2.Papillary muscle dysfunction Rupture Regurgitation
3.Myocardial Rupture Risk more=3-& days post MI Ventricular free wall rupture MI Cardiac tamponade Hemopericardium Ventricular septum rupture-VSD R/F for ruptureAge >60, Ant/Lat wall, Female, ! st MI > second MI
4.PERICARDITIS MI Myocardial inflammationPericardial inflammation2-3 day recover its own B) Post MILittle bleeding blood & plasmapericardial space--.Organised(Fibrin)Fibrinous pericarditis C) MIDamage of heart muscleNew antigen (Neo antigen)Trigger antibody productionPericarditis DRESSLER SYND ( Time:week Rx Steroid) 5.MURAL THROMBUS Thromus in heart and aortaStasis of blood/Endothelial injuryThromusEmboliSystemic thromboembolic events 6.VENTRICULAR ANEURYSM
Cardiac enzymes My : My oglobin Time : T ROPONIN I TO : T ROPONIN T C : C K MB A : A ST LL : L DH1
Cardiac enzyme start peak fall Myoglobin 2hr - 24hr Troponin 2-4hr 48hr 7-10days CK-MB 2-4 hr 24hr 48-72hrs AST/SGOT <12hr 48hr 4-5days LDH1 24hr 4-5 days After 10D Myoglobin not specific –early rise early fall Troponin I > Troponin T
Update HFABP - Hear fatty Acid Binding Protein IMA - Ischemia Modified Albumin
Flipping of LDH ratio NORMAL Blood= LDH 2>>>LDH1 HEART=LDH1>>>LDH2 MI-Blood LDH 1>>>>>LDH2 Flipping ratio
Marker of reinfarction Is TROPONIN Serial monitoring rise by .20% from base line