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Ischaemic Heart Disease / Coronary Artery Disease - Coggle Diagram

- - - - Hyperlipidaemia
      - Hypertension
      - Cigarrete smoking
      - Diabetes mellitus
- - - - Plaque rupture
      - Plaque thrombosis
        
        Plaque rupture exposes thrombogenic lipis and sub endothelial collagen
        
        Platelet activation, aggregation and thrombin generation
        
        Thrombus production
        
        Critial event leading to acute coronary syndrome (MI)
      - Vasospasm
        
        Usually in pts with pre-existing atherosclerosis
        
        Mechanism unclear
        
        May be triggered by plaque rupture and release of vasoactive molecules from platelets
        Thromboxan A2
        
        Endothelial cell dysfunction possible trigger
        
        Smoking and increased androgenergic activity are implicated
      - Plaque fissuring
      - Plaque haemorrhage
- - - - Episodic CP
        Assosiated with Exertion
        Relieved by rest
      - Stable atherosclerotic plaque causing => 75% narrowing of coronary artery
      - Term critical stenosis used if oxygen demand cannot be met
      - Treatment: Vasodilators
    - - Increased frequency CP
        At rest
      - Referred to as pre-infarction angina
      - Induced by acute plaque change
        Fissure
        Rupture
        Thrombosis
        Embolism
        Vasospasm
      - An Acute Coronary Syndrome (ACS)
    - - Not due to coronary disease
      - Often cyclical
        At rest
        Can wake from sleep
      - Associated with angiospasm
      - Response to admin of vasodilators
- - - - External rupture of infarct
      - Mural thrombi
      - Acute pericarditis
      - Ventricular aneurysms
      - Papillary muscle dysfunction
    - - Cardiac arrythmias
      - Left ventricular failure
      - Cardiogeneic shock
      - Rupture of free wall, septum, papillary muscle
      - Thromboembolism
  - - - Affects:
        Anterior and apical left ventricle
        Anterior 2/3 of interventricular septum
    - - Affects:
        Posterior wall of LV
        Posterior 1/3 of interventricular septum (in RAC-dominance)
        Right ventricle
    - - Affects:
        Lateral wall of left ventricle
        Posterior wall (LCA-dominance)
  - - - No changes on gross examination
      - Slight pallor of myocardium
    - - Microscopically:
        
        Coagulative necrosis
        
        Contraction of band necrosis
        
        Nuclear karryorhexis
    - - SLight pallor or mottling on gross examination
      - Continuing coagulative necrosis of cardiac myocytes on histology
    - - Pallor and mottling on gross examination
      - Complete coagulative necrosis of cardiac myocytes and heavy polymorphonuclear infiltration on histology
    - - Central pallor with hyperaemic border on gross exam
      - Macrophages appear
        Early disintegration and phagocytosis of dead cardiac myocytes
        Granulation tissue formtaion begins at edge of infact
    - - Yellow soft shrunkedn myocardium
      - Well developed phagocytosis
        Prominent granlution tissue fromation
    - - Firm grey myocardium on gross exam
      - Fibrosis in the myocardium replaces dead core of cells
  - - - Cardiac troponin I and T
      - Levels remain elevated 4-7 days after MI
    - - CK-MM and CK-MB
      - Total CK activity rises 2-4 hrs post infarct
        Peaks at 24hrs
        Returns to baseline at 72 hrs
      - CK-MB is more specific
    - - Used less since introducation of cardiac troponins