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L7 Pathology Ischaemic Heart disease

Lecture objectives

  1. Explain how atherosclerosis is ahte reult of casucalr wall remodeklling in response to chronic endothelial injury - response to injury hypothesis
  2. Describe the gross and microscopic changes seen in the vascular wall in chronic and complicated atherosclerosis, namely early fatty streaks matyre atherosclerotic plaques and plaques with superimposed thrombosis
  3. correlate the cilinical rpesentation of IHD- andgina pectoris VS MI with the underlying coronary artery pathology for example chronic mechanical obstructioni by stable atherosclerotic plaques and sudden vascular occlusion

context

highest killer for maori males and but non maori malea and females

Terminology

ischaemia hypoxia infaction coagulative necrosis (ghost like changes)

Risk factors of Athersclerosis

genetics family history age male gender hyperlipidaemia hypertesnion cigarette smoking diabetes inflammation

Pathogenesis of Atherosclerosis

arterial response to endothelial injury

This lecture posits that atherosclerosis is not a byproduct of hypercholesterolaemia but actually an arterial response to continued injury

This injury can include but is not limited to:

  • hypertension
  • complement
  • lipids
  • glycosylation
  • hypoxia
  • acidosis
  • cigarette smoke
  • etc…

steps of atherosclerosis (atheroma)

  1. endothelial injury and dysfunciton causes increased vascular permability and leukocyte and platelet adhesion
  2. With increased vascular permability lipoproteins (mainly LDL seem into vessel wall)
  3. cytokine release attract monocyte which go into intima turn into macrophages and consume lipid until they become foam cells
  4. further ytokine and GF release leads to smooth muscle cell recruitment
  5. smooth muscel cells make ECM and also become foam cells
  6. t cells are recruited
  7. atherosclerotic plaque is created

Morphology

early fatty streaks give way to mature plaques

complicaitons

can lead to mechanical obstruction - critical stenosis is 70% increases diffusion distance which can lead to weakening of the walls and eventual rupture

aneurysms can be fusiform, saccular, and can contain mural (wall) thrombus

haemorrhage into the plaque plque ulceration, erosion or ruptur leading to thrombosis

Pathogenesis of IHD

Chronic vascular occlusion by athersclerosis in which chronic occlusion is means stenosis from beyond 70% one of more of RCA LAD LCX arteries affectes

acute plaque change

  • intraplaque haemorrhage, erosion, rupture
  • super imposed thrombosis coronary vasospasm component

Clinical presentaion of ACS

  1. angina pectoris
    1. Ischaemia but doesnt cause infarct
    2. can be stable or unstable (unstable rapidly leads to MI and SCD)
  2. Myocardial infarction
    1. Ischaemia causing myocardial necrosis
  3. sudden cardiac death
    1. ischaemia leading to fatal arrhythmia
  4. Chronic IHD with HF
    1. due to accumulated damage

Lab diagnosis

CK-MB Troponin-T

Time is muscle and stemi vs nstemi

Nstemi is not completely transmural stemi is completely transmural

MI morphology

MI complicaiton

  • Acute heart failure

  • cardiogenic shock (2/3rds od deathin acute mI)

  • arrhythmias (all types (potentially fatal VF))

  • myocardial rupture

    • ventricular fee vall rupture
    • rupture of interventricular septum
    • papillary muscle rupture

  • Pericarditis

  • mural thrombus formation

  • ventricular aneuryms formaiont

  • progressive late heart failure

Chronic IHD with heart failure

progressive congestive heart fauilre due to accumulated ischaemic damafe over years

nutmeg liver

Graph View