Histopath - Cardio Flashcards
Causes of death after MI
Arrythmia –> cardiac arrest
Cardiogenic shock
Rupture
Causes of LV hypertrophy
HTN
Aortic stenosis
Ischaemia may contribute
ECG lead & corresponding vessels
II, III, aVF = right coronary artery (inferior)
V1 - V4 = left anterior descending (anterior)
1, V5, V6 = circumflex (lateral)
Diagnostic criteria for STEMI
> 2mm ST elevation in 2 leads?
>1mm ST elevation in 2 consecutive chest leads
Blockage of which cardiac vessel is more likely to cause arrhythmia?
Right coronary (vs LAD)
Supplies SA & AV nodes
ECG evidence of old MI
Deep Q waves
T wave inversion?
RF for atherosclerosis
Family Hx - most significant independent RF Age Sex - male Hyperlipidaemia HTN Smoking DM
RF for atherosclerosis
Family Hx - most significant independent RF Age Sex - male Hyperlipidaemia HTN Smoking DM
How do risk factors interact in atherosclerosis
Multiplicative effect
2 RF = 4 fold increased risk
3 RF = 7 fold
Pathogenesis of atherosclerosis - process
Endothelial damage
Lipoprotein accumulation (LDL)
Monocyte adhesion to endothelium + migration into intima
Monocytes –> macrophages + foam cells (ingest fat)
Platelet adhesion
Release of various pro-inflammatory factors
Smooth muscle cell recruitment –> endothelial proliferation
Lipid accumulation - extracellular + intracellular
Atheroma
Earliest atherosclerotic lesion seen
Fatty streaks - lipid filled foam cells / macrophages
present in virtually all children >10yo
Macroscopic features of atherosclerotic plaque
Raised lesion
Soft lipid core
White fibrous cap
Appear eccentric
Critical stenosis threshold
~70% occlusion OR (lumen) diameter <1mm
When demand > supply
Forms of acute atherosclerotic plaque change
Rupture - exposes pro-thrombogenic contents
Erosion - exposed pro-thrombogenic sub endothelial basement membrane
Haemorrhage into plaque - increases size
Criteria for increased risk of atherosclerotic plaque rupture
Lots of foam cells or extracellular lipid
Thin fibrous cap
Few smooth muscle cells
Clusters of inflammatory cells
Pathogenesis of ischaemic heart disease
Insufficient coronary perfusion
(imbalance of supply vs demand for oxygenated blood)
+ less removal of waste –> less well tolerated than pure hypoxia
Plaque distribution in IHD
First few cm of LAD or LCX
or entire length of RCA
Threshold for pain at rest
90% stenosis
Definition of angina pectoris
Transient ischaemia NOT resulting in myocyte necrosis
Definition of myocardial infarction
Death of cardiac muscle due to prolonged ischaemia
Timing of MI reversibility
Irreversible after 20-30 mins
Most common MI locations
LAD - 50%, anterior wall of left ventricle, anterior septum, apex
RCA - 40%, posterior wall of left ventricle, posterior septum, posterior right ventricle
LCX - 20%, lateral left ventricle (not apex)
Timeline of MI changes
<6h = none
6-24h = Macro: none. Micro: loss of nuclei, homogenous cytoplasm, necrotic cell death.
24h = Macro: pale, oedema. Micro: oedema, inflammation (neutrophils)
3-4 days = Macro: haemorrhage. Micro: coagulative necrosis, granulation, infiltration of polymorphs THEN macrophages
1-3 weeks = Macro: thin, yellow. Micro: granulation tissue, new vessels, myofibroblasts, collagen synthesis.
> 3-6 weeks = Macro: tough white. Micro: dense fibrosis, decellularising scar
Mechanism of re-perfusion injury
Oxidative stress + Ca overload + inflammation
Arrhythmias common
