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
Macroscopic features of chronic IHD
Enlarged, heavy heart
Hypertrophied, dilated LV
Atherosclerosis
+/- mural thrombi
Microscopic feature of chronic IHD
Fibrosis
Definition of sudden cardiac death
Unexpected death from cardiac cause in individuals without symptomatic heart disease OR early (1 hr) after onset of Sx
Most common cause of sudden cardiac death
Lethal arrhythmia
Acute MI –> electrical instability at site distant from conduction system
Macroscopic features of cardiac failure
Dilated heart
Scarring/thinning of walls
Microscopic features of cardiac failure
Fibrosis
Replacement of ventricular myocardium
Causes of dilated cardiomyopathy
Idiopathic
Infection - viral myocarditis
Toxic - EtOH, chemotherapy, cobalt, iron
Hormonal - hyper/hypothyroid, diabetes, peri-partum?
Genetic - haemochromatosis, Fabry’s, McArdle’s
Immuno - myocarditis
Causes of hypertrophic cardiomyopathy
Familial in 50% - autosomal dominant, variable penetrance
Beta-myosin heavy chain?
Causes of restrictive cardiomyopathy
Idiopathic
2ndary to myocardial disease - amyloid, sarcoid
Order of valves affected by chronic rheumatic valve disease
Mitral > aortic > tricuspid > pulmonary
Most common cause of aortic stenosis
Calcified aortic stenosis
Affects 70-80yo
Calcium deposits in outflow side of cusp –> impaired opening
Causes of aortic regurgitation
Rigidity - rheumatic disease, degenerative
Microbial endocarditis
Dilatation - valve insufficient to cover increased area e.g. Marfan’s, dissecting aneurysm, Ank Spond
Duke’ criteria for IE
Major:
- bacteraemia (2 cultures, 12 hours apart)
- echo findings: vegetation
Minor:
- Fever 38+
- Echo findings (not meeting major criteria)
- Vascular phenomenon: Embolisation, splinter haemorrhage, Janeway lesions
- Immuno phenomenon: Osler’s nodes, Roth spots, GN, Rh factor
- Microbiological: 1 culture +ve
- Risk factor: IVDU, predisposing heart disease
Interpretation of Duke’s criteria for IE
Diagnosed if:
2 major
OR 1 major + 3 minor
OR 5 minor
Tx of IE
Strep viridans = Benzylpenicillin + gentamicin
MSSA = flucloxacillin
MRSA - Vancomycin
Prosthetic valve = vancomycin + gentamicin + rifampicin
Features of Ventricular aneurysm
Post MI
ECG changes - ST elevation in V2-5
No chest pain, SOB or other Sx
Most common cause of constrictive pericarditis in ‘developing’ world
Tuberculosis
Effects of amyloidosis in the heart?
Restrictive cardiomyopathy
Arrhythmia
Clinical features of heart failure
Left = pulmonary oedema, SOB
Right (cor pulmonale) = peripheral oedema
Effect of mycobacteria in the heart
Calcifying pericarditis
Takotsubo’s cardiomyopathy - key features
‘Broken heart syndrome’
Develops in response to intensive physical or emotional experience
ECG changes + apical akinesia + interventricular septum hypertrophy
Cardiac enzymes, CXR, percutaneous coronary intervention NAD.
