Cardiovascular pathology I

Athersclerosis

sites (most to leats common)
- abdomial aorta
- coronary arteries
- popliteal arteries
- desc thoracic aorta
- internal carotids
- circle of willis
pathogenesis
- fatty streak in children
- athermatous plaques develop through life
- become symptomatic middle age or later
conseqeunces:
- MI/IHD/sudden death/stroke/CVA
- gangrene of extremities, gut ischaemia
- AAA - rupture
- haemorrhage into placque

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structure
- fibrous cap
- cells (smooth m. and inflamm)
- lipid
- CT and ECM
stable plaque:
- thick fibrous cap
unstable plaque:
- no thick cap; at risk of rupture/fissure causing emboli +/- thrombosis
RFs or atherosclerosis
- no modifiable: age, male, FHx, genetic abnormality
- modifiable: high lipids, HTN, smoking, DM
pathogenesis theory:
- "response to injury hypothesis"
- chronic inflam response of arterial wall inititated by chronic endothelail injury

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imbalance b/w supply and demand for oxygenated blood in the heart
90% due to atehrosclerosis of coronary artery disease
- 10%: congenital herat disease, anameia, lung disease
aggravated by anything that incr demand or decr supply:
- hypertrophy, hypotension, hypoxaemia, incr HR
risk of IHD w/ athersclerosis dep on:
- no. of vessels affected (usually > 1)
- distribution (prox LAD, prox LCX, entire RCA)
- degree of narrowing (75% reduction in x-sctional area= critical stenosis)
4 syndromes of IHD
- MI (myocyte necrosis, see elevated creatinine kinase [3d] and troponins [7-10d] w/in 4-8hrs); angina pectoris (NO necrosis); chronic IHD; sudden cardiac death
NB most dangerous lesions are 50-755 stenosis w/ lipid rich core and minimal fibrous cap- do not produce angina,high risk of rupture/fissure w/ no collaterals or preconditioning has occurred

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transmural
- full wall thickness
- assoc w/ acute thrombosis/occlusion of vessel
- occ due to vasospasm or emboli
- on distribution of singl eartery
subendocardial
- inner 1/3-1/2 of myocardium
- may extend being territory of singl eartery
- subendocardial zone is least perfused thus most at risk w/ reduced coronary flow
- usually critical stenosis but no acute plaque change
histologically can see from 4 hrs
macroscopically can see from 12 hrs
NB blood supply
- LAD: apex, anterio LV, anterior IVS
- LCX: lat LV
- RCA: inferior/posterior LV, posterior IVS, RV

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early reperfusion
- salvages sublethally injured myocytes and minimise infarct size
- risk of reperfusion injury
- despite salvage some myocytes may not function for several days: "stunned myocardium"
- repetitive short lived ischaemia may be protective (preconditioning)
complications:
- contractile dysfnction > heart failure > cardiogenic shock
- arrythmias
- myocardial rupture
  - in free wall: tamponade/ in IVS: L to R shunt
  - papillary muscle: acute severe mitral regurg
- pericarditis early or in weeks (Dressler syndrome= AI)
- mural thrombus (emoboli risk)
- ventricular aneurysm
- progressive late heart failure

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failure of heart as a pump
adaptive mechanisms to prevent/postpone failure
- dilation (incr preload due to Frank-Starling mechanism)
- hypertrophy (incr size of myocytes)
- activation of neurohumoral mechanisms
  - NA released by adrenergic cardiac nerves > incr HR
  - activation of RAA system > maintain renal function
  - release of atrial natriuretic peptide (ANP) due to high BP > aldosterone antagonist
causes:
- usually systolic dysfunction (poor contarction)
- oc diastolic dysfunction (stiff walls unable to fill properly)
L HF > pulmonary oedema, organ ischaemia (impaired renal function)
- occurs in most forms of heart disease
R HF > organ ischaemia, peripheral oedema, congestion of organs, ascites/pleural effusion
- usually secondary to LHF
- pure R HF is uncommon (cor pulmonale)

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response of herat to increased demands
- systemic hypertension
- pulmonary hypertension = cor pulmonary
hypertension leads to hypertrophy which causes:
- myocardial dysfunction
- cardiac dilation
- CCF
- sudden death

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Dx criteria
- LV hypertrophy (concentric) + Hx/pathologucal evidenc of HTN
Presentation:
- asymptomatic > ECG
- AF (w/ LA enlargement)
- CCF
gross morphology
- circumferential LV hypertrophy
- NO lV dilation
- incr heart weight
- thick wall (> stiff > impaired filling > LA enlargement)
histology
- incr myocyte size
- incr nuclear size
- interstitial fibrosis

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pulmonary hypertensive heart disease
secondary to pulmonary HTN
- due to abnormality of lungs/pulmonary vasculature
- must exclude 2nd to
  - congenital heart disease
  - disease of left heart
acute presenation:
- sudden incr in pulm BP
  - e.g. massive PE
  - see dilation of RV, no hypertrophy
chronic:
- prolonged pr overload
- RV hypertrophy

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