CR - ischaemic heart disease (ii)
MI Pathology
coronary atheroma
plaque rupture
plaque fissure (lipids exposed)
macrophages from a smooth muscle foam cells
subsequent secondary thrombosis (thrombin, fibrin, platelets) - advanced complicated lesion
ischaemia
possibly reversible for 6-12 hrs
necrosis begins 30 mins after occlusion furthest from blood supply (subendocardial myocardium)
then if STEMI progresses through full thickness of myocardium (transmural infarct) to pericardium
STEMI
Q waves (-ve deflection preceding R wave, represents left-to-right depol of interventricular septum) present
ST elevation
complete coronary art occlusion
no lumen
often acute (no collat circulation)
emergency - rush to cath lab
goal of Tx = reperfusion
thrombolysis if < 30 mins
mechanical revasc (bypass - CABG) if < 90 mins
often reversible if this is achieved
NSTEMI
Q waves absent
ST not elevated (often depressed)
incomplete occlusion
or prolonged shock
often due to severe atheroma
collat circulation often present
still a lumen
goal of Tx = prevent total occlusion
myocardial failure
fatal arrhythmia
PCI not as urgent
MI Dx
clinical
ECG
quick + easy
gives info about site + vessel involved
gives info about arrhythmias
lab
troponin I+T
both subtypes indicate damage
sensitive, not specific
stays elevated for 7-14 days
CK-MB
muscle brain fracture of creatinine kinase
found almost exclusively in myocardium (specific cardiac structural proteins)
indicate extent of infarct, significance of vessel, degree of myocardial hypertrophy + if there's collat circulation
regulatory proteins actin filaments in cardiac muscle (engage with Ca)
measured in blood via immunoassay techniques
associated with many other conditions
cardiac surgery
heart contusion (bruising as a result of trauma)
myocarditis
cardiomyopathy (esp HOCM - hypertrophic obstructive cardiomyopathy)
chemo tx (cell destruction)
renal disease
sepsis
poly/dermatomyositis
small amounts in rheumatic heart disease
MI morphological changes
up to 10 hrs: no microscopic changes seen
necrosis, inflamm, wound healing
day 1
coag necrosis (dark red, firm)
hypereosinophilia
haemorrhaging from dead vessels
day 2-7
inflamm (neutrophils + oedema) beside necrotic area
soft yellow/tanned tissue
if marked can get fever + increased WCC (bad prognosis)
day 7-14
repair
resorption of dead tissue (depressed area)
granulation tissue (redness) @ edges
wk 2-8
evolving fibrosis (blue with purple nuclei under masson trichome stain)
deceased vascularity (grey/white tissue)
wk 8
dense fibrosis (scarring)
depressed thin myocardium
risk of thrombi, aneurysm, rupture
Myocardial cell death
LVF (pump failure - wide spectrum of severity)
sinus tachycardia (>100beats/min) but normal BP + tissue perfusion
if moderate: dyspnoea + pul oedema
if severe cardiogenic shock
poor prognosis
intractable (hard to manage) hypotension
hypoperfusion
reduced EJ (SV/EDV, should be >60%)