Acute coronary syndromes include: Unstable angina Acute
myocardial infarction Sudden cardiac death Basics of
pathophysiology Stable atherosclerotic plaque unstable
atherothrombotic lesion Rupture, superficial erosion deep
haemorrhage, ulceration, fissuring. Change results in the formation
of a thrombis which causes partial or complete occlusion of the
vessel
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Stable myocardial O2 demand > ability of stenosed coronary
art. to deliver. Due to physical activity, emotional excitement or
workload. Prinzmetal Caused by vasospasm. May be no/minor
athersclerotic presence Unstable plaque rupture partially occlusive
thrombosis + vasoconstriction severe but transient in coronary
blood flow. Thromboemboli can micro infarcts. Occurs with low
exercise or at rest.
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The ischaemic episode can last from 15s up to 15 minutes,
meaning that no (/minimal?) myocyte necrosis occurs.
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Acute plaque change platelet adherence to exposed
collagen/necrotic plaque contents, combine to form microthrombi
platelets release mediators causing vasospasm TF release act.
Coagulation cascade, thrombus occludes lumen.
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Other causes Vasospasm : platelet loitering or cocaine use
Emboli: from LA due to AF, left sided mural thrombosis, infective
endocarditis vegitation, right sided source via patent foramen
ovale Low systemic BP: e.g. shock, perfusion Vasculitis, vascular
dissection Haematological issues like sickle cell causing
occlusion
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Reversible: Aerobic metabolism stops no ATP production and
accumulation of toxic metabolites (lactic acid) Loss of
contractility in 60 secs. This can cause death prior to the
production of an infarct. Irreversible: Leaky cell membrane
intracellular components leak into cardiac interstitium
microvasculature and lymph. >1hr, damage to microvasculature
Permanent myocardium damage 2 - 4hrs.
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Begins as subendocardial (dependent on cause) and then moves as
a wavefront transmurally The inner 1/3 is the least perfused region
and is therefore the most susceptible. Regionally isolated if
thrombus is lysed early Circumferential in prolonged, severe
systemic BP (shock + non-critical stenosis) Transmural infarct
gives ST elevation, subendcardial does not
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Location, severity, rate of development of coronary
obstructions Size of vascular bed perfused by occluded artery
Duration of occlusion Metabolic/O2 needs of myocardium at risk.
Collateral vessels Presence, site, severity of vascular spasm HR,
rhythm, blood oxygenation. **Necrosis is complete in 6hrs, longer
if collaterals are present**
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TimeMacroscopic featuresMicroscopic features 0-30minsNone
30mins 4hrNoneNone border fibres wavy? 4hrs 12 hrs (12 24 hrs) Dark
mottlingHaemorrhage, oedema, early coagulative necrosis (wavy
myofibrils, more space b/n cells, cells shrink and become more
dense/ darker) 1 - 3 daysMottling with yellow- tan infarct centre
Neutrophil infiltration, coagulation necrosis (myofibrils lose
nuclei) 3 - 7 daysHyperemic border, central yellow-tan softening
Macrophages performing phagocytosis at border. Dying neutrophils 10
14 daysRed-gray infarct bordersGranulation tissue (angiogenesis +
collagen) 2 8 weeksGrey-white scar, progressive from border to the
core of infarct collagen deposition, cellularity > 2
monthsScarring completeDense collagenous scar
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atherosclerotic lesion disrupted plaque regional myocardial
ischaemia fatal ventricular arrythmia Can be the first clinical
presentation of IHD AMI is the most common trigger for fatal
arrhythmias (e.g. VF, asystole) Injury can affect the conduction
system and create electrochemical cardiac instability. Fatal
arrhythmias are usually caused by electrical instability distant
from the conduction system arrythmogenic foci are often located
adjacent to scars of old MIs.
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Pulmonary HTN Congenital abnormalities Aortic valve stenosis
Mitral valve prolapsed Myocarditis Dilated or hypertrophic
cardiomyopathy Cardiac hypertrophy Genetic ( channel or proteins
which assist the channels functioning are faulty, often leading to
long QT intervals.)
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Dilated cardiomyopathy Genetic Myocarditis (sometimes due to
viruses) Alcohol and other toxins Childbirth ( volume?) Ventricular
remodelling Response to injury or changes in loading Adaptive