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Rick Allen

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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

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Robbins and Cotran