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There are many complications, which will be discussed below in chronological order:
1-3 days
Arrhythmias: sinus bradycardia, sinus tachycardia, ventricular premature contractions, ventricular tachycardia, atrial/ventricular fibrillation, asystole, atrial flutter.
Pericarditis: usually develops after a transmural infarct (not subendocardial). It occurs due to migration of underlying myocardial inflammation to pericardial surfaces.
3-5 days
Myocardial rupture: myocardial inflammation causes weakening therefore 1) rupture of ventricular wall resulting in haemopericardium + cardiac tamponade (usually fatal), 2) ventricular septum rupture leading to left-right shunt, 3) papillary muscle rupture cause mitral insufficiency . Other causes of mitral insuffiency is papillary muscle dysfunction due to ischaemia, LV dilatation (physically pulling mitral valve apart), ventricular wall necrosis nearby papillary muscle emergence.
5-10 days
Mural thrombus: local contractility problems (stasis) + endocardial damage = thrombus formation = potential thromboembolism.
10 days +
Contractile dysfunction: LV contraction impaired, causing hypotension, pulmonary vascular congestion --> interstitial transudation --> pulmonary oedema. If infarct causes 20-25% of ventricle size = abnormal ventricule function, uif 40%+ = cardiogenic shock.
Ventricular aneurysm: Anterseptal infarct heals by forming fibrotic tissue, which is thin. This paradoxically bulges during systole – causing an aneurysm.
Category: Pathology Notes
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