Myocardial infarction Part 3

Myocardial infarction Part 3: detailed Notes • • • • • • • Persistent ischaemic chest pain → radiates neck, left arm or both Occurs at rest No relief from vasodilators May be acute shortness of breath (LV failure) pain may not be noticed 10%-15% of patients the onset is asymptomatic (silent) → discovered only later by electrocardiography Usually Coronary Arterial Occlusion from atherosclerosis with: o Acute atheromatous plaque change (such as rupture) o Superimposed platelet activation, adhesion, release of mediators o Vasospasm stimulated by platelet aggregation and the release of mediators o Thrombosis with complete arterial occlusion in 90% of cases o Aggravated by increased myocardial demand (hypertrophy or tachycardia) or diminished diastolic coronary flow (hypotension) Uncommon coronary artery disease other than atherosclerosis: o o o • • Vasospasm: isolated, intense, and relatively prolonged, perhaps in association with platelet aggregation (sometimes related to cocaine abuse). NB may be incidental atherosclerosis Emboli: from left side of circulation – aortic valve disease particularly likely because of diastolic filling Others: possibly thrombosis from diseases of small intramural coronary vessels such as vasculitis or amyloid, blood disorders e.g. haemoglobinopathies, vascular dissection and inadequate protection during cardiac surgery Key early events in cardiac myocytes after onset of ischaemia o Within seconds: onset of ATP depletion o <2 min: loss of contractility o 10 min: ATP reduced to 50% of normal o 40 min: ATP reduced to 10% of normal o 20-40 mins: irreversible cell injury o >1hr: microvascular injury Later structural events in MI after onset of ischaemia o 2-3 hrs: dehydrogenase enzymes lost o 12-24 hrs: discoloured by stagnant blood o 48 hrs: yellow to tan colour with congested rim o 3-5 days: softens o By 2 weeks: enclosed by congested granulation tissue o By 6-8 weeks: converted to a fibrous scar Appearance of heart tissue post MI • Age o After 2 to 3 hours after the infarct dehydrogenase enzymes are lost o By 12 to 24 hours the affected area is discoloured by stagnant blood o By 48 hours the infarct acquires a yellow to tan colour and has a congested rim o It softens over the next 3 to 5 days o By 2 weeks it is enclosed by congested granulation tissue o Over the next few it is converted to a fibrous scar • Frequency o Several infarcts of varying age are frequently together o Repetitive necrosis may cause extension of an infarct over a period of days to weeks producing a complex appearance • Site o Left anterior descending coronary artery (40% to 50%): anterior wall of left ventricle near apex; anterior portion of ventricular septum; apex circumferentially o Right coronary artery (30% to 40%): inferior/posterior wall of left ventricle; posterior portion of ventricular septum; inferior/posterior right ventricular free wall in some cases o Left circumflex coronary artery (15% to 20%): lateral wall of left ventricle except at apex o Others • Distribution – transmural infarcts o Full or almost full thickness of the ventricular wall in the distribution of a single coronary artery o Usually acute plaque change and thrombosis o Almost always involve some of the left ventricle (including the septum). o Often some right ventricle involvement (but infarction limited to RV are rare – 13% of cases) o Involve the whole supply distribution of the occluded coronary artery (except for approx. 0.1 mm of subendocardial myocardium preserved by diffusion from the lumen) • Distribution – subendocardial (nontransmural) o Limited to the inner one third to one half of the ventricular wall ▪ May extend laterally beyond the perfusion territory of a single coronary artery. ▪ Subendocardium – least well perfused region of myocardium • Plaque disruption followed by coronary thrombus that becomes lysed or • Prolonged and/or severe reduction in systemic blood pressure, as in shock, often with mild coronary stenoses