Clinical Pathology · MU Sofia

49. Ischemic heart disease: myocardial infarction. Microscopic & gross pathomorphology. Stages, complications, outcomes.

Covers myocardial infarction as one form of ischaemic heart disease, explaining how most infarcts arise from thrombosis over a ruptured atherosclerotic plaque and how the myocardium responds over time. It sets out the coronary artery territories, the transmural versus non-transmural distinction, and a day-by-day table of gross and histopathological changes from the first hours to several weeks. It ends with the main complications, such as cardiogenic shock, papillary muscle dysfunction, rupture, pericarditis and aneurysm, and when they tend to appear.

Inside: 3 sections · 2 labelled pictures · 13 flashcards · 3 min

Topic 49 of 138 in the MU Sofia syllabus for Clinical Pathology (Medicine, Year 4). The free AceMed note covers it in 3 sections, about 585 words (3 min of reading), with 13 flashcards.

In this note

  1. Ischemic heart disease: myocardial infarction. Microscopic & gross pathomorphology. Stages, complications, outcomes
  2. Stages
  3. Complications/Outcomes

Ischemic heart disease: myocardial infarction. Microscopic & gross pathomorphology. Stages, complications, outcomes

Cardiomyocytes generate energy via oxidative phosphorylation, so oxygen is a must. IHD is a term that encompasses all conditions where there is an imbalance between cardiac perfusion and myocardial oxygen required. 90% of IHD cases are reduced coronary blood flow due to obstructive atherosclerosis, and this is what the term generally means. Manifestations of IHD are:

  • Angina pectoris (stable, unstable, Prinzmetal)
  • Acute MI
  • Chronic IHD with CHF (see below)
  • Sudden cardiac death (can occur due to MI but commonly due to lethal arrhythmia)

Here we will focus on Myocardial Infarction

  • The vast majority of MIs are caused by acute coronary artery thrombosis, generally where there is disruption of a pre existing atherosclerotic plaque that provides thrombus generation, vascular occlusion and transmural infarction of downstream myocardium
  • 10% of MIs are due to coronary artery vasospasm or embolism from other thrombi.
  • In typical MI the following events occur
  • Atheromatous plaque is disrupted exposing endothelium collagen and necrotic plaque
  • Platelets adhere, aggregate and are activated
  • Activation causes coagulation and the thrombus is generated
  • Myocardial response to MI
  • Loss of ATP production has rapid functional effect with ultrastructural changes (including myofibrillar relaxation and mitochondrial swelling). These early stages are reversible
  • Ischemia after 20-40 minutes is irreversible and leads to coagulative necrosis
  • MIs also commonly trigger arrhythmias (e.g. ventricular fibrillation)
  • We can describe infarcts as transmural or non-transmural. Transmural means that the necrosis spreads through the whole thickness of the myocardium, non-transmural does not.

Remember: which artery, which wall:

  • Left anterior descending (40–50% of MIs): anterior wall of the left ventricle, apex, anterior two-thirds of the septum
  • Right coronary (30–40%): inferior/posterior wall, posterior third of the septum, right ventricle
  • Left circumflex (15–20%): lateral wall of the left ventricle

Myocardial infarcts less than 12 hours old are not grossly apparent, however, those more than 2-3 hours old can be visualised by staining. 12-24 hours after the event, a red-blue discolouration should be visible caused by stagnated blood, over the following weeks, a fibrous scar will evolve.

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