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.