Myocardial Ischaemia

There are different levels of ischaemia which causes different levels of problems, these are described below:

• Functional ischaemia: there is no damage to cardiac muscle, so pathologically nothing special. Causes angina --> may progress to arrhythmias --> causes death.

• Slow-onset occlusion: gradual onset of ischaemia takes some time, allowing for sufficient collaterals to develop. You get fibrinous necrosis, and therefore such areas are replaced by fibrous tissue. Replacement of tissue causes cardiac hypertrophy (i.e.: existing muscle fibres get larger to subsidise for losses), and too much replacement will render “functional syncytium” useless (i.e.: compliance reduction) – heart failure.

• Rapid-onset ischaemia: MI + associated complications (i.e.: arrhythmias)

The pathological aspects of each of the above

Functional ischaemia: Angina is caused because of stable chronic plaque causing a “Fixed coronary obstruction”. This can lead to MI, LVF.

Chronic Ischaemia: usually causes “triple vessel disease” – where atheroma build up occurs in LAD, Circumflex, & RCA. Slow replacement with fibrotic tissue cause other muscle fibres to hypertrophy --> cardiac dilatation --> cardiac failure.

Rapid onset ischaemia / MI: Remember that cholesterol & lipid material infiltrate the tunica intima. This thickens it, and raises it (i.e.: look at picture above). The intima + associated atherosclerosis = atheroma. It has an overlying fibrous capsule. This breaks and exposes the lipids to blood. This induces platelet aggregation / thrombus formation  resulting in unstable angina / infarction. If this happens in LAD = anteroseptal inf., lateral angle of RCA = inferior inf., proximal lateral circumflex = lateral inf. Focal transmural inf. = post part of LV + septum, focal subendocardial infarct (known as global sub. Inf.).

Category: Pathology Notes