Pathophysiology

The vast majority of ACS is caused by thrombosis developing at the site of an atherosclerotic plaque in a coronary artery (Davies 2000). As the plaque grows, it gradually occludes the lumen of the artery, thus reducing the amount of blood flow. Plaques are composed of a lipid core covered by a fibrous cap (Jowett & Thompson 2003) (see Figure 2.1).

ACS is most frequently caused by the development of a blood clot at the site of the plaque. Usually this occurs where the outer covering of the plaque ruptures, exposing the thrombogenic inner core to blood in the arterial lumen (Davies 2000). Platelet aggregation and fibrin deposition occur (Jowett & Thompson

2003). Initially the thrombus forms in the plaque and then extends into the lumen.

The presentations of ACS are caused in slightly different ways.

• If the clot partially occludes the lumen, resulting in sharply reduced blood flow, unstable angina results.

• If the clot occludes the lumen but spontaneously dissolves or if there is distal embolisation causing myocardial damage, NSTEMI results.

• If the clot completely occludes the lumen, AMI involving the full thickness of the ventricular wall will result. This is associated with ST segment elevation on the electrocardiogram (ECG). In this case a STEMI has occurred.

Figure 2.2 shows how the pathophysiology and ECG changes are linked. The diagnosis and therefore treatment of ACS in the acute phase are based on clinical history, evidence of risk factors and the ECG changes rather than the pathological processes described above. It is recognised that there is a continuum between unstable angina and NSTEMI (British Cardiac Society 2001).

Arterial lumen

ïbrous cap

'lot formation

Fig. 2.1 Clot formation at the site of an atheromatous plaque.

Lipid pool

ïbrous cap

'lot formation

Fig. 2.1 Clot formation at the site of an atheromatous plaque.

Condition Pathophysiology

Typical ECG trace*

Biochemical markers

Stable angina Stable plaque p A t Can be normal Absent

Unstable angina jjtto Clot formation Jl T wave inversion Absent

NSTEMI jttTP 1 ■ Distal embolisation A ST segment depression Present distal embolisation _/vJ| ^^

artery occlusion ^^^

STEMI J||||y Full artery occlusion A —. ST segment elevation Present

5 These are typical ECG presentations - different ECG morphology or normal ECG is possible

Fig. 2.2 Classification in acute coronary syndrome.

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