Almost all AF patients show the pathophysiological changes that increase stroke risk.
AF’s characteristic aberrant electrical activity means that the atria do have time to contract and move the blood into the ventricles. So, blood remains in the atria and a clot may form. This, in turn, may embolise resulting in an ischaemic stroke.32 Even short AF episodes can damage the atrial endothelium, which expresses factors that activate the coagulation cascade and as well as activating platelets and inflammatory cells. As a result, even short AF episodes can increase stroke risk.5
The left atrial appendage (LAA; figure 6) is the most common site of thrombus formation in the heart.6
At least 90% of emboli that cause stroke in AF patients arise in the LAA.33 The left and right atrial appendages (sacs in the muscle wall) are embryological remnants. Nevertheless, during volume overload, the LAA can act as a reservoir and mediates adaptive responses to the reduction in circulating blood volume.4
The LAA is a long, tubular structure with a narrow opening into the atrium.4 AF means that the emptying of the LAA is often incomplete and slow.34 This makes the LAA particularly prone to blood stasis. So, thrombi are more likely to form in the LAA in patients with mitral valve disease (irrespective of underlying rhythm) and non-valvular AF than in other parts of the heart.4 AF also promotes remodelling of the LAA. Post-mortem studies suggest that the LAA is considerably larger in AF patients compared with people without AF.4
Thrombi formed in the LAA tend to be relatively large. As a result, when the thrombi embolise, the fragment commonly cause ischaemic strokes and peripheral embolism.34The next section summarises the symptoms arising from the pathological changes that underlie atrial fibrillation
Other sections to further your understanding in the disease awareness section include: