The best way to prevent cardioembolic stroke remains early detection and treatment of AF - WD Freeman
image by: Atrial Fibrillation Association - US
The diagnosis of cardioembolic stroke has two sides to the coin: on the negative side, there is the absence of evidence of another cause of stroke. On the positive side, there is evidence of a cardioembolic stroke such as a Holter recording showing intermittent atrial fibrillation, an echocardiogram showing a cardioembolic source such as thrombus in the left atrium, a ventricular aneurysm, ventricular dyskinesia or cardiomyopathy.
An additional important consideration is the clinical pattern of cerebral involvement: a patient with cortical ischaemia in multiple vascular territories should be regarded as having a cardioembolic (or aortic atheromatous) source. For example, if a right-handed patient has a left homonymous hemianopsia either simultaneous with or on a separate occasion from an episode of aphasia and weakness of the right arm, this must be regarded as cardioembolic.
Because the risk of recurrent stroke is high soon after a cardioembolic event, it is more prudent to anticoagulate the patient pending the results of investigations, rather than wait several weeks to anticoagulate the patient after the results are available from an echocardiogram and Holter recording (followed by more prolonged ECG monitoring if the initial Holter is negative). Indeed, if there is a strong suspicion of a cardioembolic source, as described above, it is now more prudent to anticoagulate the patient with a DOAC than to persist with antiplatelet therapy. Two trials of this approach in patients with ESUS are in progress.
Importance of anticoagulation for cardioembolic stroke
In considering prevention of cardioembolic stroke, it is crucial to understand that antiplatelet agents are not anticoagulants. Antiplatelet agents prevent formation of white thrombus (platelet aggregates that form in the setting of fast flow, in arteries and perhaps on heart valves). The kind of thrombus that forms in the setting of stasis, such as in the left atrial appendage in atrial fibrillation, in ventricular dyskinesia and in deep veins (leading to paradoxical embolism), is called red thrombus. It results from polymerisation of fibrin, formation of a mesh of long fibrin strands similar to cotton wool, with entrapped red blood cells. To prevent formation of red thrombus it is necessary to use anticoagulants. This is why antiplatelet agents are much less effective than anticoagulants in preventing stroke from atrial fibrillation.
Many physicians are reluctant to prescribe anticoagulants, based on bad experiences with warfarin. Haemorrhage rates are much higher in the real world than in clinical trials, and haemorrhages tend to occur early after initiation of warfarin. Gomes et al reported that among patients with a high risk of stroke from atrial fibrillation, more than 16% had a haemorrhage within 30 days of initiating warfarin. This is a serious problem; many studies report that more than half of patients who should be anticoagulated for atrial fibrillation do not receive anticoagulants at all. A higher proportion is not effectively anticoagulated: Gladstone et al reported that among patients with atrial fibrillation and first-ever stroke, after excluding patients with known contraindications to anticoagulation (not to antiplatelet therapy), only 10% were adequately anticoagulated.
Some physicians, thinking that antiplatelet therapy is safer than anticoagulation, may consider dual antiplatelet therapy for patients who are reluctant to take warfarin, or in whom it is thought that warfarin is not safe. That approach does not work; Connolly et al reported that adding clopidogrel to aspirin reduced stroke from atrial fibrillation by only 0.67%.
Probably true contraindication to anticoagulation is less common than many physicians believe. For example, reluctance to prescribe anticoagulation to elderly patients because of fear that the patient may fall is misplaced: anticoagulation is even more beneficial in the elderly than in younger patients,20 and it would take ~295 falls to equal the risk of not taking anticoagulants in atrial fibrillation. Most intracerebral haemorrhages can be prevented by effective blood pressure control, and most serious gastrointestinal haemorrhages can be prevented by treating Helicobacter pylori.
Fortunately, with the availability of new DOACs, the decision to anticoagulate for cardioembolic stroke is now much easier. For patients in whom anticoagulation truly seems contraindicated (eg, patients with recurrent intracerebral haemorrhages from amyloid angiopathy), removal or occlusion of the left atrial appendage should be considered. Most thrombi in atrial fibrillation occur in the left atrial appendage. The atrial appendage can be removed with closed chest robotic surgery, or occluded with an implant. Left atrial occlusion has become safer in recent years.
Source: J David Spence, Excerpt from Cardioembolic stroke: everything has changed, Stroke and Vascular Neurology, June 26, 2018.