Cardioembolic Stroke

Abstract

Cardiac embolism accounts for an increasing proportion of ischemic strokes and might multiply several-fold during the next decades. However, research points to several potential strategies to stem this expected rise in cardioembolic stroke. First, although one-third of strokes are of unclear cause, it is increasingly accepted that many of these cryptogenic strokes arise from a distant embolism rather than in situ cerebrovascular disease, leading to the recent formulation of embolic stroke of undetermined source as a distinct target for investigation. Second, recent clinical trials have indicated that embolic stroke of undetermined source may often stem from subclinical atrial fibrillation, which can be diagnosed with prolonged heart rhythm monitoring. Third, emerging evidence indicates that a thrombogenic atrial substrate can lead to atrial thromboembolism even in the absence of atrial fibrillation. Such an atrial cardiomyopathy may explain many cases of embolic stroke of undetermined source, and oral anticoagulant drugs may prove to reduce stroke risk from atrial cardiomyopathy given its parallels to atrial fibrillation. Non-vitamin K antagonist oral anticoagulant drugs have recently expanded therapeutic options for preventing cardioembolic stroke and are currently being tested for stroke prevention in patients with embolic stroke of undetermined source, including specifically those with atrial cardiomyopathy. Fourth, increasing appreciation of thrombogenic atrial substrate and the common coexistence of cardiac and extracardiac stroke risk factors suggest benefits from global vascular risk factor management in addition to anticoagulation. Finally, improved imaging of ventricular thrombus plus the availability of non-vitamin K antagonist oral anticoagulant drugs may lead to better prevention of stroke from acute myocardial infarction and heart failure.

Keywords: anticoagulants; atrial cardiomyopathy; atrial fibrillation; atrial myopathy; embolism; heart failure; stroke.

Figure 1

Overlap between cryptogenic stroke, embolic stroke of undetermined source, and cardioembolic stroke.

Figure 2

Relationship between systemic risk factors, atrial substrate, atrial fibrillation, and stroke. Aging and systemic vascular risk factors lead to an abnormal atrial substrate, or atrial cardiopathy, that can itself result in both AF and/or thromboembolism. Once AF develops, it directly worsens atrial contractile function and secondarily worsens the underlying atrial cardiopathy via structural remodeling, both of which further increase thromboembolic risk. At the same time, the systemic vascular risk factors that give rise to atrial cardiopathy and AF also increase stroke risk via non-atrial mechanisms such as large-artery atherosclerosis, systolic heart failure, and cerebral small-vessel disease.