Cardioembolic Stroke

Abstract

Cardiac embolism accounts for an increasing proportion of ischemic strokes, and might multiply several-fold over 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” (ESUS) as a distinct target for investigation. Second, recent clinical trials have indicated that ESUS may often stem from subclinical atrial fibrillation (AF) 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 AF. Such an atrial cardiopathy may explain many cases of ESUS, and oral anticoagulant drugs may prove to reduce stroke risk from atrial cardiopathy given its parallels to AF. Non-vitamin K antagonist oral anticoagulant (NOAC) drugs have recently expanded therapeutic options for preventing cardioembolic stroke and are currently being tested for stroke prevention in patients with ESUS, including specifically those with atrial cardiopathy. Fourth, increasing appreciation of thrombogenic atrial substrate and the common co-existence of cardiac and extra-cardiac stroke risk factors suggests benefits from global vascular risk factor management in addition to anticoagulation. Finally, improved imaging of ventricular thrombus plus the availability of NOAC drugs may lead to better prevention of stroke from acute myocardial infarction and heart failure.

Association between excessive supraventricular ectopy and subclinical cerebrovascular disease: a population‐based study

“…Therefore, the present findings suggest that the effect of increased SVEBs on ischaemic stroke may partly occur through a gradual increase in these subclinical cerebrovascular disease burdens. The present findings also emphasize the concept that an increased SVEB is considered a marker of atrial disease or atherosclerosis burden and indicate that increased SVEBs might improve risk stratification of individuals at high risk of subclinical cerebrovascular disease and consequently apparent ischaemic stroke. The advantage of using SVEBs as a novel method for detecting the association with ischaemic cerebrovascular diseases would be that SVEBs are more frequent than episodes of AF.…”

“…Increased SVEBs might represent an atrial cardiomyopathic change that forms an atrial hypercoagulable state resulting in cardioembolism, which is similar to that present in AF [6][7][8]. Increased SVEBs are also accompanied by several risk factors for atherosclerosis [9].…”

Clinical and echocardiographic characteristics of cardioembolic stroke

“…It is increasingly recognized that AF is a marker of abnormal left atrial (LA) function, i.e. an 'atrial myopathy' or 'abnormal atrial substrate', that contributes to thrombus formation even in sinus rhythm [5,6]. This further explains the lack of temporal relationship between periods of AF and CE stroke Correspondence: L. Thomas, Department of Cardiology, Westmead Hospital, Westmead, NSW 2145, Australia (tel.…”

Clinical and Neuroimaging Characteristics in Embolic Stroke of Undetermined versus Cardioembolic Origin: A Population‐Based Study

“…29 Therefore, it is important to perform a comprehensive and targeted diagnostic workup in ESUS that may include transoesophageal echocardiography exam to uncover additional cardioembolic sources of embolism (mitral annular calcification, aortic valve stenosis or calcification, atrial appendage stasis, patent foramen ovale, left ventricle dysfunction, myxoma, infective endocarditis), aortic arch atherosclerosis, cancer-related stroke (hypercoagulability syndrome, marantic endocarditis), as well as high resolution vessel wall imaging that may disclose nonstenotic, unstable, high-risk atherosclerotic plaques in extra-and intracranial arteries, or alternatively branch atheromatous disease. 11,12,[29][30][31] Interestingly, nonstenotic carotid plaques with 3 mm thickness were more prevalent ipsilateral than contralateral to the location of cerebral infarction in ESUS patients. 32 Furthermore, the ESUS Global Registry reported a prevalence of nonstenotic carotid artery plaques and aortic arch atherosclerosis of 79 and of 28%, respectively.…”