|LETTER TO EDITOR
|Year : 2020 | Volume
| Issue : 3 | Page : 183-184
Embolism somewhere, thrombus nowhere, origin is there in the left atrium: Atrial cardiomyopathy and cryptogenic stroke
Ismail Mohamed Ibrahim
Department of Cardiology, Faculty of Human Medicine, Zagazig University, Zagazig, Egypt
|Date of Submission||17-Apr-2020|
|Date of Decision||21-May-2020|
|Date of Acceptance||29-Aug-2020|
|Date of Web Publication||05-Nov-2020|
Ismail Mohamed Ibrahim
Department of Cardiology, Faculty of Human Medicine, Zagazig University, Zagazig
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Ibrahim IM. Embolism somewhere, thrombus nowhere, origin is there in the left atrium: Atrial cardiomyopathy and cryptogenic stroke. J Cardiovasc Echography 2020;30:183-4
|How to cite this URL:|
Ibrahim IM. Embolism somewhere, thrombus nowhere, origin is there in the left atrium: Atrial cardiomyopathy and cryptogenic stroke. J Cardiovasc Echography [serial online] 2020 [cited 2020 Nov 24];30:183-4. Available from: https://www.jcecho.org/text.asp?2020/30/3/183/300088
Cryptogenic stroke counts for about one-fourth of ischemic stokes. It is considered when a definite cardio-aortic embolism, large artery atherosclerosis, or small-artery disease cannot be identified. In the last decade, the concept of atrial cardiomyopathy (AC) has been revived and was considered a plausible cardiac phenotype explaining some cryptogenic strokes.
The term AC was first published in 1972. Recently, a consensus document by the European Heart Rhythm Association (EHRA) reintroduced AC and defined it as “any complex structural, architectural, contractile or electrophysiological changes affecting atria with potential to produce clinically relevant manifestations.” Accordingly, the features of AC include left atrial dilatation/deformation/dysfunction, left atrial appendage reduced flow, intra-atrial conduction block/electromechanical dyssynchrony, as well as elevated serum brain natriuretic peptide (BNP). Of course, multimodality imaging including newer echocardiographic techniques (e.g., strain rate imaging and three-dimensional echocardiography) in addition to cardiac tomography and magnetic resonance can detect some anatomical and functional features of AC.
Numerous findings support the independent association between AC and stroke risk. First, in Specialized Programs of Translational Research in Acute Stroke, AC without concomitant atrial fibrillation (AF) was found in nearly 65% of patients with cryptogenic stroke. Second, the temporal relationship between AF and stroke was lacking in many studies. Finally, in an analysis of Warfarin Aspirin Recurrent Stroke Study, the secondary prevention benefit of warfarin versus aspirin was significantly higher in patients without AF but with elevated NT-pro-BNP. Mechanistically, strokes associated with AC are perhaps mediated through atrial hypo-contractility, atrial endothelial dysfunction, as well as hyper-coagulability.
The clinical predictors of stroke risk in AF included in CHA2 DS2-VASc are congestive heart failure, hypertension, age ≥75 years, diabetes, prior stroke or thromboembolism, vascular disease, age between 65 and 74 years, and sex category. All of these predictors are known to induce atrial structural and functional remodeling. Hence, the practice of anticoagulation in AF appears to be indirectly targeting the associated AC. This notion may alter the current status of stroke prevention, shifting it to a non-AF-dependent paradigm. Currently, recent research is under way to test the hypothesis of secondary stroke prevention in patients with AC and no concomitant AF. The ongoing Atrial Cardiopathy and Antithrombotic Drugs in Prevention after cryptogenic stroke study aims at comparing secondary prevention through using apixaban versus aspirin in cryptogenic stroke patients with AC. The study results will significantly affect our understanding and management of cryptogenic strokes.
Critical thinking on AC raises many diagnostic and therapeutic issues. First, the EHRA classification is based on atrial histopathology which is clinically impractical. Second, the potential thrombogenic impact of each feature, the interplay between different features, and the final “grade” of AC have not been yet elucidated. Third, estimation of stroke burden in AC patients has not been studied in randomized controlled studies. Lastly, whether or not patients with AC are eligible for primary stroke prevention has not been studied yet. Enormous basic and translational research is encouraged to gain a better understanding of the clinical significance of AC.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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