LAUSR

Introduction: Current evidence questions the linear sequence traditionally described in atrial fibrillation, blood stasis, intracavitary thrombus, and embolization to the central nervous system. Currently, new perspectives have been described based on questions from the linearly traditional chronology of events; it is within this scope that the article has its objective. Evidences: The association of the two entities is biologically plausible and supported by different cohorts with a higher risk of developing atrial fibrillation, especially in the cardioembolic form. Concepts (temporal dissociation, biological gradient, etc.) determine the existence of other factors associated with cardioembolism, not exclusively by atrial fibrillation. The entire cascade of events associated with myopathy and atrial remodeling can generate damage to the myocyte and amplify the prothrombotic status. It is important to clarify that atrial myopathy can present itself as atrial fibrillation initially or not, but should always be considered thrombogenic in all the contexts of their clinical presentation. Considering atrial heart disease as a cause of embolic stroke, it could explain that one-third of strokes are considered cryptogenic. Conclusions: The traditional model exclusively associating the presence of atrial fibrillation in the genesis of thromboembolism is incomplete. The concept of atrial cardiopathy where cardioembolism occurs in a non-atrial fibrillation dependent manner fits better with current data. The future challenge is to effectively detect the various manifestations of atrial heart disease, generating direct implications for the identification of patients at risk of stroke and also for better management after a cardioembolic event.