Cardioembolic stroke remains one of the most severe manifestations of cardiovascular disease, with atrial fibrillation (AF) responsible for a large proportion of ischemic cerebrovascular events. Stroke prevention strategies are currently dominated by oral anticoagulation guided by CHA2 DS2 -VASc scores, which emphasize age and comorbidities and therefore have limited applicability in younger patients with low conventional risk profiles. Although bleeding risk is routinely assessed using tools such as HAS-BLED, lifelong anticoagulation may still confer a substantial cumulative hemorrhagic burden over decades of treatment. The left atrial appendage (LAA) represents the primary anatomical source of thromboembolism in AF, yet current guidelines largely restrict surgical or percutaneous LAA exclusion to patients with AF who have contraindications to anticoagulation, reflecting a predominantly reactive approach. This Perspective advocates reconsideration of prophylactic surgical LAA exclusion at the time of open mitral valve repair in younger patients. Although early mitral repair limits atrial remodeling, it does not abolish lifetime AF risk, and postoperative or late-onset AF remains frequent. Moreover, residual or recurrent mitral regurgitation promotes progressive atrial dilation and fibrosis, increasing longterm thromboembolic risk even in patients initially in sinus rhythm. By integrating atrial remodeling, LAA morphology and function, residual mitral pathology, and the limitations of lifelong anticoagulation, a selective preventive framework emerges. An anatomical brain-heart prevention strategy may reduce lifetime cerebrovascular risk and improve long-term outcomes. While prospective data are needed, existing evidence supports individualized discussion of prophylactic LAA exclusion during mitral valve repair in selected young patients with structural atrial disease.
Prophylactic surgical left atrial appendage exclusion in young patients undergoing open-heart surgery for mitral valve repair: A brain-heart preventive perspective
Jacob Zeitani
2026
Abstract
Cardioembolic stroke remains one of the most severe manifestations of cardiovascular disease, with atrial fibrillation (AF) responsible for a large proportion of ischemic cerebrovascular events. Stroke prevention strategies are currently dominated by oral anticoagulation guided by CHA2 DS2 -VASc scores, which emphasize age and comorbidities and therefore have limited applicability in younger patients with low conventional risk profiles. Although bleeding risk is routinely assessed using tools such as HAS-BLED, lifelong anticoagulation may still confer a substantial cumulative hemorrhagic burden over decades of treatment. The left atrial appendage (LAA) represents the primary anatomical source of thromboembolism in AF, yet current guidelines largely restrict surgical or percutaneous LAA exclusion to patients with AF who have contraindications to anticoagulation, reflecting a predominantly reactive approach. This Perspective advocates reconsideration of prophylactic surgical LAA exclusion at the time of open mitral valve repair in younger patients. Although early mitral repair limits atrial remodeling, it does not abolish lifetime AF risk, and postoperative or late-onset AF remains frequent. Moreover, residual or recurrent mitral regurgitation promotes progressive atrial dilation and fibrosis, increasing longterm thromboembolic risk even in patients initially in sinus rhythm. By integrating atrial remodeling, LAA morphology and function, residual mitral pathology, and the limitations of lifelong anticoagulation, a selective preventive framework emerges. An anatomical brain-heart prevention strategy may reduce lifetime cerebrovascular risk and improve long-term outcomes. While prospective data are needed, existing evidence supports individualized discussion of prophylactic LAA exclusion during mitral valve repair in selected young patients with structural atrial disease.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
