The article addresses an increasingly common practice: prophylactic left atrial appendage (LAA) exclusion in patients without atrial fibrillation (AF). It questions whether this intervention, despite its potential thromboembolic benefits, is physiologically neutral. Unlike the remodeled appendage typically found in patients with AF, the LAA in sinus rhythm remains an active, electrically integrated structure that contributes to left atrial reservoir function, atrial compliance, and atrial natriuretic peptide secretion. Based on this premise, the author proposes that its exclusion may produce a distinct phenotype of iatrogenic atrial dysfunction in a subset of patients.

The proposed mechanism involves several simultaneous consequences of LAA exclusion, including loss of mechanical function, electrical isolation, and neurohormonal changes. These effects occur in the setting of cardiac surgery, when the atrium is already exposed to inflammation, fluid shifts, autonomic activation, and atrial stretch. Together, these changes could promote atrial arrhythmias and impair atrial function, while also introducing uncertainty regarding subsequent rhythm surveillance and antithrombotic management. To provide a structured basis for investigating this hypothesis, the author proposes five clinical domains: procedural, temporal, electrical, mechanical, and management-related.

The author concludes that iatrogenic atrial dysfunction syndrome (IADS) should not currently be regarded as an established clinical entity, but rather as a proposed, unvalidated post-procedural phenotype requiring confirmation through prospective studies.

COMMENTARY:

The most interesting aspect of this article is not the proposal of a new syndrome. It is probably too early to define a distinct clinical entity. Its real value lies in questioning a practice that may gradually come to be regarded as harmless. LAA exclusion has become increasingly straightforward during cardiac surgery, and its rationale for stroke prevention in patients with established AF is well recognized. The difficulty arises when the same reasoning is extended to patients who arrive in the operating room in sinus rhythm. In these patients, we are not excluding a remodeled, poorly contractile, and electrically altered appendage, but rather a structure that remains functional, contributes to cardiac mechanics, and participates in neurohormonal regulation. This distinction changes the question. It is no longer simply whether we can prevent a potential future stroke, but whether we are altering a healthy structure before fully understanding the functional consequences. The issue is not merely whether the procedure can be performed, but in which patients it is justified and what functional effects it may produce.

The hypothesis proposed by Shuhaiber is also reasonable from a pathophysiological perspective. The LAA contributes to left atrial compliance and reservoir function, maintains electrical activity, and participates in neurohormonal regulation through atrial natriuretic peptide secretion. Its exclusion may simultaneously alter all three components. The perioperative environment of cardiac surgery, characterized by inflammation, abrupt changes in loading conditions, autonomic activation, fluid shifts, and ischemia-reperfusion injury, makes the atrium particularly vulnerable. It is therefore plausible that, in selected patients, the cumulative effect of these insults could lower the threshold for developing postoperative atrial fibrillation (POAF) or persistent abnormalities in atrial mechanics. Nevertheless, a plausible pathophysiological explanation does not establish causality. POAF is common and multifactorial, and the author himself acknowledges that LAA exclusion cannot be considered its sole cause, or probably even its dominant cause. At most, it may represent an additional contributing factor. The challenge will be to determine how much of the observed POAF can genuinely be attributed to LAA exclusion and how much simply reflects the postoperative course itself.

Another important consideration is that the potential benefits and harms do not occur on the same timescale. The anticipated benefit of prophylactic exclusion lies in the future and depends on several conditions. The patient would need to develop AF, the appendage would need to become a relevant source of embolism, and closure would have to remain complete. By contrast, any mechanical or neurohormonal changes begin at the time of the procedure. This does not necessarily mean that prophylactic LAA exclusion should be abandoned, but it does argue against allowing the procedure to become routine without solid supporting evidence. Moreover, the issue does not end with clip placement or surgical ligation. Incomplete exclusion, a residual stump, or persistent communication may diminish the expected thromboembolic benefit while creating a false sense of protection during follow-up. From a surgical perspective, the practical implication is clear: deciding to exclude the appendage is not enough. The indication, surgical technique, and confirmation of successful exclusion also matter, particularly when operating on a structure that was initially healthy.

The concept of IADS should, for now, be approached with caution. Grouping POAF, mechanical abnormalities, neurohormonal changes, and subsequent uncertainty regarding anticoagulation under a single label is appealing, but it remains unclear whether these findings truly constitute a distinct clinical phenotype. The author presents the concept as a provisional framework intended to organize a hypothesis rather than establish a diagnosis. That is probably the article’s greatest contribution. Rather than simply introducing another syndrome, it draws attention back to the physiological importance of a structure that, for years, has been viewed almost exclusively as a potential source of thrombus formation. Before considering the LAA expendable in patients without AF, we need to better understand what function is lost when it is excluded, which patients may be particularly affected by that loss, and whether the potential long-term thromboembolic benefit outweighs the possible immediate functional cost. The next step, rather than accepting a new diagnostic label, may be to design studies capable of answering these questions.

REFERENCE:

Shuhaiber JH. Iatrogenic atrial dysfunction after prophylactic left atrial appendage exclusion: a proposed post-procedural atrial phenotype. Europace. 2026 Jun 2;28(6):euag138. doi: 10.1093/europace/euag138. PMID: 42290286; PMCID: PMC13318152.