John Mandrola


March 20, 2015

The current bias of medicine is strong. When we are in doubt, when evidence is sparse, doctors do more, not less. Internists prescribe, cardiologists implant, surgeons cut. We know what we know. So it goes with the left atrial appendage and heart surgery.

A cardiac surgeon might say: why not take care of the left atrial appendage (LAA) while we are in there? It can't hurt. It can only help. The appendage is the most likely source of thrombus. And these patients are at high risk for AF and stroke.

The 2014 AF treatment guidelines advise that "surgical excision of the LAA may be considered in patients undergoing cardiac surgery." The guideline writers place this statement in category class IIb; they grade the level of evidence as C.[1] Translation: they have no idea—because there are so few data. Recall, also, that class-IIb, level-C statements hover precariously close to class III—not useful and possibly harmful.

I wonder how many left atrial appendages have been clipped, stapled, and excised in the name of helping patients.

A study presented (as an oral abstract) at the American College of Cardiology 2015 Scientific Sessions casts some doubt on yet another bias of medicine.[2]

The Study

A group of researchers from the Mayo Clinic analyzed their cardiovascular surgical database of 10 663 adults who underwent coronary artery bypass or valve surgery from 2000 to 2005. They excluded patients with concurrent or prior history of maze procedures, catheter ablation, or congenital heart disease.

The purpose of the study was to determine the short- and long-term risks and benefits of prophylactic LAA closure at the time of cardiac surgery. The researchers counted three easy measures as outcomes: postoperative AF, ischemic strokes, and death.

The study was not a randomized trial. The cohort included 9323 patients who did not have LAA exclusion and 468 who had LAA closure. The research team used propensity-score matching to reduce imbalances between the groups. Each patient who underwent LAA closure was matched (on 26 covariates) to one patient who underwent no LAA closure. The median follow-up was 5.6 years. AF prior to surgery was noted in 25% of both groups.


The unadjusted data before propensity matching are shown in this table.

Outcome LAA closure (%) No LAA closure (%) P
Postop AF 68.4 31.9 <0.001
Ischemic stroke 4.3 5.1 NS
Mortality 25.7 23.2 0.05

To account for imbalances in the groups, the researchers reported results after propensity matching.

Patients who underwent LAA closure were nearly three times more likely (OR=2.83) to have postop AF.

LAA closure had no effect on long-term stroke (OR 0.80, 95% CI 0.53–1.22) or mortality (OR 0.99, 95% CI 0.80—1.22).

Conclusions and Caveats

Although surgical LAA closure was safe, it was associated with a threefold increased risk of postoperative AF and did not significantly influence the long-term risk of stroke or death.

The authors pointed out that LAA closure was not randomly assigned, and although the groups were well matched on many variables, unmeasured confounders could have influenced the result. The bullet point on the final slide of the abstract urged caution when interpreting results.


I spoke with cardiac arrhythmia surgeon Dr Ralph Damiano (Washington University, St Louis, MO) about the study. He emphasized that this was retrospective nonrandomized data. "We don't know why certain patients had appendage closure. Propensity matching is better than no matching, but there is a strong possibility of selection bias," he said.

On the matter of postoperative AF, Damiano added that "in animal models, any sort of atriotomy predisposes to AF, probably because of inflammation."

By email, electrophysiologist and outcomes researcher Dr Mintu Turakhia (Stanford University, CA) also noted the limits of propensity matching. In this study, "many things could have influenced treatment selection [LAA closure] and outcome, including frailty, pump time, surgical approach, or attending physician and/or team."

Limitations aside, I believe these are thought-provoking data. They come from the real world. It is a large database from a respected medical center. And it adds (something) to an area where there is little evidence—just eminence.

These data raise questions about add-on surgical LAA closure. For instance:

Three times the risk of postoperative AF. Why is that? It is not meaningless, is it?

In patients with enough heart disease to undergo surgery, LAA closure did not associate with lower risks of stroke or death over long-term follow-up. That's interesting. Was it all statistics, or do focal treatments (LAA closure) struggle against systemic diseases (stroke)?

What does this say about the concept—the fundamental underpinnings—of LAA closure? Although many of these patients did not have documented AF before surgery, most had elevated CHADS-VASC scores.

At the very least, these data support the role of inflammation as a mechanism in AF, urge caution about prophylactic appendage closure, and provide a strong hypothesis for randomized trials, such as the Left Atrial Appendage Occlusion Study III (LAAOS III). which is currently enrolling patients and not expecting results until 2019.

And . . . if you would allow a tiny shred of doubt to enter your mind, these data might just soften the sinister image of the left atrial appendage. Could it be there for a reason?



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