Aortic Wall Thrombus in TAVI Patients Portends Thromboembolic Events

Severe aortic wall thrombus (AWT) on multidetector CT imaging foreshadows higher risk of thromboembolic events in patients undergoing transfemoral TAVI, a prospective cohort study shows.

The results were published yesterday in JACC: Cardiovascular Interventions.

Brahim Harbaoui, MD, PhD (Hospital Croix-Rousse and Hospital Lyon Sud, France), the study’s senior author, pointed out that while periprocedural complications with TAVI have waned over the years, thromboembolic events and stroke have remained a problem. The incidence tops out at 3% even in low-risk patients, he observed. “It’s a major concern for patients and for us, because despite the increasing experience and the newer devices, we haven’t managed to decrease the incidence of stroke.”

AWT historically has been considered a trivial finding, one that doesn’t merit precise assessment, said Harbaoui. Importantly, while the new results confirm stroke rates are higher in patients with AWT, what’s unclear is whether the AWT is itself provoking the events. “With this study we cannot say if aortic wall thrombus is a risk factor or is a risk marker,” he stressed.

With further research, though, Harbaoui said this characteristic might one day be used to guide management. Options for mitigating risk in patients with severe AWT, he noted, include use of alternative access routes, adaptations during transfemoral access (eg, a longer sheath), and cerebral protection devices.

For this last option, the randomized PROTECTED TAVR trial failed to show that cerebral embolic protection reduced all stroke in patients undergoing TAVI. Some in the structural field, however, have held out hope that these devices might, when used correctly, mitigate risk, especially for more serious stroke types and in patients at the highest risk—pinpointing that subset has proved elusive.

These observations with AWT may point to a way forward, Harbaoui suggested. “[If] such a trial is performed in selected patients with aortic wall thrombus, perhaps the results would not be the same.”

With this study we cannot say if aortic wall thrombus is a risk factor or is a risk marker. Brahim Harbaoui

Toby Rogers, MD, PhD (MedStar Washington Hospital Center, Washington, DC), commenting on the results for TCTMD, said that AWT is “certainly a theoretical concern and there have been papers in the past that have shown the very mobile thrombus, or mobile atheroma, in the arch may be associated with thromboembolic events.”

Here, the association is indeed strong, Rogers confirmed. “What’s nice about this is it’s a very systematic study in a cohort of transfemoral patients, which is what the vast majority of TAVR procedures are in this day and age, and they provide a scoring scheme to identify patients at high risk.”

Severe AWT Stands Out

Led by Marc Bonnet, MD (Hospital Croix-Rousse and Hospital Lyon Sud), the researchers enrolled 641 transfemoral TAVI patients treated between January 2011 and April 2022. All were prospectively evaluated for the presence of AWT using Brilliance 64 and iCT (Philips) or Discovery CT750 HD (GEMS) multidetector CT scanners.

For each of the 617 patients whose aorta was visualized in its entirety on CT, Bonnet et al quantified AWT using a 0-10 score based on thrombus type, thickness, and size as well as the number of aortic segments involved, with values of ≥ 8 considered severe. In the aorta, the most common locations of the AWT were infrarenal/renal, zones 8-9 (24.8%) and thoracic descending, zones 3-4 (20.4%).

The primary endpoint (a composite of thromboembolic events that included ischemic stroke, blue toe syndrome, bowel ischemia, and other solid organ infarction) occurred in 3.3% of the cohort.

Severe AWT—identified in 11.4%—was associated with a substantially higher risk of the primary outcome (13.7% vs 1.8% without severe AWT; OR 8.48; 95% CI 3.36-21.40) that persisted after adjustment for comorbidities and procedural characteristics. No such associations were seen for moderate or none/mild AWT. The only other factor to significantly predict the primary outcome was peripheral vascular disease (OR 4.48; 95% CI 1.64-11.20).

Additionally, severe AWT was linked to more stroke (OR 5.66; 95% CI 2.00-15.30) and procedural death (OR 4.66; 95% CI 1.80-11.30), relationships that again persisted after adjustment. Certain AWT characteristics, as well as specific AWT locations, also conferred higher risk.

What’s Driving the Link?

Like Harbaoui, Rogers, too, stressed that the current analysis, by design, doesn’t speak to mechanism.

“There are a few things that go against this being a direct causal link [where] a piece of atheroma breaks off and goes to the brain,” he said, noting that most of the observed AWT was located past the aortic arch. “It is at least a little hard to understand how thrombus there could get to the brain, because it would have to go upstream.”

It’s possible that AWT is “a marker of more diffuse atherosclerotic disease” that in turn increases patients’ risk of stroke, Rogers said.

Harbaoui said the researchers are currently in touch with industry in the hopes of conducting a randomized trial that employs embolic protection in high-risk patients who have severe AWT as a way to reduce stroke.

The potential for a targeted approach like this, Rogers agreed, “is certainly a very interesting question to be answered prospectively.”

In PROTECTED TAVR, for example, “there were no obvious risk factors that identified patients who would benefit from cerebral embolic protection,” he pointed out. “Before that study, we all thought we were smart [and] could recognize a patient who has high risk of stroke during TAVR,” such as those with a prior stroke, who had a bicuspid aortic valve, or were undergoing a valve-in-valve procedure.

“None of those things came out of that dataset as being predictors,” said Rogers, but AWT wasn’t looked at in the trial. “If that turned out to predict benefit from cerebral embolic protection, then that could certainly be practice-changing—that study just needs to be done.”

Beyond a device-based solution, Bonnet and colleagues highlight the possibility of pharmacologic strategies for prevention. Importantly, they add, their findings could also have relevance to other endovascular procedures.

Yousif Ahmad, MD, PhD, and Alexandra J. Lansky, MD (both from Yale School of Medicine, New Haven, CT), in an editorial accompanying the study, point out that the Sentinel device (Boston Scientific) tested in PROTECTED TAVR is not alone: other tools for cerebral embolic protection are being developed that might be more effective.

The current study injects a fresh perspective, they say. “Rather than purely focusing on new devices or technical factors, an alternative global strategy to reducing stroke and other embolic complications after TAVR is to focus on identifying patients at highest risk for stroke who would benefit the most from protection.”