Fewer Strokes After AFib Screening Only With Risky Genes

In one post hoc analysis, yes, but the finding is preliminary. The LOOP trial as a whole, in 6,004 adults aged 70 to 90, found no significant stroke reduction from loop recorder screening (hazard ratio 0.80). When 5,656 participants were split by a polygenic risk score for AFib, screening was linked to fewer strokes or embolisms in the above-median half (hazard ratio 0.65) and not in the below-median half (1.06). The interaction was significant (P = 0.006). The authors call the result hypothesis-generating.

Did AFib screening reduce stroke in the LOOP trial overall?

Not significantly. LOOP randomized 6,004 adults aged 70 to 90 with at least one stroke risk factor. One quarter got an implantable loop recorder. Three quarters got usual care.

Screening tripled detection. AFib was diagnosed in 31.8% of the loop recorder group and 12.2% of controls. Anticoagulation was started in 29.7% against 13.1%.

The primary outcome was stroke or systemic embolism. It occurred in 4.5% of the screened group and 5.6% of controls, a hazard ratio of 0.80 (95% CI 0.61 to 1.05). Major bleeding was 4.3% against 3.5%. Neither gap reached significance.

The authors wrote that not all AFib may be worth screening for. That left open which people gain most.

What did the genetic-risk analysis find?

It found an interaction. The analysis covered 5,656 AFib-naive participants aged 70 or older with genetic data. Each had a polygenic risk score for AFib. Median follow-up was 5.4 years. AFib was diagnosed in 969 people (17.1%). Stroke or systemic embolism occurred in 296 (5.2%).

The score did track AFib itself. The hazard ratio per standard deviation increase was 1.20 (95% CI 1.13 to 1.28).

Screening effects split by score. In people at or above the median score, screening was linked to fewer strokes or embolisms, with a hazard ratio of 0.65 (0.43 to 0.97). Below the median it was 1.06 (0.72 to 1.57). The interaction between arm and score was significant at P = 0.006.

This is a prespecified post hoc analysis. The authors describe the findings as hypothesis-generating.

Does genetic risk change the bleeding picture too?

It did in this analysis. Screening was linked to more major bleeding at lower genetic risk (interaction P = 0.036). In the below-median half the hazard ratio was 1.71 (95% CI 1.12 to 2.64).

The same analysis found that each standard deviation of score raised the odds of an AFib episode lasting 24 hours or longer. The odds ratio was 1.35 (1.02 to 1.78).

Together the pattern is one of more benefit and fewer harms at higher score. It rests on subgroups of a single trial.

How does this fit with other AFib screening trials?

Other trials have not shown a stroke reduction from screening either. GUARD-AF screened people aged 70 and older in primary care with a 14-day patch monitor. Among 11,905 participants, stroke hospitalization was 0.7% with screening and 0.6% with usual care (hazard ratio 1.10, 95% CI 0.69 to 1.75). That trial stopped enrolling early and reported low event rates. See the GUARD-AF results.

None of these trials used a consumer wearable. Whether finding more AFib with any device prevents strokes is covered in whether finding more AFib prevents strokes.

On genetics generally, a 2021 review describes many variants tied to AFib susceptibility. It frames using that knowledge to pick who gets screening or treatment as an open question. The LOOP analysis is an early data point on that question.

What does this not settle?

It is one subgroup analysis in one trial. Interaction tests across a risk score can produce chance findings, and the authors label theirs hypothesis-generating. No second trial has confirmed it.

The population was narrow. All participants were 70 or older with stroke risk factors and a loop recorder implanted. Results may not carry to younger people, to people without risk factors, or to wearable-based detection. The 296 stroke or embolism events are also few for subgroup work.

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