Clinical Benefits of Concomitant Surgical Ablation for Atrial Fibrillation in Patients Undergoing Mitral Valve Surgery

[www.practiceupdate.com]

I had a MVR (mitral valve repair) and MAZE minimally invasive surgery at Penn in 2012. This was due to a severely leaky valve, and I was in constant AFIB at the time. Thereafter I had no recorded AFIB until 1/2021, when I had a CV.

I have 2 thoughts about the study:
1. Could the MAZE procedure have kept me from getting tPA following a stroke while still at Penn?
2. Does the previous MAZE preclude/suggest any of the current CA techniques?

Note that I have 2 scheduled EP consults this week for a possible CA.
BTW, this forum is great, I check it out several times a day!

Quote
autks
1. Could the MAZE procedure have kept me from getting tPA following a stroke while still at Penn?
2. Does the previous MAZE preclude/suggest any of the current CA techniques?

1. Possibly. If the stroke occurred right after the MAZE procedure, before the incisions had had time to heal, then tPA would probably be considered too risky.

2. No, shouldn't matter.

[www.ncbi.nlm.nih.gov]

They tested stopping anticoagulation after 3 months on this MAZE trial. Group A continued taking anticoagulation. 5 bled. One died from a stroke while on an anticoagulant two years later while another had a stroke immediately after waking up from anesthesia. No reported strokes for group B for those who took nothing. How can that be? It’s a small sample but still I wonder.

Bullet point:

“Embolism secondary to atrial fibrillation, which accounts for 25% of all ischemic strokes, has a 60% rate of death and severe disability.[1,2] Unfortunately, due to its risks and inconveniences, anticoagulation therapy is underused in real-world practice.”

Nothing to be concluded from that paper because of the sample size. With only 2 strokes and 5 bleed events, random chance could easily have reversed those numbers.

I agree and had mentioned it was a small sample . I shared it because of the italic bullet point message mentioned in the study.

Reading the paper, almost all the subjects were using warfarin. There are issues keeping INR in the 2 to 3 therapeutic range. Other thoughts to keep in mind are a) there are other causes of stroke; b) warfarin or other anticoagulants do not provide 100% stroke risk reduction. There were 8 subjects in the OAC group with prior stroke vs 2 in the non OAC group. Lastly, subjects weren't randomized in to the OAC vs non OAC groups, it was based on what their docs decided. It is possible that the docs put their subjects in the OAC group for reasons that were related to the docs' sense of their stroke risk.