High Fibrosis at Greater Risk of Stroke and Precludes Catheter Ablation: Lessons Learned from the DECAAF Trial
By Steve S. Ryan, PhD
Presenter: Dr. Nassir Marrouche of the Comprehensive Arrhythmia Research and Management Center (CARMA) at the University of Utah Health Sciences gave a presentation entitled “The Ablation Lesion or the Atrial Disease? Lessons Learn from DECAAF.”
Background: In his BAFS 2011 presentation, (see BAFS 2011: MRI [Magnetic Resonant Imaging) Applied to A-Fib), Dr. Marrouche described the data enhancement (also called “delayed-enhancement”) MRI process which uses a metallic Gadolinium contrast dye to see in 3D and identify collagen fibrotic areas in the heart. Dr. Marrouche uses MRI to separate A-Fib patients by their degree of fibrosis into four “stages:” In addition to other factors, the amount of fibrosis in the left atrium is key to ablation treatment success.
• “Utah Stage 1” low scarring or fibrosis
• “Utah Stage 2” 5%-20% fibrosis
• “Utah Stage 3 20%-35% fibrosis
• “Utah Stage 4: greater than 35% fibrosis
Detecting Fibrosis with the DE-MRI
To begin, Dr. Marrouche showed slides of how the delayed-enhancement MRI (DE-MRI) is used to detect fibrosis.1 Using “Masson trichome” staining he showed slides of how normal myocytes (heart muscle) appear normal and red, while areas of collagen (fibrosis) appear blue and almost blot out the red myocytes in someone with extensive A-Fib.
DECAFF Study Findings
The Delayed Enhancement-MRI Determinant of Successful Catheter Ablation of Atrial Fibrillation trial (DECAAF) was conducted at 15 different centers worldwide between 2010 and 2011. The degree of fibrosis in patients with atrial fibrillation was followed before and after their catheter ablation.2
The DECAFF study showed that patients with more fibrosis (Utah Stage III and IV) had less successful ablation outcomes. They also had a greater risk of stroke. MRI was also used to detect ablation scarring and gaps in ablation lesions. (The various centers used different types of catheter ablation such as PVI with RF or with Cryo.) In a somewhat controversial statement, Dr. Marrouche had previously stated, “encircling the (pulmonary) veins with lesions as seen on the MRI was not important in terms of treatment success.”3
These findings support Dr. Marrouche’s previous presentation at the Boston A-Fib Symposium (see BAFS 2011: MRI [Magnetic Resonant Imaging] Applied to A-Fib).
The only predictor of atrial fibrosis was hypertension (p=0.004).
The predictors of recurrence after ablation were:
- Left atrial fibrosis (p<0.0001) Each 1% increase in fibrosis was associated with a 6% increased risk of recurrence.
- Mitral valve disease (p<0.0001)
- Left Ventricular Ejection Fraction (p<0.05)
Dr. Marrouche discussed what he called residual fibrosis “fibrotic tissue not covered with ablation lesions.” Residual fibrosis is measured by subtracting ablated scar area from pre-ablation DE-MRI. The more residual fibrosis, the more there is an increased risk of recurrence.
DECAFF Conclusions: Utah Stage III & IV Fibrosis Levels Not Recommended For Catheter Ablation
Dr. Marrouche concluded from the DECAFF study that “Atrial fibrosis detected using DE-MRI is a strong and independent predictor of procedural outcome in patients undergoing ablation of atrial fibrillation.” For all patients in Utah Stage IV and for many in Utah Stage III, they are not recommended for catheter ablation but should be put on life-long medication instead. Because of the extent of their fibrosis, they have less successful ablation outcomes.
Patients with High Levels of Fibrosis More at Risk of Stroke
One of the most important findings for patients from Dr. Marrouche’s studies is that patients with high levels of fibrosis are more at risk of stroke. Utah Stage IV patients were four times more likely to have a stroke than patients with a low level of atrial fibrosis. In his previous work, Dr. Marrouche found that even patients in simple early-onset paroxysmal A-Fib can have high levels of fibrosis. (Many other factors besides A-Fib can produce fibrosis in the heart.) Anyone in A-Fib should probably have an MRI to measure their level of fibrosis. Instead of the less empirical CHADS2 score, an MRI would quantify whether or not a person needs to be on anticoagulants. MRIs to measure fibrosis should become a routine diagnostic tool.
Hypertension Produces Fibrosis
In Dr. Marrouche’s studies, hypertension was the only guaranteed predictor of developing fibrosis. We already knew that hypertension was a cause or trigger of A-Fib. Thanks to Dr. Marrouche, we also now know that hypertension causes or triggers fibrosis. If you have real hypertension, do what you can to lower it (diet, exercise, medications, etc.) Though sometimes this is very hard to do.
More research needs to be done on the link(s) between hypertension, fibrosis and A-Fib. If we induce hypertension, for example in animal studies, does it produce both fibrosis and A-Fib at the same time? Or does the A-Fib develop first, then produce fibrosis?
High Fibrosis Precludes Catheter Ablation
Sad news for patients? According to Dr. Marrouche’s studies, high levels of fibrosis preclude having a catheter ablation, that catheter ablation has a poor success rate in cases of high fibrosis (Utah Stages III and IV). Dr. Marrouche recommends that these high fibrosis patients reconcile themselves to living the rest of their lives on meds, that they can’t be cured of their A-Fib by catheter ablation. (It must be devastating for a patient to hear this.)
But many centers and doctors specialize in ablating patients with persistent and long-standing persistent A-Fib. For example, in a live case ablation at the 2014 Boston A-Fib Symposium at Orlando, Dr. Mélèze Hocini from the Bordeaux Group using ECGI successfully ablated a patient with persistent A-Fib and a fibrosis score of 22% (Utah Stage III) who also had a huge dilated left atrium. Fibrotic heart tissue doesn’t preclude or prevent making catheter burns in the heart. Rather, high levels of fibrosis are usually associated with more difficult-to-ablate cases where there are more A-Fib signals sources than just in the pulmonary veins. But some doctors and centers do these kinds of ablations all the time with high success rates.
If someone tells you that you have too much fibrosis to have a successful catheter ablation, get a second opinion. But you probably shouldn’t go to your local EP. Instead you need to go to more experienced doctors and centers like the Bordeaux group who specialize in tracking down, mapping and isolating A-Fib signal sources coming from other spots in the heart than the pulmonary veins. (See my list of EPs specializing in Persistent and Long-standing Persistent A-Fib.)
“encircling the (pulmonary) veins with lesions as seen on the MRI was not important in terms of treatment success.”
Practically all the centers in the study started by isolating the PVs. But success (freedom from recurrence) in the DECAAF study was dependent on the previous amount of fibrosis. However, the PVs usually do need to be isolated for treatment success.
“Residual Fibrosis”, from the perspective of A-Fib patients, isn’t all that different from ablation burns. Catheter ablation doesn’t change fibrotic heart tissue to normal tissue. In both cases the heart tissue is scarred, dead, immobile, with little or no blood flow and transport function. That’s why most EPs try to keep catheter ablation burns to a minimum.
Stuart, C. MRI may help identify best candidates for ablation. Cardiovascular Business. Feb 05, 2014. Last accessed March 16, 2014, URL: http://tinyurl.com/DECAAFTrial
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Last updated: Saturday, February 13, 2016
- VIDEO: 3D Model of Left Atrium Demonstrating Left Atrial Fibrosis in a Patient with Atrial Fibrillation. Last accessed March 16, 2014. URL: http://tinyurl.com/DECAAF3DModel↵
- Marrouche NF, et al. Association of atrial tissue fibrosis identified by delayed enhancement MRI and atrial fibrillation catheter ablation: the DECAAF study. JAMA. 2014 Feb 5;311(5):498-506. doi: 10.1001/jama.2014.3. PubMed PMID: 24496537.↵
- O’Riordan, Michael. DECAFF Published: MRI Aids in AF Ablation Success. Heartwire, February 5, 2014. http:”//www.medscape.com/viewarticle/820230↵