Do you know your Ejection Fraction? In three short video clips, Dr. Robert Fishel, discusses the ejection fraction (EF) a measurement of the pumping efficiency of the heart and why cardiac patients should know their EF. Dr. Fishel is Director of Cardiac Electrophysiology at JFK Medical Center; Uploaded on Jun 22, 2011.
♦ What is an Ejection Fraction? (:34)
♦ Who should know their EF? (:54)
YouTube video playback controls: When watching this video, you have several playback options. The following controls are located in the lower right portion of the frame: Turn on closed captions, Settings (speed/quality), Watch on YouTube website, and Enlarge video to full frame. Click an icon to select.
If you find any errors on this page, email us. Y Last updated: Saturday, February 18, 2017
Yes! There benefits from a catheter ablation even when the patient’s A-Fib has not been eliminated. Research has shown that the intensity or duration A-Fib symptoms may lessen, and medications that were ineffective before the ablation may now work.
A-Fib is a progressive disease that over time re-models and changes your heart. One of the remodeling effects of A-Fib is a reduction in the heart’s pumping ability (that’s why you might feel faint or dizzy during an A-Fib episode).
A key indicator of heart health is your Ejection Fraction (EF), a percentage of blood that is pumped out of your heart by the left ventricle during each beat. A heathy heart has an EF between 50 to 75 percent; an EF below 50% means your heart is no longer pumping efficiently. An EF of less than 35% means a seriously weakened heart.
In a meta-analysis of 26 A-Fib research studies, investigators found additional ‘side’ benefits to catheter ablation. The studies involved 1,838 A-Fib patients who had undergone a catheter ablation. Post-ablation follow-up averaged 23 months.
Follow-up data revealed a significant 13% improvement in left ventricular ejection fraction (EF).
In addition, there was a significant reduction in the number of patients who formerly had an ejection fraction of less than 35%, i.e., their EF ratio improved. (Might these ‘side’ benefits be attributed to an improvement in left ventricular ejection fraction?)
A catheter ablation can profoundly change one’s life—even if you need a second ablation (or a third)—know that you may reap ‘side’ benefits from each ablation.
11. “What is the heart’s ejection fraction? As an A-Fib patient, is it important to know my EF?”
Ejection Fraction (EF) is a percentage of blood that is pumped out of the heart during each beat. Your EF is a key indicator of your heart health.
“Ejection” refers to the amount of blood that is pumped out of the heart’s main pumping chamber (the left ventricle) during each heartbeat. “Fraction” refers to the fact that, even in a healthy heart, some blood always remains within this chamber after each heartbeat. Therefore, an Ejection Fraction is a percentage of the blood within the chamber that is pumped out with every heartbeat.
EF is most commonly measured in your doctor’s office during an echocardiogram. Your EF should be between 50 to 75 percent to indicate the heart is pumping well and able to deliver an adequate supply of blood to the body and brain.
If your EF falls below 50%, this means your heart is no longer pumping efficiently to meet the body’s needs and indicates a weakened heart muscle. An EF of less than 35% increases the risk of life-threatening irregular heartbeats.
Your EF can go up and down, based on your heart condition and your treatment therapies.
What does this mean to you? Most likely your EF was measured when you were first diagnosed with A-Fib. Ask your doctor if your Ejection Fraction is above 50% and how often you should have it checked? Your EF can help your doctor determine the effectiveness of your A-Fib treatment plan.
Keep in mind that Ejection Fraction is just one measure of heart function.
Atrial Fibrillation patients often have loads of “Why?” and “How?” questions. Here are answers to the most frequently asked questions by patients and their families. (Click on the question to jump to the answer.)
1. Causes: “Why does so much Atrial Fibrillation come from the Pulmonary Vein openings?”
Related Question: “What causes Paroxysmal A-Fib to turn into Persistent (Chronic) A-Fib?”
Related Question: “A-Fib and Flutter—I have both. Does one cause the other?”
2. Hereditary: “Is my Atrial Fibrillation genetic? Will my children get A-Fib too?”
3. PSVT: “Is Atrial Fibrillation (A-Fib) different from what doctors call Paroxysmal Supraventricular Tachycardia?”
4. Adrenergic/Vagal: “What is the difference between “Adrenergic” and “Vagal” Atrial Fibrillation? How can I tell if I have one or the other? Does it really matter? Does Pulmonary Vein Ablation (Isolation) work for Adrenergic and/or Vagal A-Fib?”
5. Stiff Heart: “I’ve heard about ‘stiff heart’ or diastolic dysfunction. When you have A-Fib, do you automatically have diastolic heart failure? What exactly is diastolic dysfunction?”
6. Stem Cells: “I’ve read about stem cells research to regenerate damaged heart tissue. Could this help cure A-Fib patients?”
7. EF: “What is the heart’s ejection fraction? As an A-Fib patient, is it important to know my EF?”
8. Anesthesia: “I read that the local anesthesia my dentist uses may trigger my A-Fib. Why is that?”
9. Fibrosis: “How can I determine or measure how much fibrosis I have? Can something non-invasive like a CT scan measure fibrosis?”
10. Treatment Options: “My surgeon wants to close off my LAA during my Mini-Maze surgery. Should I agree? What’s the role of the Left Atrial Appendage?”
Related Question: “My cardiologist recommends a pacemaker. I have paroxysmal A-Fib with “pauses” at the end of an event. Will they stop if my A-Fib is cured? I am willing, but want to learn more about these pauses first.”
Related Question: “My EP won’t even try a catheter ablation. My left atrium is over 55mm and several cardioversions have failed. I am 69 years old, in permanent A-Fib for 15 years, but non-symptomatic. I exercise regularly and have met some self-imposed extreme goals. What more can I do?
If you find any errors on this page, email us. Y Last updated: Tuesday, February 14, 2017
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
Return to Index of Articles: AF Symposium: Steve’s Summary Reports
Last updated: Thursday, January 26, 2017
- 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↵