Non-Valvular Atrial Fibrillation & Left Atrial Appendage
The left atrial appendage (LAA) is a small, muscular out-pocketing of the left atrium, one of the upper chambers of the heart. It fills with and empties blood when the left atrium relaxes and contracts.
There is still a bit of uncertainty around the function of the LAA, however it is believed to act as a decompression chamber during times of high atrial pressure.
Typically, the LAA is of little concern, however it may be problematic for individuals with atrial fibrillation (Afib). In a normal heart, the left atrium contracts before the ventricle to allow for sufficient blood flow from the left atrium to the left ventricle to subsequently supply the rest of the body. Afib is characterized by a disruption of electrical signals of the heart causing an irregular beat (arrhythmia) manifesting as a quivering of the left atrium rather than a normal contraction.
Cross section of the heart showing left atrium, LAA, and left ventricle
Usually electrical signals begin at the sinoatrial node and lead to atrial activation and then travel down to the AV node for ventricular activation. This is what drives the movement of blood from the atria to the ventricles and subsequently to the rest of the body.
In Afib the electrical impulses in the atria are disorganized leading to an irregular and rapid beating pattern. The contraction of the atria are not coordinated with the ventricles causing inadequate blood flow between the chambers of the heart and to the body.
Afib is generally classified as non-valvular and valvular.
Valvular Afib predominantly results from mitral stenosis. There is no therapy other than warfarin approved for anticoagulation of valvular afib.
Non-valvular Afib is caused by factors other than valve diseases, such as high blood pressure or an overactive thyroid gland.
Chaotic and uncoordinated contraction of the heart causes blood to remain in the left atrium and left atrial appendage for longer periods of time. This results in stasis (blood standing still) consequentially, blood will begin to collect in the LAA and is prone to forming clots. Thus, in patients with Afib, the LAA is a common site for clot formation. If a clot dislodges it may exit towards the arteries leading to the brain and cause stroke.
Blood pools in LAA due to irregular contractions.
Site for clot formation.
The blood clot dislodges from the LAA, travels through the arterial system, and lodges itself in a blood vessel leading to the brain. This
obscures blood flow and causes a stroke.
What does this mean for me?
It is important to manage your heart health with your medical team to reduce the risk of stroke. This involves lifestyle changes such as healthy eating and exercise as recommended by your physician, and medications that slow the heart rate, and thin the blood. However, many people may not be suitable candidates for blood thinners if they bleed excessively. Thus, given that most clots originate from the left atrial appendage, a procedure has been developed to close the appendage, and significantly reducing your risk of stroke.
Atrial fibrillation symptoms include:
Palpitations (rapid, uncomfortable, and irregular heartbeat)
Shortness of breath
Reduced exercise capacity
Normal heartbeat rhythm of 60 beats per minute
Abnormal heartbeat rhythm of 140 beats per minute
A normal heart rate is anywhere between 60-100 beats/minute, whereas the heart rate in atrial fibrillation can range from 100-175 beats/min. What causes the heart to beat so abnormally fast?
Let’s take a look at what produces the heart beat in the first place. The heart is made up of a special type of tissue called cardiac muscle. Unlike the vast majority of structures in our bodies, cardiac muscle is myogenic. This means that it is capable of contracting on its own without the input of the nervous system.
The heart accomplishes this with a small cluster of cells called the sinoatrial (SA) node. The SA node is the pacemaker of the heart because it generates electrical impulses required for contraction and controls the heart rate. Electrical signals produced by the SA node prompts atrial contraction causing blood to be pushed into the ventricles. The signals then follow a path from the SA node down to the atrioventricular (AV) node, and then to the purkinje fibres which prompt ventricular contraction and subsequent ejection of blood to the body.
Signal conduction pathway in the heart
Atrial fibrillation (Afib) puts a hamper on this system of smooth contractions. In Afib, the electrical signals are random and chaotic resulting in a quiver instead of a full contraction. But why do some people develop atrial fibrillation?
Common causes for Afib:
High blood pressure
Coronary artery disease
Congenital heart defects (defects you are born with)
Metabolic imbalance (ie. Hyperactive thyroid)
Exposure to stimulants such as caffeine, tobacco, and other heart rate elevating narcotics
Previous heart surgeries
Sleep disorders (ie. Sleep apnea)
Risk factors for developing Afib:
Age: most individuals who experience Afib are 65 or older
Heart disease: valve problems, congenital heart disease, congestive heart failure, coronary artery disease, heart attack
Long Term Health Implications
Long Term Health Implications
Clot formation in the LAA can result in the following complications, which have a direct impact on your immediate health and wellbeing:
Stroke: A chaotic rhythm causes blood to pool in the upper chambers of the heart known as the atria and may form clots. Blood clots may dislodge form the heart and travel to the brain. This results in a blockage of blood flow consequently resulting in a stroke.
The risk of a stroke in individuals with Afib gets higher with age. High blood pressure, diabetes, history of heart failure, and pervious occurrence of stroke also increase the risk of developing a stroke.
Heart Failure: Insufficient amount of blood is circulated throughout the body. The heart attempts to beat harder and faster as a result which puts you at risk for heart failure.
As a result of inadequate contractions of the heart, blood can pool in the pulmonary veins resulting in fluid pockets in the lungs. That causes fatigue and shortness of breath.
Next steps: investigation plan
Your doctor will review your signs and symptoms, past medical history, and physical examination. If your doctor suspects that you have Afib, they may conduct several tests to determine your condition. These tests include an ECG, Holter monitor, event recorder, echocardiogram, blood tests, stress tests, and a chest X-ray.
Electrocardiogram (ECG): as the primary tool for diagnosing Afib, an ECG uses small electrodes that are attached to your chest and arms to record electrical signals as they travel through your heart
Holter monitor: If your doctor suspects Afib they would want a prolonged look at your heart rhythms. A Holter monitor is a portable ECG device that is carried on the patient either in your pocket or worn as a belt and or shoulder strap and records the hearts activity for 24 hours or longer.
Event recorder: This portable ECG device monitors the heart activity over a span of few weeks to a few months. The event recorder records the heart rhythm at the time of your symptoms. When a fast heart rate is being experienced, you push a button and the ECG strip of the preceding few minutes and following few minutes is recorded.
Echocardiogram: A wand-like device known as a transducer is held at your chest, and sounds waves help to create a movable picture of your heart. Occasionally, a tube-like transducer is guided down your throat into the esophagus. The echocardiogram helps to diagnose or rule out any structural heart disease or blood clots that might be present in the heart.
Blood tests: A blood test helps in ruling out any thyroid problems or other possible substances than lead to Afib.
Stress test: stress tests monitors the heart rate during a strenuous exercise, generally a short jog or run at increasing speeds
Chest X-ray: this test helps your doctor to assess the condition of your lungs and heart, as well diagnose conditions other then Afib that may be causing you symptoms.
The Heart Team
At PMCC, we believe that multidisciplinary teams improve patient care. After you meet with a PMCC cardiologist, your case will be discussed by the "Heart Team". The Heart Team is a team of professionals with a high degree of specialization, that has been assembled to deliver the best possible care for our patients. It consists of Cardiologists, Heart Surgeons, Anesthesiologists, Radiologists, echocardiographers, and specialized nurses. During the “Heart Team” conference, all of your clinical data is presented, including results from the diagnostic imaging tests, as well as your history and other conditions.
The Heart Team will aim to come up with a consensus about the most reasonable course of action for your specific case taking into account all of your clinical features.
Reminder: clots are formed because Afib causes blood stasis (slow movement) resulting in coagulation. A clot can dislodge from the site of formation and impair blood flow elsewhere. Impaired blood flow to the brain can result in stroke. A major site for clot formation is in the left atrial appendage.
Treatment Options & Stroke Prevention
The risk of stroke secondary to Afib can be mitigated by taking important steps towards living a healthy lifestyle which includes but is not limited to a heart-healthy diet, engaging in physical activity, avoiding cigarette smoking, stress reduction, and limiting your caffeine intake.
Treatment options can vary depending on your risk factors. Often, individuals with Afib are prescribed with anticoagulation/blood thinning medications to prevent the formation of a clot.
Blood thinners work to prevent blood coagulation to reduce the risk of clot formation or keep an already existing clot from getting larger.
How do doctors decide if a patient is a good candidate for anticoagulation therapy?
The CHADS2 score is a risk assessment schema that doctors use to determine the susceptibility of a patient with Afib to suffer a stroke. The score helps doctors make informed decisions on whether or not a patient is a good candidate for anticoagulation therapy.
The risk of stroke is determined by a patient’s CHADS2 score which depends on age and comorbidities
· A score of 0 means low risk of stroke. The patient will not need anticoagulation therapy
· A score of 1-2 is moderate risk and may require anticoagulation therapy
· A score of 3-6 is high risk and will require anticoagulation therapy
A physician will decide whether a patient will be on anticoagulation therapy depending on his/her CHADS2 score.
A serious side effect of anticoagulation therapy however, is the risk of heavy bleeding. Even a cut on your finger can bleed excessively and it would be difficult to manage.
Thus, another treatment option for patients who are not good candidates for oral anticoagulants is to close the LAA. Since more than 90% of clot formation occurs in the LAA, it’s closure reduces the risk of stroke significantly.
The LAA can be closed using a parachute shaped, self-expanding device called the WATCHMAN Device. Its placement does not require surgery but patients may be put under general anesthesia. To insert the device, a catheter sheath is inserted through the femoral vein (near the groin) and guided all the way up to the heart where it crosses the septum and enters the LAA. The device is placed in the opening of the LAA to prevent blood from collecting inside it.
The WATCHMAN Device plugs the LAA to reduce the risk of clot formation and subsequent stroke.
The WATCHMAN Device has been used since 2010 to successfully close the LAA and has been proven to be an effective alternative to anticoagulation therapy.
AMPLATZER Amulet Occluder
Another alternative to anticoagulation therapy is to plug the LAA with the Amplatzer Amulet Occluder. This device is comprised of a connecting lobe and disc that seals the opening of the LAA. The amulet's design allows for a more flexible placement within the LAA.
AMPLATZER Amulet Occluder
Patients may be placed under general anesthesia for this procedure. A physician gains access through the femoral vein to insert a catheter sheath that is guided to the heart, and through the septum where the opening of the LAA can be reached.
Based on the investigation, your doctor will discuss all options with you to create an individualized treatment plan.
LAA Occlusion Procedure
Patients are taken off of blood thinners/anticoagulants for 3-4 days before the day of the procedure
Patients are admitted to the hospital on the same day of the procedure
Patients must fast for 6 hours prior to the procedure
On the day of the procedure, patients will also be given antibiotics to reduce the risk of device infection
While under general anesthesia, patients will require a breathing tube and a transesophageal echocardiogram (TEE), which is important to visualize the correct position of the device and assist with the transseptal puncture
Patients are given heparin (blood thinner) during the procedure to reduce the risk of stroke
The procedure is initiated with access through the femoral vein near the groin
A catheter is inserted to measure pressures in the right heart, and saturations of the chambers of the heart
The procedure is divided into two main steps:
1) Transseptal puncture - a hole is made through the interatrial septum (between the left and right atrium) using a needle. After obtaining access, a balloon is used to enlarge the hole in the septum to put devices through easily.
2) A delivery system carries the device used to plug the opening of the LAA. This is guided with the TEE.
Patients will remain in the hospital overnight
Patients will have a small wound over the right groin. They are advised not to partake in strenuous activities for 6 months after the procedure
Patients will be on two anti-platelet medications for 6 months
A transthoracic echocardiogram is conducted a few months after the procedure to look at the end result of the device
Frequently Asked Questions
Will LAA closure change the functioning of my heart?
No, this procedure will not change the functioning of your heart. It will simply block the opening to the left atrial appendage to avoid blood pooling there.
Are there any lifestyle restrictions following LAA closure? What can I expect post-procedure?
Your doctor will advise you to avoid strenuous activity, such as long distance walking, running, and heavy lifting, for the first week following your procedure. For 6 months following the procedure, it is advised to avoid contact sports, as well as keep up with antiplatelet therapy that your doctor will prescribe.
Will OHIP (public insurance) cover my LAA closure?
How urgent is the treatment?
The urgency of this procedure varies between patients. This is an elective procedure that reduced the risk of stroke and is mainly done for individuals who are not suitable for anti-coagulation therapy.
Cross-section of heart: https://www.medscape.org/viewarticle/803859_transcript
Normal heart vs. Atrial fibrillation: https://www.diversalertnetwork.org/health/heart/atrial-fibrillation
Blood clot in LAA: https://intl.sentreheart.com/patient/laa-closure/
Normal heart beat: https://watchlearnlive.heart.org/CVML_Player.php?moduleSelect=arrhyt
Atrial fibrillation: https://watchlearnlive.heart.org/CVML_Player.php?moduleSelect=arrhyt
Stroke symptoms: https://www.thrombosisadviser.com/signs-symptoms-risks-of-stroke/
Electrical signals of the heart: https://www.youtube.com/watch?v=lK32IfBw4hI
Device placed in LAA: https://www.watchman.com/en-UK-HCP/about-watchman-implant.html
Amplatzer Amulet Occluder: https://www.dicardiology.com/content/st-jude-medical-launches-amplatzer-amulet-laa-occluder-trial
Amplatzer Amulet Occluder St. Jude Medical https://www.businesswire.com/news/home/20161102005979/en/Largest-Observational-Study-Date-St.-Jude-Medical