TAVR Complications

Case Presentation:

You are working in the CCU on TAVR Thursdays when a 75 year old male with PMH of severe symptomatic aortic stenosis, non-ischemic cardiomyopathy with EF 50-55%, HTN, HLD, and uncontrolled diabetes returns from the cath lab after successful TAVR procedure. You obtain a routine EKG after the procedure.

Ask Yourself:

Questions:

What should be ordered for the patient after he returns from the cath lab?
What do you think of this patient’s EKGs? What differences do you notice from the first, second, and third?
Why did this EKG change occur acutely after a successful TAVR? How can this be further managed?
What other complications do you have to look out for after TAVR?

EKG Prior to Procedure:

EKG 2 Days After Procedure:

EKG 1 Week After Procedure:

Background:

The advent of Transvalvular Aortic Valve Repair (TAVRs) has helped to revolutionize the field of cardiology as aortic stenosis is one of the main valvular diseases affecting the elderly. At first, Surgical Aortic Valve Repairs (SAVRs) that required open heart surgery were the standard of care for those patients with severe aortic stenosis until TAVRs came along as an alternative for patients who were high risk for undergoing open heart surgery. As time passed and the catheters and technology became more advanced, TAVRs have become the mainstay of treatment for severe aortic stenosis as they are cheaper, less invasive, and overall safer procedures than their SAVR counterparts.

While TAVR has been found to be non-inferior and, in some cases, superior to SAVR, there are some patients who might be better SAVR candidates. Specifically, if the patient is younger (<65 years old), they can get a mechanical valve via SAVR as this can last patients their entire lives vs the bioprosthetic TAVR which usually only lasts about 10-20 years. The downside of a mechanical valve is that patients need to be on lifelong anticoagulation with warfarin. Other instances in which SAVR may be preferable is when a patient’s anatomy makes TAVR technically difficult. Lastly, if patients are going to be getting open heart surgery anyways and they have even moderate aortic stenosis, they should have the their aortic valves replaced then.

Reasons for Aortic Stenosis:

Congenital: Usually presents with uni-or bicuspid valves. Patients are typically young (<30 years old)
Calcified bicuspid: Age 40-60 years old
Rheumatic heart disease: Age 40-60 years old

Senile degeneration: > 70 years (most common)

Figure 1 shows an apical five chamber view (i.e. an apical four chamber view of the left atrium, left ventricle, right atrium, and right ventricle with the addition of the aortic valve). When patients have stenotic aortic valves, this will impede blood flow out of the aortic valve. The picture on the right shows the difference between a normal vs stenotic aortic valve when the valve opens and closes.

Workup:

Symptoms:

Chest pain:

As the aortic stenosis worsens, this causes increased afterload on the left ventricle and increased wall stress. The heart will compensate by undergoing left ventricular hypertrophy. Usually, blood goes from the aorta to the coronaries, which is from a high to low pressure system. As the pressures within the left ventricle increase, there is less of a gradient from the aorta to the left ventricle and it becomes harder for blood to flow into the coronary arteries. As a result, patients may experience angina.
As muscle thickness within the left ventricle increases, there can be an oxygen mismatch, which can also cause anginal symptoms

Syncope

A stenotic aortic valve may impede flow, which may lead to decreased brain perfusion and cause syncope

Dyspnea

A stenotic aortic valve can cause lead to poor perfusion, leading to poor peripheral oxygenation and feelings of fatigue
Overtime, the heart may lose its ability to compensate. When this happens, the EF can decrease, causing patients to experience heart failure symptoms.

Physical Exam:

Heart sounds:

Crescendo-decrescendo murmur that may move to the carotids
Lack of S2 when stenosis is severe
S4 due to stiffening of the left ventricle
Slow rising carotid pulse (pulsus tardus) with decreased amplitude (pulsus parvus)

On TTE, you may be able to see the calcified aortic valve. You may also see concentric left ventricular hypertrophy, as the stenosis causes increased afterload in the left ventricle and increased wall stress. Overtime, this can cause diastolic dysfunction due to a stiffer ventricle.

There are measurements on TTE that we look at to measure the extent of the aortic stenosis. Specifically, we look at the aortic jet velocity, the mean gradient, and valve area, and then classify the aortic stenosis as normal, mild, moderate, or severe (Table 1).

Note: Sometimes TTE can overestimate gradients. If the patient looks like they have significant stenosis on the TTE but the numbers look normal, these patients may either need repeat TTEs or even be candidates for catheterization to figure out the exact pressures, velocities, and gradients.

How We Figure Out Aortic Valve Area:

Being able to make these calculations depends on the Continuity Equation, which basically states that whatever goes through one side of a system (i.e. the left ventricular outflow tract, LVOT) must come out through the rest of the system (i.e. the aortic valve). When we are dealing with aortic stenosis, the variable we are trying to solve for is the aortic valve area (Figure 2).

Figure 3 gives us a step by step of how to get the variables for the continuity equation. First, we set up the TTE so that we get an apical five chamber view. Then, we set up our dopplers so that it goes through the LVOT and aortic valve. We then measure the diameter of the LVOT to get the area of the LVOT. Next, we use the pulse wave doppler to get the velocity of blood through the LVOT. Finally, we use the continuous wave doppler to get the velocities through the aortic valve. Once we have the LVOT area and velocity, as well as the aortic valve velocities, we can solve for the area of the aortic valve.

What’s the difference between pulse wave doppler (PWD) and continuous wave doppler (CWD)? Simply put, the PWD uses one beam to send out short bursts of ultrasound and will analyze the reflected waves between pulses. This works well for accurately measuring the velocities of things that are closer to the probe (i.e. the LVOT). Unlike the PWD, the CWD will continuously transmit and analyze ultrasound waves, which allows for higher velocities to be measured.

Figure 4 shows the continuous wave doppler (seen in green) of the velocities through the aortic valve. The velocities appear to be negative (i.e. are below the thick green line) because these velocities are moving AWAY from the ultrasound probe. Normal velocities < 2 m/s. However, note how in this picture velocities are >4m/s, which indicates severe aortic stenosis.

Continued…

A Word on Low Flow, Low Gradient Aortic Stenosis:

Overtime, the heart might not be able to compensate for the aortic stenosis. When this happens, the heart may be too weak to generate the force needed to effectively pump enough blood out to the body. As a result, the gradient will decrease despite the fact that the body needs a higher gradient given the stenosis.

Another phenomena called pseudo aortic stenosis occurs when the valve appears to be stenotic. However, it will open more if needed. Many times, it may be difficult to distinguish between these two entities on TTE. Therefore, you will need to order a dobutamine stress echocardiogram. If the cardiac output and gradient increases, the patient does not have true aortic stenosis.

In most cases, access is obtained through the femoral artery. A guide wire is threaded up the aorta into the aortic arch, then into the stenotic aortic valve. Then, the artificial valve is guided through to the aorta and LV using a balloon catheter over the guide wire. The balloon is inflated, which opens up the old valve and makes room for the new valve.

Indications for aortic valve replacement:

When considering if patients are candidates for aortic valve replacement, we take into consideration the patient’s symptoms and the severity of the patient’s aortic stenosis.

The table pictured is from the 2020 AHA/ACC recommendations regarding class 1 indications for when aortic valve replacement is indicated:

Class of Recommendation (COR); Level of Evidence (LOE); A: A level of evidence; B—NR: B level of evidence, non-randomized

Complications of TAVR:

Conduction Issues:

A major complication that can develop after TAVR is conduction abnormalities, specifically left bundle branch block (LBBB) and atrioventricular block (AVB), which can necessitate pacemaker placement. The reason this occurs is due to how close the conduction system is to the aorta (specifically with the bundle of HIS at the membranous interventricular septum near the aortic valve and the left bundle branch at the level of the non coronary aortic cusp below the inferior membranous septum edge) – Figure 5.

Direct insult to the conduction system can occur because of inflammation, ischemia, hematoma, edema, or direct mechanical injury secondary to the implantation of the artificial valve. As such, you should get an EKG a few hours and 24 hours after the procedure. Both LBBB and AVB usually develop within 24 hours of TAVR placement. While some of these conduction issues may resolve within 30 days, about 55% of patients end up having persistence of their blocks. In the PARTNER 3 trial, the incidence of new LBBB after 1 year was 23.7% post TAVR. Patients with LBBB after TAVR have a 2-fold increased risk for requiring pacemaker implantation.

Figure 5 shows demonstrates three major complications from a TAVR procedure, namely occlusion of the left coronary artery by the TAVR device, conduction abnormalities due to the TAVR pushing against the conduction system (specifically pictured with the left bundle branch), and tamponade (which can occur due to aortic dissection).

Coronary Occlusion / STEMI: Due to anatomy, TAVR placement in the aorta is adjacent to the coronary ostia. If a patient has a higher-riding ostia, the TAVR may push against the coronary and can cause a functional occlusion ( Figure 5). Most compressions will be seen while the patient is still in the cath lab as ST elevations and widening of the QRS. A stent must be placed immediately to restore coronary blood flow.

In order to prevent this, we get a CT TAVR prior to the procedure so we can understand the coronary anatomy and better anticipate if patients are at high risk of coronary compression.

Stroke: Although there is less of a stroke risk with TAVR than SAVR, strokes remain a major complication of TAVR. Calcification particles from the aortic valve, aorta, and left ventricle can embolize during the procedure due to the manipulations of the catheter and cause ischemic stroke. Strokes can also occur secondary to hypoperfusion during the procedure as well.

The overall stroke risk post TAVR is about 3-6%; 50% of strokes that occur after TAVR occur within 24 hours and 50% occur after about 10 days due to thrombus formation. It’s important to monitor these patients for signs of any neuro deficits and begin antiplatelet therapy like aspirin for at least 6 months post TAVR.

Aortic Dissection: Acute aortic dissection is a rare but fatal complication of TAVR. As TAVR involves the introduction of multiple wires and devices in the aorta, the stiff wires can disrupt the intima and lead to aortic dissection. Dissection can occur either from the wires themselves, the manipulation of the valve during retraction, or during the balloon valvuloplasty. One of the major complications of aortic dissection include tamponade, which can best be seen by the subxiphoid view on a bedside TTE (Figure 6).

Figure 6 shows a bedside subxiphoid POCUS of a pericardial effusion.

Vascular Complications/Bleeding: Vascular complications can occur anywhere from the aortic valve to the femoral access site. In addition to the complications already mentioned, access site hematoma is another severe complication. Since TAVRs require arterial access, these hematomas can grow to be quite significant and potentially even impede arterial flow to distal extremities. As such, monitoring for hematoma formation and ensuring good peripheral pulses is crucial.

Acute Kidney Injury: AKI occurs in 1 out 6 patients undergoing TAVR due to the use of IV contrast during the procedure. AKI after TAVR doubles the mortality risk after 1 year. Patients with preexisting CKD prior to having TAVR are at a higher risk of developing AKI along with patients who have vascular complications/bleeding during the procedure.

Other complications: Other complications that are uncommon but can still occur include residual infection, hypotension, sub-valvular hypercontractile hypertrophic obstructive cardiomyopathy-like obstruction, acute aortic regurgitation, and left ventricular (LV) perforation.

Back to the Case:

1. What should be ordered for the patient after he returns from the cath lab?

When patients return from the cath lab, you should make sure to order an EKG immediately for that day and an EKG for the next morning, due to high concerns for conduction abnormalities that may develop. You should also order a TTE for next day to ensure no pericardial effusion develops and the valve is still in good position.

Although TAVRs do not require full anticoagulation with warfarin like the mechanical valves of SAVR, patients should be started on an antiplatelet medication, such as aspirin, for at least 6 months post TAVR procedure.

2. What do you think of this patient’s EKGs? What differences do you notice from the first, second, and third?

The first is the patient’s baseline EKG showing atrial fibrillation with a notable right bundle branch block with rates in the low 100s. The second EKG after the procedure is concerning for significant bradycardia with rates in the 30s caused by AV block. Due to the patient’s conduction abnormalities, he actually required transvenous pacing and was ultimately given a pacemaker. The third EKG shows a functional left bundle branch block with new left axis deviation caused by the patient’s newly implanted pacemaker. If you look closely, you can see little vertical lines before the QRS complexes which indicate paced beats.

3. Why did this EKG change occur acutely after a successful TAVR? How can this be further managed?

The patient’s EKG changed acutely due to conduction abnormalities caused by the TAVR procedure. Since the bundle of HIS is adjacent to the aortic valve, the TAVR device must have pushed up against the conduction system and caused a functional AV block. As the patient was very bradycardic and symptomatic with poor chronotropic response, he required transvenous pacing until he was able to get a pacemaker.

4. What other complications do you have to look out for after TAVR?

In addition to conduction abnormalities, you should also be on the lookout for coronary occlusion / STEMI, femoral access hematomas that can cause distal extremity arterial occlusions, stroke, tamponade from aortic dissection, and AKI.

Further Learning:

Resident Responsibilities

Make sure to order an EKG when the patient returns from the cath lab to monitor for any conduction abnormalities or coronary occlusions. You should also order an EKG and TTE to be done the next day to continue to look for conduction issues and to evaluate for any pericardial effusions.
Remember! Conduction abnormalities can occur days after the TAVR procedure!
As the TAVR procedure uses arterial access, it is important to monitor closely for femoral access site hematoma and to assess distal pulses as hematomas can prevent good distal arterial flow!
Be sure to evaluate for signs of stroke after TAVR with a thorough neuro exam. Any focal neuro deficit should be taken very seriously.
All patients who have had a TAVR procedure should be started on an antiplatelet agent, usually aspirin, to be continued for at least 6 months post procedure.

Further Reading:

PARTNER 3 trial

TAVR has been shown to be a safe procedure that is non-inferior to superior toto SAVRs

PROGRESS trial

Comparing TAVRs to close monitoring for patients who have moderate aortic stenosis with at least one risk factor

2020 ACC/AHA Guideline for the Management of Patients with Valvular Heart Disease
- https://www.ahajournals.org/doi/10.1161/CIR.0000000000000923#d1e4304