Preview of the ACC: Percutaneous Mitral Valve Repair

"[The procedure is] very new and involves repairing my leaky valve using a clip device, without open heart surgery, so that my heart will function better"

-Elizabeth Taylor, via Twitter 6 Oct 2009

Percutaneous mitral valve repair will be the talk of the ACC Scientific Sessions for interventional cardiology this year, especially since coronary artery stent procedures are so, well, yesterday.

One valve repair technology popularized by Ms. Taylor's tweet that corrects a leaky mitral valve will be presented Sunday morning at the ACC meeting in Atlanta when the EVEREST II trial results are released (Larry Husten over at Cardiobrief.org has a nice outline of the late-breaking clinical trial schedule).

The EVEREST II trial is a phase 3 trial that compares the percutaneous mitral valve repair head-to-head with more conventional open mitral-valve surgery. The trial is sponsored by E-valve, Inc. (bought a year ago by Abbott). Since our center has participated in the trial (note to SEC: I have no clue about the results), it might be interesting to review the background and provide a few pictures on the technology. (By the way, this was NOT Elizabeth Taylor's procedure!)

(Important disclaimer: This device is NOT YET APPROVED for use in the US. Further, I have no financial interest in the manufacturer(s) and was not an investigator for the EVEREST I or EVEREST II trials, but I do work at one of the trial centers).

Background

In 1998, a report of correcting mitral valve insifficiency (leakage) was reported by Ottavio Alfieri and colleagues in the European Journal of Cardiovascular Surgery describing a technique to plicate (suture together) the mid-portion of the mitral valve, effectively creating a "bowtie" orifice to correct the leakage:

The experimental technique reported in this study could permit minimally invasive correction of the mitral insufficiency. These patients are often not referred for surgical repair, because they are believed “too sick” for conventional surgery. The experimental technology described in this report would avoid cardiopulmonary bypass and its consequences, and thus represents a more palatable alternative for these patients.

The long-term results of this technique were favorable and lead to the development of a minimally-invasive (yet transthoracic) approach for this same repair and later, thanks to the wonders of clever engineers, a completely percutaneous approach using a clip instead of sutures.

Equipment

(Note: Thanks to Dr. Ted Feldman for use of these great pictures) and the clinical trial nurses who make this all possible.

While minimally invasive, this procedure takes a village, so to speak, to perform: the interventional cardiologists, an echocardiographer and a well-hidden anesthesiologist (can you say "Where's Waldo?") barely seen behind the plastic drapes above the patient's head (yes, the patient gets to sleep for the procedure):

The personnel and equipment required to perform percutaneous repair of the mitral valve as viewed from the patient's feet. Note the Frankenstein-like steering-and-release contraption with all the IV tubing coming from it in front of the doctors used to place the mitral clip.
(Click image to enlarge)

A view from behind the implanting physicians. Note that all eyes are on the echocardiographic images to the right as the clip is positioned, rather than the fluroscopic images immedicately in front of the operators.
(Click image to enlarge)

The back end of the catheter delivery system looks just a bit complicated, since it steers the clip, grasps each leaflet of the mitral valve, and releases the clip when seated properly:

Click image to enlarge

The business end of the device is a small mechanical clip that grasps the center of the posterior and anterior leaflets of the mitral valve in an attempt to replicate the "bowtie" surgical repair originally described:

A cartoon rendition (top) and a photo of the clip (bottom) used to clip together the leaflets of the mitral valve

While the fluoro images of the procedure are interesting to view as the device is deployed:

An RAO fluoroscopic view of the mitral valve clip passed to the left atrium above the mitral valve.

The mitral valve clip is advanced below the mitral valve into the left ventricle in preparation of grasping the mitral valve.

The valve leaflets are grasped and the side "wings" of the clip closed.

The clip is deployed and fixes permanently to the mitral valve leaflets.

Although these fluoroscopic images are amazing, this procedure would not be possible without the ability to see the valve leaflets in realtime using transesophageal echocardiography:

Transesophageal echocardiographic images of the clip (outlined in orange) being placed below the mitral valve leaflets.

The clip is withdrawn until the leaflets of the mitral valve are engaged in the clip. (Note the "wings" of the clip are still open)

The wings of the clip are closed tightly to grasp the valve leaflets.

Will the Device Work?

Although preliminary results of the EVEREST I trial were promising, the EVEREST II trial will be the pivotal comparative effectiveness study comparing this approach to open mitral valve repair.

One thing's for sure after seeing all this: innovation in cardiology is alive and well!

See you Sunday!

-Wes

Blaming It All on Mitral Valve Prolapse

Chicago is still reeling from the aftermath of the Chicago Marathon as they struggle to ascertain why Chad Schieber, an otherwise healthy 35 year old police officer, could die during the event. Certainly, everyone’s heart goes out to the grieving family, and at times like this, we all search for “the cause” – why should an otherwise fit individual die?

The coroner’s report that described “mitral valve prolapse” as the cause. But for those of us in the cardiac field, we wonder, how the heck can the presence of mitral valve prolapse cause death?

Mitral valve prolapse is caused by a redundancy of the mitral valve that causes the mitral valve (which separates the left atrium from the main pumping chamber of the heart, the left ventricle) to bow, or prolapse, into the left atrium. The leaflets are prevented from bowing too far back into the left atrium during systole by strong strands of tissue (called chordae) that act to tether the leaflets to the left ventricular chamber (think of the lines attached to a parachute that serve to hold air inside the parachute). Some patients have some leakage of the valve from the left ventricle backward into the left atrium caused by the bowing leaflets. Tons of folks live just fine with a minor leakage. But if the leakage gets too severe, or if one of the chordae ruptures, the flow of blood backward into the lungs can be so severe that the lungs fill abruptly with fluid, and respiratory collapse and perhaps death, occurs.

We are given limited information in the coroner’s report if a chordal rupture occurred in Mr. Stokes, only that he had “mitral valve prolapse.” So if he did NOT have chordal rupture, then we are left to wonder, would the mitral valve prolapse in and of itself, have killed him? Likely not. So if not, what other causes might explain his untimely demise?

First, let me say, I doubt we will ever know. But much more common in marathoners running on a hot day is the presence of heat stroke and electrolyte abnormalities. Given the hype about the need for water and the experience of this runner, it’s hard to imagine that heat stroke would be the most likely cause here, but it can’t be excluded. Electrolyte abnormalities, on the other hand, may have played a significant role.

There are two main “electrolytes of life,” as I like to call them: sodium and potassium. Sodium is the major electrolyte outside of cells, and potassium is the main electrolyte inside of cells. Sweat is important cooling mechanism for the body, since evaporative heat loss is a very effective way to lose heat. But with sweat goes sodium and a small amount of potassium, too. And so the marathoner drinks water – lots of water – but often, does not replace any of the sodium lost with sweating.

And the results for the heart can be catastrophic. An important study was recently reported in the New England Journal of Medicine regarding hyponatremia (low sodium levels) in marathon runners in the Boston Marathon. This weekend, I had a chance to see this first-hand on Sunday when a marathon runner presented to our ER with hyperventilation, confusion and muscle fasciculations (diffuse fine twitching) and positive cardiac markers. Here were his lab studies:

Sodium 125 (ref: 133-145 meq/L)
Potassium 3.4 (ref: 3.5-5.3meq/L)
Chloride: 90 (ref:98-108 meq/L)
CO2 17 (ref: 23-32 meq/L)

Myoglobin: 1453 (ref: 21-98)
CK-MB 62.5 (ref:0.6-6.3)
Troponin-I 0.31 (ref: 0.0-0.06)

His EKG was normal.

What was striking were his confusion and muscle fasciculations. If effect, his sodium was so low that it was affecting all of the excitable tissues: his neurons and muscles. Fortunately for this individual, he did not have any skipped heart beats.

But throw a few extra heart beats into a heart exposed to that low sodium (which certainly could happen in the setting of mitral valve prolapse) and fatal cardiac arrhythmias can occur abruptly and irreversibly, resulting in sudden death.

So could this have been the real cause of death for this young man? Perhaps. Perhaps not. But blaming it all on mitral valve prolapse sends the wrong message to the thousands of patients living with this common heart valve anomaly.

-Wes