Echo Case: A Classic Case of… You Tell Me

Ronald H. Wharton, MD

Disclosures

February 28, 2018

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Hello and welcome to another imaging case study. This is Ronald Wharton. I am a cardiologist at Montefiore Medical Center and assistant professor of medicine at the Albert Einstein College of Medicine, Bronx, New York. I thought I'd show a few images of—well, you tell me. Go through them quickly and dissect, and then see if you can figure out what's going on.

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You will see several images. You'll see some M-modes. You'll see some 2D images. You'll see some spectral Dopplers. There are different manifestations of the same underlying pathology, so let's get started.

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Here we have a parasternal long-axis 2D image. Take a look at it for a few seconds. Look at the motion of all of the walls. Look at the size of the chambers. Those are hints.

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In this slide, you can see an M-mode through the aortic valve. Note that the heart rhythm is regular. Look closely at the aortic valve opening and closing.

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Here is an apical four-chamber 2D image. Again, look at the motion of all the walls—not just in the ventricles but in the atria as well. Look around the heart.

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Now, you see a pulsed-wave Doppler through the left ventricular outflow tract (LVOT). Note also, again, that the heart rhythm is regular.

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This shows it's the same thing, except now we have a pulsed-wave Doppler of the mitral inflow instead of the LVOT. The rhythm is still regular.

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The next slide shows a continuous-wave Doppler through the mitral valve. You can see some of the flow heading towards the left ventricular outflow tract inside the continuous-wave Doppler during systole.

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In the next slide, you can see the lateral mitral annular tissue Doppler velocities. Take a look at them.

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Here, you see the medial annular tissue Doppler velocities. Take a look at those and compare them with the image you just saw.

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Finally, in this slide, you see a 2D subcostal image with the inferior vena cava.

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Let's take a look at all of these closely. Do you notice the septal bounce? Do you notice that in this parasternal long axis, as the image plays, sometimes the septum dives down, comes back up, and then dives down? The left atrial size is large. We'll talk about why a little later.

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This is the M-mode of the aortic valve. You'll notice that the ejection period is not identical from beat to beat. I think it's most dramatically different between the first beat and the second beat. You can see that the ejection period, which you can measure by the aortic valve opening-to-closing time, is much longer in the first beat than in the second beat and then starts getting a little longer again. The rhythm is regular, so you can't attribute that to changes in filling periods.

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Take a look again at the motion of the intraventricular septum. Sometimes it bounces towards the right abruptly and then comes in towards the left. Look also at the interatrial septum. Do you notice also that that's bouncing back and forth between the left atrium and the right atrium? Sometimes it goes to the left and goes to the left again. These are all reflections of varying pressures between the right side and the left side of the heart.

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Here you can see the LVOT flow. You'll notice that not only is the LVOT flow variable from beat to beat but also the pre-ejection flow, or the flow that occurs with the atrial kick, seems to be changing in parallel. That's a finding that I don't know has been necessarily described in the literature, but I see it all the time anecdotally. When the atria contract its left ventricle, the flow sort of swirls around, hits the apex, and then starts swirling around towards the LVOT. You can actually see the flow heading towards the LVOT during atrial systole, obviously not enough that it opens the valve, but you could see it.

You'll notice that in this slide, as the LVOT flow increases in velocity, there is a parallel increase in velocity in the atrial kick that comes before it.

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Here, you see the variability in the pulse-wave Doppler through the mitral valve from beat to beat.

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If you look at this continuous-wave Doppler—and I actually marked these in green— you can see that there are variabilities in the isovolumic relaxation time (IVRT).

For instance, take the first green measurement that I marked, which is just before the third mitral inflow. You can see that there's a small E wave, and there's a very small amount of flow in the IVRT during which the IVRT is relatively long. In the next beat, the E wave is larger and the isovolumic relaxation time is shorter.

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You also see that the velocity in the lateral mitral annulus, which is supposed to be higher than the medial mitral annulus, is in fact lower. The lateral mitral annular velocity is within the vicinity of 6 to 7 cm/s. The medial mitral annular velocities are frequently in excess of 8 cm/s.

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Finally, also notice in the next slide that the inferior vena cava is dilated and plethoric.

What were we looking at? This is all constrictive pericarditis. The variabilities that we saw in all of these images have to do with the fact that the filling of one ventricle is occurring at the expense of the other. During inspiration, the right-sided pressures are higher and the septum will bow to the left. During expiration, the left side's filling is increased and the septum bows to the right.

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Not only does that happen, but there are corresponding increases in pressures in the left atria and the right atria as well, such that during inspiration, the right atrial pressure goes higher and the filling to the left side is reduced. Not only is the E velocity smaller, but the isovolumic relaxation period becomes longer because the left atrial pressure is lower. During expiration, when the left atrial pressure becomes higher, the septum in the atrium bows to the right. The isovolumic relaxation period actually becomes shorter because the left atrial pressure goes up.

All of these findings support constrictive pericarditis. The annular velocities are what's referred to as annulus paradoxus. Why is that? The pericardial constriction tethers the lateral wall preferentially compared with the septal wall. Unlike virtually every other case that you see, where the lateral velocities in the mitral annulars are higher than the medial velocities, here it's reversed.

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Now, finally, I want to give you the punch line. What was the etiology of the constriction in this case? Well, this is a patient who presented with heart failure, as many constrictive pericarditis patients do. This is a patient who had constrictive pericarditis after a cardiac transplant, which is why the left atrium is so large. Constrictive pericarditis is in the differential diagnosis of heart failure after heart transplant, a much less common cause than rejection.

Sometimes, after a heart transplant, you can just get a little pericardial fluid around the heart. It becomes inflammatory and you get constrictive physiology. That's a situation where sometimes a pericardiotomy can cure the patient instead of other things that you would traditionally think about, like immunosuppressives to prevent rejection. Here, this was a constrictive pericarditis problem, not a problem with LV function, per se.

I hope you like the case. Thank you again for listening. This is Ron Wharton from Bronx, New York, for theheart.org | Medscape Cardiology. Thanks for listening.

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