Echo Case: Problem Pill or Is There a Pill for This Problem?

Ronald H Wharton, MD


October 29, 2015

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Ronald H Wharton, MD: Hello, and greetings from Bronx, New York. This is Ronald Wharton. I'm a cardiologist at Montefiore Medical Center in the Albert Einstein College of Medicine.

Today I thought I'd present something which I think you'll find educational and somewhat amusing. I title this, Is the problem the pill, or is there a pill for this problem? Next slide.

Here's the history. This is a 45-year-old gentleman who was admitted to the inpatient service. He came in because of shortness of breath. His history is bad. He'd been told in the past of a very high LDL cholesterol and high triglycerides. He was started on a high-potency statin. He is not taking any other medications. He comes to the emergency room because he just feels fatigued. It's getting worse; he is getting more and more short of breath. Next slide.

Here's some pertinent things on his labs. His physical exam wasn't particularly revealing other than the fact that he's obese. He had a standard cardiac troponin T, which came back at 0.15 ng/mL, the reference in our lab is less than 0.11 ng/mL. He also had a very high total CK, almost 14,000 U/L. The CK-MB was 0.6% of the total CK. Histransaminases were also elevated, and he was admitted to telemetry.

So, is there something wrong with his heart? Is this all a case of statin-induced myositis and statin-induced hepatitis?

Well, everybody gets an echocardiogram nowadays, and this gentleman was no exception. You can see here, he has a parasternal long-axis 2D image and in this image, you can see the LV systolic function is good, the RV systolic function looks good. If you look closely, there's some early diastolic collapse of the RV free wall.

In the next slide, you can see a similar thing. This is now parasternal, short-axis at the level of the aortic valve. Again, you can see that there is some early diastolic collapse of the free wall of the right ventricular outflow tract.

In the next slide, you can see these findings on M-mode. Here we have an M-mode of the aortic valve, and you'll notice that after the aortic valve closes, the tricuspid valve should be opening up and the RV should be getting bigger. But there's a bit of a delay between when the aortic valve closes and when the right ventricular outflow tract (RVOT) starts expanding.

In the next slide, you can see something similar in the mitral M-Mode. You'll notice that after the mitral opens, there's a bit of a delay before the RVOT starts to get bigger. They're both 2D and confirmatory M-mode findings demonstrating tamponade physiology.

Take a look for a second at this apical four-chamber view. You can see that there is a circumferential pericardial effusion; the function of the RV and the LV appear to be normal.

Similarly, if you look at the two-chamber view on the next slide, you can see that the anterior and inferior walls appear to thicken normally, and again note the circumferential pericardial effusion.

The next slide demonstrates a pulse-wave Doppler through the mitral valve, and you'll notice that there is significant respiratory variation in the mitral inflow depending on whether the patient is taking a deep breath in or a deep breath out. During inspiration, the mitral velocities are reduced; during expiration the mitral velocities are higher. So here are some questions.

Is there a regional abnormality? There doesn't seem to be-the wall thickening in all the views that I showed you (parasternal long axis, apical four and apical two chambers) all looked okay. Certainly no echo evidence of any previous infarction. Is there tamponade physiology? Well, we covered that. You can see it in the imaging very clearly. If you don't, you can also look at the M-mode images, which give you the additional time resolution, demonstrating that the RVOT starts to expand considerably after the aortic valve is closed and after the mitral valve has opened. Next slide.

You can see those again. I'll show you the M-mode again. Take a look at where the aortic valve is closing, see where the RVOT starts to come up.

In the mitral valve, you'll notice that the mitral valve always opens probably a good 100 ms or more-I didn't measure it on the slides-but that's probably at least 100 ms before the RV starts to get bigger. So, what do we do? He's on a statin, that's all he's taking. His CKs are off the wall, his transaminases are high, he has evidence of pericardial tamponade physiology with a moderate circumferential pericardial effusion. You can probably guess that that effusion didn't get there overnight from its size. Considering its size, these findings of tamponade aren't pleasant, but they're not the worst case we've ever seen on an echocardiogram.

Do we stop the statin? Do we do a pericardiocentesis? Do we do both? Do we do neither?

One other thing to think about, should we look at an imaging study, look at constriction? Is this constrictive pericarditis? Maybe the statin has nothing to do with it. After all, he has a pericardial effusion, maybe that's part of some inflammatory process involving the pericardium and he has constrictive physiology. There is a ventricular interdependence, you saw that very clearly on the pulse-wave Doppler through the mitral valve as well as the 2D and M-mode imaging. His liver functions are abnormal, that's how constriction presents, isn't it? Maybe this is all constriction.

Well, it's a great thought, but there's only one problem. Did you notice through all of those images, despite the tamponade physiology, that his heart rate is only about 60 beats per minute? He's not taking a beta-blocker, he's just taking a statin.

So, what's the answer? Drum roll. Well, what did we do? Did we do a pericardiocentesis? Did we do a liver biopsy? Or did we just do a blood test?

It was a blood test.

The patient's thyroid-stimulating hormone (TSH) was also 400 µg/mL. If you look at the next slide, and with my apologies to Dr Seuss,

There is no statin hepatitis,

There is no statin myositis,

The statin here is not to blame,

The thyroid here is not so tame.

The thyroid here is what is sick,

This is the answer to my trick,

And finally here is the thrill,

Of what can happen with a pill.

(That is, if the pill is levothyroxine.)

Here's a repeat echocardiogram 8 months later. The patient did not have any procedures, no needles were stuck anywhere. Here's a parasternal long axis, same patient. No effusion.

Apical four-chamber in the next slide. Normal LV, normal RV. No effusion, so in summary

The myositis is gone, the liver is better and the pericardium is finally no longer wetter. I won't quit my day job just yet, but I hope you enjoyed this, a nice case of thyroid disease causing all of these other problems. My appreciation to my colleagues in the division of endocrinology at Montefiore for sharing the case with me. Hope you liked it. In any case, this is a very nice illustration of how the thyroid can cause a conundrum of other problems, and I hope you enjoyed it.

This is Ronald Wharton for the division of cardiology at Montefiore Medical Center, Albert Einstein College of Medicine, at on Medscape. Thanks for watching.

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