Ronald H Wharton, MD

Disclosures

February 26, 2015

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Dr Ronald Wharton: Good afternoon. This is Dr Ronald Wharton. I am an assistant professor of medicine at the Albert Einstein College of Medicine in the Bronx, New York City, and attending cardiologist at Montefiore Medical Center in the Bronx. Today, I thought I would share with you two echocardiograms done on the same patient about a week apart. I titled this "Who Needs an ECG?" because the echocardiograms demonstrate some interesting hemodynamics as well as some interesting things that relate to an echocardiogram that I thought might be of interest to the cardiology and echocardiography public out there.

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This is a patient who has end-stage renal disease, who has to get hemodialysis three times a week. It sets patients up for infectious sequelae, which often occur, regrettably. This patient developed an acute febrile illness associated with dyspnea and a murmur.

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You can see here in the parasternal long axis of the first image that the left ventricle is somewhat dilated. She is rather small, and when you adjust this for body surface area, the left ventricle (LV) is mild to moderately dilated. There is an obvious vegetation on either the right or the left noncoronary cusp. You really can't tell which on this view, but there is vegetation. In addition, you can see the left atrium is enlarged. The coaptation of the mitral leaflets is apically displaced.

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When we put color on this image, you can see that the mitral regurgitation is severe and the aortic regurgitation is torrential. No mystery here: the endocarditis has led to severe aortic insufficiency probably via dilatation of the left ventricle and dilatation of the mitral annulus; there is secondary severe mitral regurgitation.

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There are some nice findings here on the aortic-valve M-mode— specifically, the fluttering of the leaflet during diastole, which is usually a known sine qua non of endocarditis.

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You can see two findings in the M-mode of the mitral valve that are interesting: number one, the diastolic fluttering of the interior mitral leaflet, which is a qualitative sign of aortic insufficiency, but also the premature closure of the mitral valve. Notice that the mitral valve closes considerably before the onset of electrical systole. This demonstrates that the LV filling pressures are so high that the mitral valve is closing before electrical systole has started, so the filling pressures are very high.

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This is now an apical four-chamber view just showing the same things. The torrential aortic insufficiency

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and the not-quite-as-torrential mitral regurgitation.

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If you notice here the aortic insufficiency has a continuous-wave Doppler that you would expect with a severe acute or subacute aortic regurgitation. A very dense diastolic signal with a very steep deceleration time, demonstrating that the LV and aorta are equilibrating rapidly in diastole.

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You can see the Doppler signal of the mitral regurgitation. Notice that the mitral regurgitation starts in diastole. That should be expected, because the mitral valve is closing prematurely. What's happening here is that we have a restrictive physiology, because the left ventricle is being flooded by a volume from the severe aortic insufficiency for which it has not sufficiently dilated to accommodate. Therefore, its pressures rise so much that the mitral regurgitation starts in diastole. So for all of those of you who are listening who are taught in medical school that mitral regurgitation is purely a systolic phenomenon, well, clearly it isn't.

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This is a Doppler of the tricuspid valve in the same patient. You can see here that the peak tricuspid regurgitation velocity approaches 3 m/s, so you can assume that the patient probably has mild to moderate pulmonary-artery systolic hypertension. If the right atrial pressure were 10 mm Hg, we would be talking about a pulmonary-artery systolic pressure of approximately 46 mm Hg, and the tricuspid regurgitation signal, as you can see, unlike its mitral counterpart, starts exactly when it's supposed to, with the onset of electrical systole (right after the QRS), which is right above the signal.

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This patient gets very, very aggressive treatment with the inotropic support she needed, because frankly she was in shock. This was a Staphylococcus aureus infection, and about a week later, her hemodynamics seemed to be a little better as judged by the physicians in charge of her care. I was not involved in her direct care.

Another echocardiogram is repeated a week later.

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Here is another parasternal long access; a week later there's a small pericardial effusion or a trace pericardial effusion, depending on how you want to read it, that wasn't there previously. The vegetation on the aortic valve is still present. The systolic function of the left ventricle looks about the same. Left ventricular size doesn't look particularly different.

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Similarly, when we put color on the valves, there is still no obvious change here. We have severe mitral regurgitation and torrential aortic regurgitation, nothing different here.

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Here is the continuous-wave Doppler signal of the mitral valve, again here; notice that the mitral regurgitation is also starting in diastole, reflecting the premature closure of the mitral valve from restrictive filling, which is still present.

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But, look what happened; this is the tricuspid regurgitation on the same patient, and now the velocity is almost the same. It probably is the same if you account for subtle changes in fluid status and the angle of the beam. The TR velocity is measured at about 2.8 m/s. But, look what's different; the tricuspid regurgitation is now starting in the middle of diastole, too. It didn't before, but it is now.

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Why is that happening? The initial study demonstrated diastolic mitral regurgitation because of the restrictive filling imposed by severe acute aortic regurgitation, but what about the diastolic tricuspid regurgitation? Certainly the patient didn't develop severe pulmonic insufficiency. We can't say that there was something parallel happening on the right side of the heart that would account for that. So what happened?

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Let's take a look at the first echocardiogram, and specifically I want you to notice that the PR interval in this electrocardiogram is normal. Probably, in the vicinity of about 160 to 180 ms.

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Contrast that with the second electro-cardiogram. Notice now that the PR interval is approaching 280 ms (or something in that vicinity). It's much longer.

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The diastolic tricuspid regurgitation is not consequent to the aortic endocarditis per se, because the aortic regurgitation doesn't increase the filling pressures on the right ventricle, only on the left ventricle. However, because the PR interval has prolonged, we now allow the atrial diastole to occur before the onset of ventricular systole. That allows the driving force of tricuspid regurgitation to start in diastole, because ventricular systole is delayed because of the prolonged PR interval.

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Why is this important? Don't forget this patient has aortic endocarditis, and one of the electrocardiographic clues to the presence of aortic-valve endocarditis and also possibly to the development of an aortic-root abscess is the presence of concomitant sinus tachycardia with prolongation of the PR interval. Normally the same catecholamines that rev up the sinus node accelerate (if you will) the conduction through the AV node. However, in this case, what is happening is that despite the high catecholamine state, the AV conduction is prolonged. That can often happen in the presence of an inflammatory condition around the AV node, such as aortic endocarditis.

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I thought I would show this case because you have two valves with diastolic regurgitation that normally aren't supposed to have diastolic regurgitation. The MR, which can be explained completely on the physiology of the aortic regurgitation, and the TR, due to prolonged AV conduction because of the presence of inflammation in the vicinity of the AV node.

As an aside, this patient underwent surgery successfully and did quite well. If anyone asks you if mitral regurgitation and tricuspid regurgitation occur in diastole, the answer is, sure. Don't pay any attention to what they taught you in medical school.

This is Ronald Wharton from Bronx, New York and Montefiore Medical Center on behalf of theheart.org at Medscape Cardiology and I hope you enjoyed this. Thank you.

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