A 76-year-old man with a prior history of hypertension, hyperlipidemia, benign prostatic hypertrophy, and no known heart disease presented with a 5-week history of generalized malaise, intermittent fevers, loss of appetite, weight loss, and progressive dyspnea on exertion. He was brought to the emergency department by his wife after he became lethargic.
On admission, he was febrile to 38.5°C (101.5°F). His blood pressure was 130/50 mmHg. His heart rate was regular at 110 bpm, and oxygen saturation was 89% on room air. The lungs exam revealed diffuse rales with decreased breath sounds at both bases. A soft systolic murmur at the right upper sternal border was noted. There was bilateral pretibial pitting edema.
Laboratory findings were notable for an elevated white blood count of 17,000/mcl with 93% neutrophils, normocytic anemia with hemoglobin of 9.1 g/dL, and an elevated erythrocyte sedimentation rate of 75 mm/hour. All 6 blood cultures promptly grew Streptococcus gordonii, a viridans member of the human oral flora.
The clinical diagnosis of subacute bacterial endocarditis with acute decompensated heart failure was established. The patient was referred for a transthoracic echocardiogram and transesophageal echocardiogram that revealed severe aortic regurgitation (AR) (Video 1), preserved left ventricular (LV) ejection fraction (Video 2), and marked pulmonary hypertension with an estimated pulmonary artery systolic pressure of 65 mmHg.
Video 1
Video 2
Figures 1-5 include four still echocardiographic images from this patient with severe acute AR and one still echocardiographic image from another patient without severe AR.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Which of these figures does NOT support the diagnosis of severe acute AR?
Show Answer
The correct answer is: C. Figure 3
This case is an example of severe acute AR due to bacterial endocarditis. Other causes of acute AR include type A aortic dissection and chest trauma. Severe acute AR is a life-threatening emergency requiring prompt diagnosis, appropriate medical therapy, and surgical intervention.
Echocardiography is the primary imaging modality for establishing the diagnosis of severe acute AR. Video 1 demonstrates endocarditis with flail right cusp of the aortic valve as the cause of severe acute AR in this patient.
The fundamental hemodynamic abnormality in severe acute AR is massive volume overload of a nondilated left ventricle leading to a rapid rise of LV diastolic pressure. This acute rise leads to a series of hemodynamic abnormalities that can be visualized on echocardiography.
Explanation for Answer A
The presence of a nondilated left ventricle as shown in Video 1 and Figures 1 and 6 indicates that severe AR is acute rather than chronic.
Figure 6
Explanation for Answer B
Due to a marked rise in LV diastolic pressure, the mitral valve closes prematurely, as shown in Figure 2 and lower panel of Figure 7. Note that in this patient, the mitral valve closes well before the QRS complex on the electrocardiogram. This is in contrast to the timing of mitral valve closure after the onset of the QRS in a healthy individual, as shown in the upper panel of Figure 7.
Figure 7
Explanation for Answer C
Due to a large regurgitant orifice, there is rapid equalization of diastolic pressures between the ascending aorta and the left ventricle. This leads to rapid deceleration and a short pressure half-time of the aortic regurgitant jet on spectral Doppler tracings, as shown in the lower panel of Figure 8. This is in contrast to chronic and/or less severe AR in which the deceleration slope is less steep and the pressure half-time is typically longer. Thus Figure 3 is NOT consistent with severe acute AR, and answer C is the correct answer.
As stated in the 2017 American Society of Echocardiography guidelines for evaluation of native valvular regurgitation, a pressure half-time >500 msec suggests mild AR, and <200 msec suggests severe AR. However, pressure half-time is determined not only by the size of the aortic regurgitant orifice but also by compliance of the left ventricle. Thus, patients with severe chronic AR and a compliant left ventricle may have a pressure half-time in the ''moderate'' range. In contrast, in patients with severe diastolic dysfunction and only mild AR may have short pressure half-time. Because vasodilator therapy decreases diastolic blood pressure independent of the AR, pressure half-time method is less useful for monitoring AR in patients receiving vasodilators.
Figure 8
Explanation for Answer D
Another marker of the elevated LV diastolic pressure is the development of diastolic (pre-systolic) mitral regurgitation, as shown in Figures 4 and 9.
Figure 9
Explanation for Answer E
Normally there is only brief retrograde flow in the descending thoracic and abdominal aorta that occurs in early diastole. With severe AR, whether acute or chronic, the retrograde flow in the descending thoracic and abdominal aorta occurs throughout diastole. Holodiastolic flow reversal in the abdominal aorta, as shown in Figures 5 and 10, is a more specific sign of severe AR than holodiastolic reversal in the descending thoracic aorta.
Figure 10
After prompt initiation of antibiotic therapy, our patient underwent urgent surgical aortic valve replacement and is doing well 3 years later.
References
Zoghbi WA, Adams D, Bonow RO, et al. Recommendations for Noninvasive Evaluation of Native Valvular Regurgitation: A Report from the American Society of Echocardiography Developed in Collaboration with the Society for Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr 2017;30:303-71.
Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;63:2438-88.
Benenstein R, Saric M. "Aortic Regurgitation: Risk stratification – timing of surgery." In: Lang R, Goldstein SA, Kronzon I, Khandheria BK, Mor-Avi V, eds. ASE's Comprehensive Echocardiography, 2nd Edition. Philadelphia, PA: Elsevier; 2016:450-52.
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