CLINICIAN UPDATE
Acute Aortic Regurgitation
Yasmin S. Hamirani, MD; Charles A. Dietl, MD; Wyatt Voyles, MD; Mel Peralta, MD;
Darlene Begay, RCS; Veena Raizada, MD
A ortic regurgitation (AR) is char-
acterized by regurgitation of blood
from the aorta to the left ventricle (LV)
management plans for each case (Figure
1A and 1B).
ventriculoatrial gradient causes the mi-
tral valve to close prematurely before
the onset of the next systole (Figures
during diastole and is attributable to Case 1 2G and 3A). The premature mitral
diverse congenital and acquired abnor- A 23-year-old man admitted to an valve closure is beneficial in the sense
malities of the aortic valve or the wall intensive care unit with Staphylococ- that the high LVDP is not transmitted
of the aortic root. AR can be either cus bacteremia presented with soft to the pulmonary venous system, thus
chronic or acute. The classic features heart sounds and a to-and-fro murmur, preventing pulmonary edema and clin-
of chronic AR have been known to which progressed to a silent precordium ical left heart failure. However, the
clinicians for nearly 2 centuries. Cor- within 24 hours. Bedside transthoracic protection afforded by premature mi-
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rigan described chronic AR in 1832 in 2-dimensional and M-mode echocardio- tral valve closure is lost when a further
his text “On Permanent Patency of the gram (TTE) and transesophageal echo- rise in the ventriculoatrial gradient
Mouth of the Aorta, or Inadequacy of cardiogram (TEE) revealed aortic valve opens the mitral valve in late diastole,
the Aortic Valves.”1 Patients with vegetations, severe AR, premature mitral leading to diastolic mitral regurgita-
valve closure, and diastolic and early tion. Mitral regurgitation in acute AR
chronic AR remain asymptomatic for
may occur either in diastole or in
many years as the LV becomes grad- systolic mitral regurgitation, indicative
systole (when the LVDP exceeds the
ually enlarged; cardiac symptoms and of acute left heart failure necessitating
left atrial pressure) (Figure 2E, 2F, and
clinical congestive heart failure then ventilatory support and urgent replace-
2H). It is likely that persistence of the
develop. On the other hand, acute se- ment of the aortic valve and aortic root
ventriculoatrial gradient, as a result of
vere AR, if untreated, leads to ad- with a homograft (Figure 2).
extension of the high LVDP level to
vanced heart failure and early death. Acute AR results in the develop- the isovolumic contraction period and
Acute severe AR may be difficult to ment of a distinct syndrome, the patho- the early systole, causes the mitral valve
recognize clinically and is often er- physiological features of which differ to open during this period, resulting in
roneously diagnosed as another acute from those of chronic AR (Figure 3A early systolic mitral regurgitation. Mitral
condition such as sepsis, pneumonia, and 3B).2 Acute severe AR imposes a regurgitation is usually effective to lower
or nonvalvular heart disease. Acute sudden excessive volume load on an LVDP; the left atrium thus serves as a
or subacute infective endocarditis, unprepared LV that is normal in size, reservoir for blood regurgitated from the
aortic dissection, and aortic valve resulting in a dramatic extreme rise in aorta to the LV. However, left atrial
damage caused by trauma are known LV diastolic pressure (LVDP), which pressure may rise further, leading to
causes of acute AR. We present 2 may approach or indeed equal the aor- pulmonary edema and circulatory fail-
cases of acute AR (case 1, infective tic diastolic pressure. Because LV ure, as in our patient.
endocarditis; case 2, Stanford type A pressure exceeds the left atrial pressure Premature mitral valve closure is
aortic dissection), and we propose during diastole, the resulting rapid present when AR is both acute and
From the Division of Cardiology and Cardiothoracic Surgery, University of New Mexico, Albuquerque, NM.
Correspondence to Veena Raizada, MD, MSC 10-5550, 1 University of New Mexico, Albuquerque, NM 87131-0001. Email [email protected]
(Circulation. 2012;126:1121-1126.)
© 2012 American Heart Association, Inc.
Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIRCULATIONAHA.112.113993
1121
1122 Circulation August 28, 2012
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Figure 1. Proposed management plan for acute aortic regurgitation (AR) due to infective endocarditis (A) and aortic dissection (B). CHF
indicates congestive heart failure; TTE, transthoracic echocardiogram; TEE, transesophageal echocardiogram; IE, infective endocarditis;
AR, aortic regurgitation; PMVC, premature mitral valve closure; DMR, diastolic mitral regurgitation; ESMR, early systolic mitral regurgi-
tation; ICU, intensive care unit; EKG, electrocardiogram; LVOT, left ventricular outflow tract; and AV, aortic valve.
severe, and it is best demonstrated by traction; leaflet closure occurs 40 ms up to 200 ms before the Q wave.3 Such
M-mode echocardiography with simul- after the onset of the QRS complex. patients, in comparison with those with
taneous electrocardiography. Premature Premature mitral valve closure is mild grade I premature mitral valve closure,
mitral valve closure is a specific and (grade I) when coaptation of the anterior exhibit extreme elevations in LVDP and
sensitive noninvasive indicator of acute and posterior mitral leaflets occurs at or volume, and may be only marginally
severe AR, and the extent of premature before the initial inscription of the QRS compensated (Figure 1A).
mitral valve closure has been correlated (ie, up to 50 ms before the Q wave but A prompt and accurate diagnosis of
with the degree of rise in LVDP. Nor- after the P wave); premature mitral valve acute AR is of great importance, be-
mally, the mitral valve does not close closure is very marked (grade II) when cause urgent or emergent aortic valve
until shortly after the onset of LV con- the mitral valve closes very prematurely, surgery is life-saving. Such patients
Hamirani et al Acute Aortic Regurgitation 1123
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Figure 1 (Continued).
are critically ill but show minimal or ing, because it is difficult to distin- Austin Flint murmur is not affected by
no clinical signs of AR. Thus, the guish diastole from systole. This is premature mitral valve closure; the short
classic decrescendo diastolic murmur because the heart sounds are soft or diastolic filling time and the high left
and the eponymous classical peripher- absent, and diastole becomes shorter atrial pressure are accompanied by tur-
al arterial signs may be lacking. An than systole. The mitral valve closes bulent blood flow through the mitral
early diastolic murmur is often heard, prematurely and opens late, because of valve. The flow dynamics are similar to
but, compared with that of patients prolongation of the systolic ejection those associated with mitral stenosis.
with chronic AR, the murmur is softer time caused by volume and pressure Second, A2 is soft because of destruc-
and shorter. This, together with the loading of the LV. This leads to a tion of valve tissue and impairment of
presence of a short and soft systolic reversal of the normal relationship be- the valve closure mechanism. Third, the
murmur, often results in development tween systole and diastole. soft systolic murmur is attributable to
of a soft to-and-fro murmur. Occasion- How can the characteristic cardiac increased flow through the aortic valve
ally, such murmurs are absent. These auscultations be explained? First, pre- and/or development of diastolic mitral
findings, combined with a soft or ab- mature mitral valve closure is respon- regurgitation and early systolic mitral
sent first heart sound (S1) or A2 (aortic sible for softness or absence of the S1 regurgitation.
component of second heart sound), because the mitral valve is closed at Patients with infective endocarditis
sometimes create a silent precordium. the beginning of LV systole. A short are at risk of developing acute and
S4 and the presystolic component of early diastolic murmur and a short mid- severe AR that can be detected by TTE
the Austin Flint murmur are absent, diastolic murmur (terminating with a and TEE. Aortic valve surgery may be
but a short mid-diastolic component of soft premature mitral valve closure timed with reference to whether the
the Austin Flint murmur is often pres- sound) produce a palpable summation premature mitral valve closure is mild
ent. Auscultation signs can be confus- gallop. The mid-diastolic portion of the or severe. The use of echocardiogra-
1124 Circulation August 28, 2012
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Figure 2. Aortic valve (AV) vegetations (A) with aortic root abscess (B), confirmed at surgery (C), severe AR (D), diastolic mitral regurgi-
tation (DMR) (E), early systolic mitral regurgitation (ESMR) (F), premature mitral valve closure (PMVC) (G), and DMR and ESMR (H). AR
indicates aortic regurgitation; TTE, transthoracic echocardiogram; and TEE, transesophageal echocardiogram.
phy permits AR severity to be graded by medical therapy; the decision on mography of the chest. The dissection
and facilitates medical and surgical early aortic valve replacement should flap originated at the level of the aortic
management of such patients. We pro- include consideration of both relative valve and involved the entire thoracic
pose that AR patients exhibiting grade hemodynamic severity (as judged by aorta, including the ascending aorta,
II premature mitral valve closure re- physical examination and echo-Dopp- the aortic arch, and the origins of the
quire urgent aortic valve replacement. ler findings) and the severity and extent innominate, left common carotid, and
Patients with grade II premature mitral of infection (including intra- and extra- left subclavian arteries. TTE and intra-
cardiac complications (Figure 1A). operative TEE revealed severe AR, a
valve closure and mitral regurgitation
dissection flap at the level of the non-
should undergo emergent aortic valve
coronary cusp of the aortic valve, and
replacement. Surgery in these 2 groups Case 2 premature mitral valve closure (Figure
of patients should proceed regardless A 59-year-old man presented to the 4). Emergent surgery was performed
of infection status and without waiting emergency department with chest and with the aortic root and aortic valve
for completion of antibiotic therapy. back pain and syncope. A chest x-ray replacement by use of a St Jude com-
Patients with grade I premature mitral revealed a widened mediastinum, and posite valve conduit, with coronary
valve closure and who do not show a diagnosis of Stanford type A dissec- reimplantation (Bentall procedure),
clinical heart failure can be managed tion was confirmed by computed to- followed by an uneventful recovery.
Hamirani et al Acute Aortic Regurgitation 1125
Figure 3. Schematic representations contrasting the hemodynamic, echocardiographic, and phonocardiographic manifestations of
acute severe (A) and chronic severe (B) AR.1 Ao indicates aorta; AR, aortic regurgitation; EDP, end-diastolic pressure; LV, left ventricle;
LA, left atrium; AML, anterior mitral leaflet; PMC, posterior mitral leaflet; ECHO, echocardiogram; PCG, phonocardiogram; C, mitral
valve closure; S1, first heart sound; S2, second heart sound; SM, systolic murmur; and DM, diastolic murmur.
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Acute type A aortic dissection is several hours, but survival levels have to 67% of all such patients. Intraop-
an uncommon but catastrophic acute improved in recent years. Clinical rec- erative TEE is indispensable to demon-
event with an annual incidence of 3 to ognition is now prompt; definitive di- strate the mechanism of AR and to
4 cases per 100 000 of the general agnostic testing with the use of TEE facilitate the choice among aortic valve
population in the United Kingdom and and/or chest computed tomography is surgical procedures, resuspension, or re-
the United States; preadmission mor- available; and emergent surgery has be- placement. These mechanisms include
tality is 20%, and inpatient mortality is come established. AR is an important dilatation of the aortic root and annulus
30%. Early-stage mortality is as high complication of proximal aortic dissec- (Figure 5A), pressure of a false lumen on
as 1% to 2% per hour over the first tion; an AR murmur is detected in 16% 1 cusp causing asymmetrical cusp coap-
Figure 4. Severe AR (A) and dissection flap at the level of non coronary cusp of the AV (B). AR indicates aortic regurgitation; AV, aortic
valve; and TTE, transthoracic echocardiogram.
1126 Circulation August 28, 2012
Figure 5. A through D, Mechanisms of AR in proximal aortic dissection explained in the text.4 AR indicates aortic regurgitation.
Reprinted with permission from Isselbacher et al.4 Copyright Elsevier, 1997.
tation (Figure 5B), flail of an aortic cusp Acknowledgments clinical recognition and management. Ann
attributable to annular support disruption Intern Med. 1977;87:223–232.
We thank Linda Jeffcoat for her assistance
3. Pridie RB, Benham R, Oakley CM. Echocar-
(Figure 5C), and prolapse of a mobile with the preparation of this manuscript.
diography of the mitral valve in aortic valve
intimal flap through the aortic valve disease. Br Heart J. 1971;31:296 –304.
(Figure 5D).4 4. Isselbacher EM, Eagle KA, Desanctis RW.
Disclosures
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In summary, patients with infective None.
Diseases of the aorta. Figure 45-8. Braun-
endocarditis and aortic dissection are wald’s Heart Disease: A Textbook of Car-
at risk of developing acute severe AR diovascular Medicine. Vol 2. 5th ed. Phila-
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AR (Figure 1A and 1B). severe aortic regurgitation. Pathophysiology, aortic regurgitation