Acute Aortic RegurgitationYasmin S. Hamirani, MD; Charles A. Dietl, MD; Wyatt Voyles, MD; Mel Peralta, MD;Darlene Begay, RCS; Veena Raizada, MD
Aortic regurgitation (AR) is char-acterized by regurgitation of blood
from the aorta to the left ventricle (LV)during diastole and is attributable todiverse congenital and acquired abnor-malities of the aortic valve or the wallof the aortic root. AR can be eitherchronic or acute. The classic featuresof chronic AR have been known toclinicians for nearly 2 centuries. Cor-rigan described chronic AR in 1832 inhis text “On Permanent Patency of theMouth of the Aorta, or Inadequacy ofthe Aortic Valves.”1 Patients withchronic AR remain asymptomatic formany years as the LV becomes grad-ually enlarged; cardiac symptoms andclinical congestive heart failure thendevelop. On the other hand, acute se-vere AR, if untreated, leads to ad-vanced heart failure and early death.Acute severe AR may be difficult torecognize clinically and is often er-roneously diagnosed as another acutecondition such as sepsis, pneumonia,or nonvalvular heart disease. Acuteor subacute infective endocarditis,aortic dissection, and aortic valvedamage caused by trauma are knowncauses of acute AR. We present 2cases of acute AR (case 1, infectiveendocarditis; case 2, Stanford type Aaortic dissection), and we propose
management plans for each case (Figure1A and 1B).
Case 1A 23-year-old man admitted to anintensive care unit with Staphylococ-cus bacteremia presented with softheart sounds and a to-and-fro murmur,which progressed to a silent precordiumwithin 24 hours. Bedside transthoracic2-dimensional and M-mode echocardio-gram (TTE) and transesophageal echo-cardiogram (TEE) revealed aortic valvevegetations, severe AR, premature mitralvalve closure, and diastolic and earlysystolic mitral regurgitation, indicativeof acute left heart failure necessitatingventilatory support and urgent replace-ment of the aortic valve and aortic rootwith a homograft (Figure 2).
Acute AR results in the develop-ment of a distinct syndrome, the patho-physiological features of which differfrom those of chronic AR (Figure 3Aand 3B).2 Acute severe AR imposes asudden excessive volume load on anunprepared LV that is normal in size,resulting in a dramatic extreme rise inLV diastolic pressure (LVDP), whichmay approach or indeed equal the aor-tic diastolic pressure. Because LVpressure exceeds the left atrial pressureduring diastole, the resulting rapid
ventriculoatrial gradient causes the mi-tral valve to close prematurely beforethe onset of the next systole (Figures2G and 3A). The premature mitralvalve closure is beneficial in the sensethat the high LVDP is not transmittedto the pulmonary venous system, thuspreventing pulmonary edema and clin-ical left heart failure. However, theprotection afforded by premature mi-tral valve closure is lost when a furtherrise in the ventriculoatrial gradientopens the mitral valve in late diastole,leading to diastolic mitral regurgita-tion. Mitral regurgitation in acute ARmay occur either in diastole or insystole (when the LVDP exceeds theleft atrial pressure) (Figure 2E, 2F, and2H). It is likely that persistence of theventriculoatrial gradient, as a result ofextension of the high LVDP level tothe isovolumic contraction period andthe early systole, causes the mitral valveto open during this period, resulting inearly systolic mitral regurgitation. Mitralregurgitation is usually effective to lowerLVDP; the left atrium thus serves as areservoir for blood regurgitated from theaorta to the LV. However, left atrialpressure may rise further, leading topulmonary edema and circulatory fail-ure, as in our patient.
Premature mitral valve closure ispresent when AR is both acute and
severe, and it is best demonstrated byM-mode echocardiography with simul-taneous electrocardiography. Prematuremitral valve closure is a specific andsensitive noninvasive indicator of acutesevere AR, and the extent of prematuremitral valve closure has been correlatedwith the degree of rise in LVDP. Nor-mally, the mitral valve does not closeuntil shortly after the onset of LV con-
traction; leaflet closure occurs 40 msafter the onset of the QRS complex.Premature mitral valve closure is mild(grade I) when coaptation of the anteriorand posterior mitral leaflets occurs at orbefore the initial inscription of the QRS(ie, up to 50 ms before the Q wave butafter the P wave); premature mitral valveclosure is very marked (grade II) whenthe mitral valve closes very prematurely,
up to 200 ms before the Q wave.3 Suchpatients, in comparison with those withgrade I premature mitral valve closure,exhibit extreme elevations in LVDP andvolume, and may be only marginallycompensated (Figure 1A).
A prompt and accurate diagnosis ofacute AR is of great importance, be-cause urgent or emergent aortic valvesurgery is life-saving. Such patients
Figure 1. Proposed management plan for acute aortic regurgitation (AR) due to infective endocarditis (A) and aortic dissection (B). CHFindicates 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.
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are critically ill but show minimal orno clinical signs of AR. Thus, theclassic decrescendo diastolic murmurand the eponymous classical peripher-al arterial signs may be lacking. Anearly diastolic murmur is often heard,but, compared with that of patientswith chronic AR, the murmur is softerand shorter. This, together with thepresence of a short and soft systolicmurmur, often results in developmentof a soft to-and-fro murmur. Occasion-ally, such murmurs are absent. Thesefindings, combined with a soft or ab-sent first heart sound (S1) or A2 (aorticcomponent of second heart sound),sometimes create a silent precordium.S4 and the presystolic component ofthe Austin Flint murmur are absent,but a short mid-diastolic component ofthe Austin Flint murmur is often pres-ent. Auscultation signs can be confus-
ing, because it is difficult to distin-guish diastole from systole. This isbecause the heart sounds are soft orabsent, and diastole becomes shorterthan systole. The mitral valve closesprematurely and opens late, because ofprolongation of the systolic ejectiontime caused by volume and pressureloading of the LV. This leads to areversal of the normal relationship be-tween systole and diastole.
How can the characteristic cardiacauscultations be explained? First, pre-mature mitral valve closure is respon-sible for softness or absence of the S1because the mitral valve is closed atthe beginning of LV systole. A shortearly diastolic murmur and a short mid-diastolic murmur (terminating with asoft premature mitral valve closuresound) produce a palpable summationgallop. The mid-diastolic portion of the
Austin Flint murmur is not affected bypremature mitral valve closure; the shortdiastolic filling time and the high leftatrial pressure are accompanied by tur-bulent blood flow through the mitralvalve. The flow dynamics are similar tothose associated with mitral stenosis.Second, A2 is soft because of destruc-tion of valve tissue and impairment ofthe valve closure mechanism. Third, thesoft systolic murmur is attributable toincreased flow through the aortic valveand/or development of diastolic mitralregurgitation and early systolic mitralregurgitation.
Patients with infective endocarditisare at risk of developing acute andsevere AR that can be detected by TTEand TEE. Aortic valve surgery may betimed with reference to whether thepremature mitral valve closure is mildor severe. The use of echocardiogra-
Figure 1 (Continued).
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phy permits AR severity to be gradedand facilitates medical and surgicalmanagement of such patients. We pro-pose that AR patients exhibiting gradeII premature mitral valve closure re-quire urgent aortic valve replacement.Patients with grade II premature mitralvalve closure and mitral regurgitationshould undergo emergent aortic valvereplacement. Surgery in these 2 groupsof patients should proceed regardlessof infection status and without waitingfor completion of antibiotic therapy.Patients with grade I premature mitralvalve closure and who do not showclinical heart failure can be managed
by medical therapy; the decision onearly aortic valve replacement shouldinclude consideration of both relativehemodynamic severity (as judged byphysical examination and echo-Dopp-ler findings) and the severity and extentof infection (including intra- and extra-cardiac complications (Figure 1A).
Case 2A 59-year-old man presented to theemergency department with chest andback pain and syncope. A chest x-rayrevealed a widened mediastinum, anda diagnosis of Stanford type A dissec-tion was confirmed by computed to-
mography of the chest. The dissectionflap originated at the level of the aorticvalve and involved the entire thoracicaorta, including the ascending aorta,the aortic arch, and the origins of theinnominate, left common carotid, andleft subclavian arteries. TTE and intra-operative TEE revealed severe AR, adissection flap at the level of the non-coronary cusp of the aortic valve, andpremature mitral valve closure (Figure4). Emergent surgery was performedwith the aortic root and aortic valvereplacement by use of a St Jude com-posite valve conduit, with coronaryreimplantation (Bentall procedure),followed by an uneventful recovery.
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). ARindicates aortic regurgitation; TTE, transthoracic echocardiogram; and TEE, transesophageal echocardiogram.
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Acute type A aortic dissection isan uncommon but catastrophic acuteevent with an annual incidence of 3 to4 cases per 100 000 of the generalpopulation in the United Kingdom andthe United States; preadmission mor-tality is 20%, and inpatient mortality is30%. Early-stage mortality is as highas 1% to 2% per hour over the first
several hours, but survival levels haveimproved in recent years. Clinical rec-ognition is now prompt; definitive di-agnostic testing with the use of TEEand/or chest computed tomography isavailable; and emergent surgery has be-come established. AR is an importantcomplication of proximal aortic dissec-tion; an AR murmur is detected in 16%
to 67% of all such patients. Intraop-erative TEE is indispensable to demon-strate the mechanism of AR and tofacilitate the choice among aortic valvesurgical procedures, resuspension, or re-placement. These mechanisms includedilatation of the aortic root and annulus(Figure 5A), pressure of a false lumen on1 cusp causing asymmetrical cusp coap-
Figure 3. Schematic representations contrasting the hemodynamic, echocardiographic, and phonocardiographic manifestations ofacute 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, mitralvalve closure; S1, first heart sound; S2, second heart sound; SM, systolic murmur; and DM, diastolic murmur.
Figure 4. Severe AR (A) and dissection flap at the level of non coronary cusp of the AV (B). AR indicates aortic regurgitation; AV, aorticvalve; and TTE, transthoracic echocardiogram.
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tation (Figure 5B), flail of an aortic cuspattributable to annular support disruption(Figure 5C), and prolapse of a mobileintimal flap through the aortic valve(Figure 5D).4
In summary, patients with infectiveendocarditis and aortic dissection areat risk of developing acute severe ARthat can be detected with the aid ofTTE and/or TEE. These techniquespermit AR severity to be graded andfacilitate appropriate medical and sur-gical management of patients with acuteAR (Figure 1A and 1B).
AcknowledgmentsWe thank Linda Jeffcoat for her assistancewith the preparation of this manuscript.
DisclosuresNone.
References1. Corrigan DJ. On permanent patency of the
mouth of the aorta or inadequacy of the aorticvalves. Edinbh Med and Surg J. 1832;37:225–245.
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.
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