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\begin{document}

\title{Asymptomatic Chronic Traumatic Aortic Valve Perforation with Severe
Aortic Regurgitation}



\author[1]{Neeta Bachani}%
\author[1]{Avishek Bagchi}%
\author[1]{Kunal Sinkar}%
\author[1]{Jaipal Jadwani}%
\author[2]{Bhavik Dhirawani}%
\author[1]{Harshad Shah}%
\author[1]{Sanjeev Vichare}%
\author[1]{Brian Pinto}%
\affil[1]{Holy Family Hospital}%
\affil[2]{Holy Family Hospial}%


\vspace{-1em}



  
  \date{March 14, 2025}


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\selectlanguage{english}
\begin{abstract}
Here we present a young asymptomatic male incidentally diagnosed to have
aortic regurgitation (AR). The patient had a history of a blunt trauma
to the thorax two years back but did never have any symptoms.
Transthoracic echocardiography showed a moderately dilated left
ventricle with normal systolic function and severe AR with normal
nondilated aortic root and tri-leaflet aortic valve. To diagnose the
etiology of the AR a trans-esophageal echocardiogram (TEE) was done,
which revealed a perforation in the non-adjacent leaflet (NAL) and
confirmed severe AR with two AR jets being clearly visualised, one
through the point of incomplete coaptation and other one through the
perforated area in the NAL. The patient was treated with aortic valve
replacement and was doing well on follow-up.%
\end{abstract}%



\sloppy


\textbf{Introduction}

Aortic leaflet perforation leading to aortic regurgitation is a known
complication of blunt chest trauma. There are some case
series\textsuperscript{1-2} and case
reports\textsuperscript{3-12}describing such cases. These patients
report either immediately or within weeks of the trauma, with dyspnea
and chest pain. They need to be operated urgently with either aortic
valve replacement or repair as found suitable. Here we describe a
patient who was asymptomatic 2 years after blunt chest trauma and was
incidentally detected to have severe aortic regurgitation (AR) caused by
a tear in the non-adjacent leaflet (NAL).

\textbf{Case Report}

A 26-year-old man was found to have cardiomegaly on chest x-ray on a
routine pre-employment health check-up. He was asymptomatic with no
history suggestive of any cardiac illness or any pre-existing
co-morbidity. He did not have a history of fever, weight loss, drug
abuse or rheumatic fever. However, on repeated interrogation he
remembered blunt trauma to his face and chest due to a vehicular
accident 2 years ago. He did not have a Marfanoid habitus. The BP was
140/40 mm Hg. The pulse rate was 100/min, regular and collapsing in
character; pistol shot sounds were also present. A Grade 4/6 high
pitched moderately long diastolic murmur was heard in the left third
intercostal space.

Echocardiography revealed a moderately dilated left ventricle with
normal systolic function. There was severe AR with significant diastolic
reversal of flow in descending thoracic aorta. The aortic valve was
tri-leaflet, with no significant dilation of the aortic root (Video 1).
The Effective Regurgitant Orifice of the AR jet by the Proximal
Isovelocity Surface Area method was 0.5 cm\textsuperscript{2} with a
regurgitant volume of 96 ml/beat. The pressure half time of the AR jet
was only 250 ms. The right coronary leaflet appeared elongated and the
NAL showed everted edges (Video 2). There was no evidence of rheumatic
affection or endocarditis.

We performed a Trans Esophageal Echocardiography (TEE) to delineate the
etiology of AR and aortic valve pathology. Normal tri-leaflet valve and
aortic root were confirmed (Figure1, Video 3) and there was evidence of
tissue gap in the NAL suggestive of perforation (Figure 2). There was no
vegetation. Colour Doppler study confirmed severe AR with two AR jets
being clearly visualised, one through the point of incomplete coaptation
and other one through the perforated area in the NAL (Figure 3; Videos
4). He underwent surgery; intra-operatively the large perforation of the
NAL was confirmed (Figure 4). There was no evidence of endocarditis or
calcification. The valve was replaced with a 21 mm St Jude Trifecta
tissue valve. Post-operative recovery was uneventful, and he is doing
well at 18 months follow up.

\textbf{Discussion}

The basic pathophysiology behind post traumatic AR can be either acute
rupture of the thoracic aorta at the isthmus where the mobile thoracic
aorta joins the firmly fixed aortic arch \textsuperscript{13,14},
leaflet injury \textsuperscript{3-12} or avulsion of the
commisures\textsuperscript{15}. The mechanism behind such injuries
involves increased pressure inside the aortic root with a closed aortic
valve and low left ventricular pressure in diastole, leading to high
transvalvular gradient. The left coronary sinus being a more posterior
structure is less commonly involved in such trauma\textsuperscript{6}.
Since the left and right coronary sinuses have the origin of coronary
arteries, they are pressure release areas; thus, the non-adjacent sinus
bears the major brunt and a tear of the NAL is commonest
pathology\textsuperscript{5}.

Patient presenting late with AR after blunt trauma to
chest\textsuperscript{5,8} have been described in literature, but they
are mostly upto few months. Patients presenting late mostly have a tear
in one of the leaflets which is small and insignificant to start with
and gradually progresses with time. In these patients the collagen in
the spongiosa is gradually replaced by mucopolysaccharides leading to
myxomatous degeneration and progressive weakness of the leaflet, causing
further damage\textsuperscript{16}. Our case is unique because a patient
remaining asymptomatic for 2 years after trauma and incidentally being
diagnosed with severe AR has not been reported.

Management of patients presenting late with severe asymptomatic AR is
always a matter of debate and traditionally onset of ventricular
dysfunction, acute pulmonary edema, and a systemic diastolic blood
pressure of less than 50 mm Hg are indications for immediate
surgery.\textsuperscript{17} Waiting for symptoms or ventricular
dysfunction might lead to some irreversible ventricular damage not
correctable by surgery\textsuperscript{10}; thus early surgery in
asymptomatic patients might be a pragmatic option\textsuperscript{6} as
done in our patient. Another point regarding surgery requires a special
mention. Traditionally valve replacement was the standard approach in
such patients, but multiple repair techniques are now being explored in
patients with limited damage to a single leaflet\textsuperscript{18}.
However, the assessment of the valve leaflets preoperatively by imaging
or intra-operatively by hand and eye assessment are imperfect as there
is a report of microscopic degeneration in an otherwise healthy-looking
leaflet, which could progress with time\textsuperscript{19}.Thus, valve
replacement is the standard approach in these cases.

\textbf{Conclusion}

A detailed history taking is always important to solve a medical puzzle.
The etiology of the case would have been overlooked had it not been for
the history of blunt trauma two years prior to presentation. We should
also keep in mind the fact that traumatic AR can present late and these
patients can rarely remain asymptomatic. In patients with severe AR,
without any evidence of rheumatic heart disease, endocarditis or a
bicuspid valve and with an AR jet though a leaflet should raise the
suspicion of traumatic AR. TEE is mandatory and diagnostic as it readily
confirms the pathology. Surgical management should be the general
approach with valve replacement being the standard treatment of choice.

Conflict of interest: None

\textbf{References:}

1. Howard CP. Aortic Insufficiency Due to Rupture by Strain of a Normal
Aortic Valve. Can Med Assoc J. 1928 Jul;19(1):12-24

2. Pr\selectlanguage{ngerman}être R, Faidutti B. Surgical management of aortic valve injury
after nonpenetrating trauma. Ann Thorac Surg. 1993 Dec;56(6):1426-31.

3. Penderleath D. Case of death from rupture of one of the semilunar
valves of the aorta. London Medical Gazette 1830; 7:109.

4. Najafi H, Dye WS, Javid H, Hunter JA, Julian OC. Rupture of an
otherwise normal aortic valve. Report of two cases and review of the
literature. J Thorac Cardiovasc Surg 1968;56: 57--62.

5. Li W, Ni Y, Chen X, Ma L. Aortic valve tear with severe aortic
regurgitation following blunt chest trauma. Cardiothorac Surg. 2011 Jun
19; 6:84. doi: 10.1186/1749-8090-6-84.

6. Maini R, Dadu RT, Addison D, Cunningham L, Hamzeh I, Wall M Jr,
Lakkis N, Tabbaa R. Isolated perforation of left coronary cusp after
blunt chest trauma. Case Rep Cardiol. 2015; 2015:235629. doi:
10.1155/2015/235629. Epub 2015 Feb 23.

7. Meunier JP, Berkane N, Lopez S, El Ghobary T, Teboul J, Malzac B,
Isetta C, Jourdan J. Traumatic aortic regurgitation: aortic
valvuloplasty controlled by aortoscopy. J Heart Valve Dis. 2001
Nov;10(6):784-8.

8. Turk T, Vural H, Ata Y, Eris C, Yavuz S. Acute aortic insufficiency
after blunt chest trauma: a case report. J Cardiovasc Surg (Torino).
2007 Jun;48(3):359-61.

9. Bernabeu E, Mestres CA, Loma-Osorio P, Josa M. Acute aortic and
mitral valve regurgitation following blunt chest trauma. Interact
Cardiovasc Thorac Surg. 2004 Mar;3(1):198-200.

10. Kin H, Minatoya K, Mukaida M, Okabayashi H. Successful valve repair
in traumatic aortic valve regurgitation. Interactive Cardiovascular and
Thoracic Surgery. 2011;12(5):869--871. doi: 10.1510/icvts.2010.262097.

11. Kan C-D, Yang Y-J. Traumatic aortic and mitral valve injury
following blunt chest injury with a variable clinical course. Heart.
2005;91(5):568--70. doi: 10.1136/hrt.2004.045104.

12. Unal M, Demirsoy E, Gogus A, Arbatli H, Hamzaoglu A, Sonmez B. Acute
Aortic Valve Regurgitation Secondary to Blunt Chest Trauma. Tex Heart
Inst J. 2001; 28(4): 312--4.

13. Sturm JT, McGee MB, Luxenberg MG. An analysis of risk factors for
death at the scene following traumatic aortic rupture. J Trauma 1988;
28:1578--80.

14. Baliga RR, Nienaber CA, Bossone E, Oh JK, Isselbacher EM, Sechtem U,
Fattori R, Raman SV, Eagle KA. The role of imaging in aortic dissection
and related syndromes. JACC Cardiovasc Imaging. 2014 Apr;7(4):406-24

15. Payne DD, Deweese JA, Mahoney EB, Murphy GW. Surgical treatment of
traumatic rupture of the normal aortic valve. Ann Thorac Surg 1974;
17:223--9.

16. Kassem S, Polvani G, Al Jaber E, Gennari M. Acute aortic
insufficiency due to rupture of an aortic valve commissure. J Card Surg.
2014 Jul;29(4):497-8. doi: 10.1111/jocs.12276. Epub 2014 Jan 12.

17. Crosby IK Muller WH Jr. Acquired disease of the aortic valve. In:
Sabiston DC Jr, Spencer FC, editors. Gibbon's Surgery of the chest. 4th
ed. Vol 2. Philadelphia: WB Saunders; 1983. p. 1280--305.

18. Asbach S, Siegenthaler MP, Beyersdorf F, Bode C, Geibel A. Aortic
valve rupture after blunt chest trauma. Clinical Research in Cardiology.
2006;95(12):675--679. doi: 10.1007/s00392-006-0441-4.

19. Egoh Y, Okoshi T, Anbe J, Akasaka T. Surgical treatment of traumatic
rupture of the normal aortic valve. Eur J Cardiothorac Surg. 1997;
11:1180--1182. doi: 10.1016/S1010-7940(96)01116-5.



\textbf{Figure and Video Legends}

Figure 1: TEE showing tri-leaflet aortic valve with a normal aortic root
in mid-esophageal long axis view

Figure 2: TEE showing a tissue gap in the non-adjacent leaflet of the
aortic valve suggestive of perforation in mid-esophageal long axis view

Figure 3: TEE showing severe AR. Two AR jets are clearly visualised; one
through the point of incomplete coaptation and the second through the
perforation in the non-adjacent leaflet.

Figure 4: Pathologic specimen showing the three leaflets with a large
perforation in the non-adjacent leaflet

Video 1: Echocardiogram in modified apical 5 chamber view showing
tri-leaflet aortic valve without any significant dilation of the aortic
root

Video 2: Echocardiogram in parasternal long axis view showing elongated
right coronary leaflet and everted edges of the non-adjacent leaflet,
with severe AR

Video 3: TEE showing tri-leaflet aortic valve in mid-esophageal long
axis view with a tissue gap in the non-adjacent leaflet of the aortic
valve suggestive of perforation without any significant dilation of the
aortic root.

Video 4: TEE with Colour Doppler study confirming severe AR with two AR
jets, one through the point of incomplete coaptation and other one
through the perforation in the non-adjacent leaflet.\selectlanguage{english}
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