Canadian Journal of Cardiology 27 (2011) 263.e21–263.e23 www.onlinecjc.ca
Case Report
Ventricular Septal Defect as a Result of Direct Trauma From Mechanical Mitral Valve Prosthesis Marian Kotrec, MD,a Davinder S. Jassal, MD, BSc, FRCPC, FACC,a,b,c Shelley Zieroth, MD, FRCPC,a,c Darren H. Freed, MD, PhD, FRCSC,c,d and James W. Tam, MD, FRCPC, FACCa a
Section of Cardiology, Department of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada b c
d
Department of Radiology, University of Manitoba, Winnipeg, Manitoba, Canada
Institute of Cardiovascular Sciences, St. Boniface Research Centre, Winnipeg, Manitoba, Canada
Section of Cardiac Surgery, Department of Surgery, University of Manitoba, Winnipeg, Manitoba, Canada
ABSTRACT
RÉSUMÉ
We present a case of a patient with preexisting mechanical mitral valve who developed a traumatic ventricular septal defect following a motor vehicle accident. Serial transthoracic echocardiography revealed the progressive nature of the defect. Surgical repair was delayed due to significant noncardiac comorbidities. The ventricular septal defect was found in an unusual location in the membranous portion of the interventricular septum. We discuss the possible etiologic mechanisms of injury as well as the importance of timely surgical repair.
Nous présentons le cas d’un patient portant une valvule mitrale mécanique qui a développé une communication interventriculaire traumatique à la suite d’un accident d’automobile. Une série d’échocardiographies transthoraciques a révélé la nature progressive de la communication. La réparation chirurgicale a été retardée en raison de comorbidités non cardiaques significatives. La communication interventriculaire a été trouvée dans un endroit inhabituell de la portion membraneuse du septum interventriculaire. Nous avons discuté tant des mécanismes étiologiques probables de la blessure que de l’importance de la réparation chirurgicale rapide.
Acquired ventricular septal defect (VSD) or rupture (VSR) is a recognized but uncommon complication following blunt chest trauma. We describe a case of isolated membranous VSD in a patient with prior mechanical St. Jude mitral valve prosthesis and systolic dysfunction.
was persistent preoperative New York Heart Association class II/III symptoms with a left ventricular ejection fraction (LVEF) of 25%-30% that did not improve post MVR. Nine months after the MVR, the patient sustained a head-on motor vehicle accident (MVA). She was hypotensive, tachycardic, and tachypneic. Physical examination demonstrated an open right femoral fracture, right undisplaced patellar fracture, multiple rib fractures with sternal in drawing, crepitus under the left breast, and paradoxical breath movements. Cardiovascular examination revealed no new cardiac murmurs. Laboratory examination showed an elevated troponin T at 1 g/L. On ECG, a third-degree heart block with a stable widecomplex escape rhythm was seen. Shortly after arrival, the patient developed hemorrhagic shock requiring aggressive volume resuscitation, intubation, and inotropic support. Intraoperative transesophageal echocardiography (TEE) at the time of noncardiac surgery revealed an LVEF of 35%-40%, moderate tricuspid regurgitation, and normal functioning mechanical mitral valve. Three days postoperatively, her respiratory status deteriorated significantly. Transthoracic echocardiography (TTE) demonstrated a new paravalvular leak along the
Case Presentation A 48-year-old woman with a history of rheumatic heart disease underwent a mechanical mitral valve replacement (MVR) with a 29-mm St. Jude valve for severe symptomatic rheumatic MVR in 2007. Postoperatively, there was echocardiographic improvement in pulmonary pressures from 84 mm Hg preoperatively to 35 mm Hg 5 months after MVR. There Received for publication February 21, 2010. Accepted June 16, 2010. Corresponding author: Dr James W. Tam, University of Manitoba, WRHA Cardiac Sciences Program, Y3015, St Boniface General Hospital, 409 Tache Ave, Winnipeg, Manitoba, R2H 2A6, Canada. Tel.: ⫹1-204-2581290; fax.: ⫹1-204-233-9162. E-mail address:
[email protected] See page 263.e23 for disclosure information.
0828-282X/$ – see front matter © 2011 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved. doi:10.1016/j.cjca.2010.12.022
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Canadian Journal of Cardiology Volume 27 2011
Figure 1. (A) Parasternal long-axis view of transthoracic echocardiography demonstrates a ventricular septal defect (arrow) in the membranous portion of the interventricular septum. (B) Color Doppler imaging shows turbulent left-to-right flow through the defect. LA, left atrium; LV, left ventricle; RV, right ventricle; Ao, aorta.
lateral annulus of the MVR. Follow-up TTE 1 week later revealed a new perimembranous VSD with left-to-right shunting on color Doppler (Fig. 1). On re-view of earlier TTE, minor disruption on the left aspect of the membranous septum was identified, without overt VSD. Right heart catheterization demonstrated the following intracardiac pressures: right atrium 21 mm Hg, right ventricle 103/7 mm Hg, left ventricle 171/23 mm Hg, pulmonary artery 99/22 mm Hg, and left ventricular end-diastolic pressure 23 mm Hg. The left-to-right shunt (Qp/Qs) was calculated at 1.8:1. After multiple delays related to ongoing noncardiac issues, the patient underwent surgical VSD repair 11 months after the MVA. The VSD, measuring 2 cm, was found just below the aortic valve, in the membranous portion of the interventricular septum, and was repaired with a bovine pericardium patch. The interatrial septum was opened whereby the paravalvular leak of the mitral valve was identified on the lateral margin and sutured closed using the transatrial septal approach. Tricuspid valve regurgitation was repaired with annuloplasty. TEE before the end of surgery revealed no residual VSD, no mitral paravalvular insufficiency, and only mild to moderate tricuspid regurgitation. Discussion VSD is a rare complication following blunt chest trauma. Various mechanisms have been described: rapid deceleration
injury of the chest resulting in a thrust of the heart against the sternum1; acute compression of the heart between the sternum and the spine2,3; and acute contusion resulting in myocardial devascularization with subsequent necrosis and late perforation.4,5 Ventricular septal rupture occurs most typically in late diastole or early systole when both the atrioventricular and semilunar valves are closed and the intraventricular pressures are high.4,6 Sudden elevation of pressure caused by the impact gives way to the rupture of the ventricular septum. Traumatic VSD in our patient occurred in the setting of prior mechanical MVR. This has not previously been reported. There are reports of traumatic VSDs with prosthetic aortic but not mitral prosthetic valves.7 Delayed closure of VSD can lead to deterioration of congestive heart failure. At the time when our patient was diagnosed with VSD, the Qp/Qs ratio was 1.8, and it reached 3.1 by the time of surgery. Current recommendations suggest repair if the ratio exceeds 1.5. Surgery did not lead to significant clinical improvement in our patient. This may be due to significant delay and/or preexisting systolic congestive heart failure. It is unclear whether earlier VSD repair may have led to more significant improvement. Pierli et al.4 reported a case of a 64-year-old man who with blunt chest trauma resulting in a new holosystolic heart murmur. He was diagnosed with traumatic VSD 40 years later with Qp/Qs
Kotrec et al. Ventricular Septal Defect in Patient With MVR
ratio 1.7. He was treated conservatively until an additional 9 years later, when Qp/Qs was 1.8. He then underwent VSD repair, which failed to prevent the development of right ventricular failure. This is similar to our patient’s situation, where delayed VSD repair did not prevent further deterioration of right heart failure. In the literature, the most common localization of traumatic ventricular defect is in the muscular septum.8,9 We are not aware of a report of traumatic VSD in the membranous part of the septum. Isolated membranous VSD is the least common septal defect.10 We hypothesize that this could have been caused by direct trauma to the membranous septum from the adjacent mechanical mitral valve prosthesis. VSD may develop over a period of few hours to days.2,8 In our case, the VSD became apparent at the time of the third echocardiogram 12 days after MVA and was not seen on the day 1 TEE or day 4 TTE. According to some authors, the initial small traumatic tear leads to secondary defect that is larger, which becomes apparent with delay.2 Another theory suggests that acute contusion results in myocardial devascularization with subsequent necrosis and late perforation.4 In clinical practice, this warrants high vigilance even when initial cardiac assessments are negative for VSD. The threshold for repeating TTE should be low when a new hemodynamic instability occurs or when there is a new pansystolic murmur. Conclusion We present the case of a patient with a VSD following blunt chest trauma that is unique for the combination of unusual location in the membranous septum, delayed development, and preexistent mechanical mitral valve prosthesis with systolic congestive heart failure. To our knowledge, similar co-occurrence of these features has never been reported. Funding Sources No external funding was used in preparation of this manuscript.
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Disclosures The authors have no conflicts of interest to disclose.
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