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Ann Thorac Surg 2006;82:1093-1095
© 2006 The Society of Thoracic Surgeons
AOUOORR Centro Cardiologico Lancisi, Ancona, Italy
Accepted for publication January 5, 2006.
* Address correspondence to Dr Matteucci, Cardiac Surgery, AOUOORR Centro Cardiologico Lancisi, Via Conca 71, 60020 Ancona, Italy (Email: sacha-m{at}libero.it).
| Abstract |
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| Introduction |
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A 33-year-old policeman was admitted to the emergency room of a local hospital after a motorcycle crash. Clinical evaluation revealed Glasgow Coma Scale 13 without hemodynamic impairment and severe multiple trauma to the head, thorax, and abdomen. A total body computed tomographic scan was performed, revealing absence of encephalic damage as well as thoracic and abdominal viscera involvement, and evidence of pelvis and left ischiopubis crus luxation with multiple face and right hand fractures.
After orthopedic correction of the hand fractures, while the patient was recovering in the intensive care unit, tachycardia developed and a murmur suggesting AR was first heard 10 days after admission. Patient was submitted to transthoracic echocardiogram with evidence of severe AR and type I De Bakey aortic dissection with an intimal tear in the right sinus of Valsalva.
The patient was transferred to our institution and a transesophageal echocardiogram revealed massive AR caused by complete detachment of the right coronary cusp everting into the aorta and mimicking an intimal tear in the ascending aorta (Fig 1), without any implication in the ascending aorta or the arch.
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| Comment |
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Heart involvement, particularly right ventricle free wall rupture, is a rare occurrence and is more frequent in patients with penetrating trauma than with blunt chest trauma. Although AV is only rarely affected, it is the valve most frequently involved in blunt cardiac injury survivors [3]. Parmley and colleagues [4] found only one case of an isolated injury of the AV in 546 autopsies on patients dying as a result of blunt chest trauma. Posttraumatic AR is related either to valve lesion itself (ie, ruptured cusps) or to trauma of the ascending aorta (ie, subadventitial rupture with prolapse of the underlying AV cusp). Therefore, the most frequent valve lesion is the isolated injury of the noncoronary cusp (ie, a tear or an avulsion of the cusp itself or of a commissure) [3].
The mechanism of AV rupture has been experimentally demonstrated after blunt trauma to the sternum, particularly during early diastole, when significative pressure gradient can be generalized across a competent AV [3].
The clinical picture of posttraumatic AR is generally rapidly progressive, and the ineffectiveness of medical treatment has underlined the importance of early surgery. In the literature, a delay is frequent between trauma and the onset of AR symptoms. We might speculate that this delay may be caused by an initial small tear of the cusp at its attachment to the valve ring that progressively extends as a result of hemodynamic stress. As the valve cusp becomes separated from its annular attachment, AR progresses with a compensatory increase in the force of ejection and consequent increased hemodynamic stress to the valve cusp [3].
The diagnosis of posttraumatic AR is based on the history of blunt chest trauma and sudden onset of signs and symptoms of AR and transesophageal echo findings.
In the pre-echocardiograpic era, traumatic disruption of a previously normal valve, while suggested by history of chest trauma and clinical findings of AR, has been confirmed only at autopsy or operation. Transthoracic echocardiography is limited by poor resolution, especially in patients with rib fractures and those requiring chest drain tubes (ie, the group that may be at highest risk for traumatic cardiac involvement). Transesophageal echocardiography can overcome these limitations because it is inexpensive, rapid, and relatively safe, and because it has become the noninvasive technique of choice to diagnose and assess wall motion and valve function [5], allowing differential diagnosis between traumatic AR, acute bacterial endocarditis, and aortic dissection.
In our case, the history of chest trauma and absence of typical endocarditic findings helped us to preoperatively exclude acute bacterial endocarditis.
Only transesophageal echocardiography performed several days after the crash achieved the correct diagnosis, excluding the misleading picture of aortic dissection.
Despite the number of posttraumatic AR treated with conservative surgery, it is increasing in recent literature [6]. German and colleagues [7] reported a post-repair high recurrence rate [7]. We suggest that indications to valve replacement or repair depend on the extent of leaflet injury, and on the number of cusps or commissures involved. Despite that there was only one cusp involved in our case, we decided to replace the valve, because we were concerned by the chance that normal leaflets not involved in the laceration would be affected by posttraumatic tears visible only on microscopic examination, as reported by Egoh and colleagues [3], with a high risk of post repair AR.
The singularity of this case was based on the fact that (1) there was a delay between the trauma and the evidence of AR, and (2) there was a right coronary cusp detachment mimicking a transthoracic echocardiographic image of intimal tear on the ascending aorta, thus resulting in a misleading diagnosis of aortic dissection.
We conclude that in patients surviving blunt chest trauma, even when asymptomatic, a high index of suspicion is needed to avoid potentially lethal consequences and repeated physical examination aided by transesophageal echocardiography should be performed. Because traumatic perforation of the AV is often complicated with various abnormalities of the vessel, careful preoperative and intraoperative judgement are essential [3]. Furthermore, as long-term results of valve repair in posttraumatic AR are not yet available, we consider valve replacement the gold standard.
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