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Ann Thorac Surg 2009;88:1664-1666. doi:10.1016/j.athoracsur.2009.03.064
© 2009 The Society of Thoracic Surgeons

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Case Reports

Post-Traumatic Rupture of the Anterolateral Papillary Muscle

Giovanni Domenico Cresce, MDa,*, Alessandro Favaro, MDa, Augusto D'Onofrio, MDa, Caterina Piccin, MDa, Paolo Magagna, MDa, Massimo Spanghero, MDb, Alessandro Fabbri, MDa

a Division of Cardiac Surgery, San Bortolo Hospital, Vicenza, Italy
b Division of Cardiology, San Bortolo Hospital, Vicenza, Italy

Accepted for publication March 18, 2009.

* Address correspondence to Dr Cresce, Division of Cardiac Surgery, San Bortolo Hospital, Viale Rodolfi 37, Vicenza, 36100, Italy (Email: gd.cresce{at}yahoo.it).


    Abstract
 Top
 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 
Rupture of cardiac valves as a consequence of nonpenetrating cardiac trauma is an uncommon phenomenon. We report the case of a 24-year-old patient with a "two-stage" traumatic rupture of the anterolateral papillary muscle of the mitral valve, after a blunt chest trauma, who successfully underwent emergency mitral valve replacement.


    Introduction
 Top
 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 
Nonpenetrating thoracic trauma often results in injury to the heart, which may vary in severity from asymptomatic cardiac contusion to an immediately fatal cardiac rupture. The mechanisms of injury could be the sudden elevation of the intraventricular pressure due to the compression of the heart between the sternum and the vertebral column, or due to the sudden deceleration of the chest with the heart being pushed forward against the sternum. The rupture of the anterolateral papillary muscle caused by blunt thoracic trauma is relatively rare. This report refers to a young patient who had delayed, severe mitral valve regurgitation develop 24 hours after a motorcycle accident.

A 24-year-old man was admitted to the emergency room of our hospital after a motorcycle accident. He arrived conscious and complaining of shortness of breath and chest pain. The electrocardiogram showed a heart rate of 120 beats per minute and a right bundle branch block. His blood pressure was 100/65 mm Hg. All peripheral pulses were present. A fracture of both forearms was found. A computed tomographic scan showed a fracture of the sternum with important retrosternal hematoma and compression of the right sides of the heart. Transesophageal echocardiography confirmed the diagnosis of acute cardiac tamponade and showed a thinning of the free wall of the right ventricle. The troponine I value was 70 ng/mL. The patient was moved to the operating room for emergency surgery. During the operation the patient was noted to have a transverse sternal fracture (causing bleeding in the anterior mediastinum) and a subsequent cardiac tamponade due to an extrinsic compression. A big hematoma of the thymus gland and of the anterior mediastinum was found. After opening the pericardium, a cardiac contusion of the lateral wall was noted without any sign of free-wall rupture. An intraoperative transesophageal echocardiography showed the competence of both the mitral and aortic valves and good left ventricular function. A careful reconstruction of the sternum was performed. The patient was then transferred to the intensive care unit in hemodynamic stable condition. After 24 hours, his condition suddenly and rapidly deteriorated. The arterial gas analyzer showed significant oxyhemoglobin desaturation. His systolic blood pressure decreased to 70 mm Hg, despite inotropic drugs administration. Two episodes of ventricular fibrillation occurred. A transesophageal echocardiography demonstrated a complete avulsion of the anterolateral papillary muscle, causing massive mitral regurgitation (Fig 1). An intra-aortic balloon pump was then placed, and the patient was immediately moved to the operating room. The chest was reopened through the previous midline sternotomy. Standard cardiopulmonary bypass with bi-caval cannulation was instituted. The aorta was cross clamped and crystalloid cardioplegia was given for myocardial protection. Mitral valve exposure was achieved through a bi-atrial transeptal approach. The examination of the mitral valve showed a complete detachment of the anterolateral papillary muscle with rupture of accessory chordae tendinae. The anterior mitral leaflet was resected (Fig 2). A 31-mm Bicarbon (Sorin Biomiedica, Saluggia, Italy) mechanical valve was implanted. Before weaning from cardiopulmonary bypass, an intraoperative coronary angiography was performed to exclude a coronary rupture and disease, or both. At the end of the operation, the patient was transferred to the intensive care unit with a high dosage of inotropic drugs and intra-aortic balloon pump support. His postoperative course was uneventful. He was extubated on postoperative day 4. He was moved out of the intensive care unit on postoperative day 5, and he was discharged from the hospital on postoperative day 10 in satisfactory clinical condition.


Figure 1
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Fig 1. A transesophageal echocardiography revealed complete detachment of the anterolateral papillary muscle (arrow). (LA = left atrium; LV = left ventricle.)

 

Figure 2
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Fig 2. Anterior leaflet of the mitral valve with attached anterolateral papillary muscle.

 

    Comment
 Top
 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 
Cardiac injury after a blunt chest trauma is a relatively common event, but it is rarely seen in the operating room because of its high mortality. Cardiac contusion represents the most common form of nonpenetrating cardiac trauma and usually results in a benign clinical course. More severe degrees of cardiac injury are rupture of the free wall, ventricular septum, aortic cusp, and atrioventricular valves. Mitral valve rupture is very rare. In a series by Parmley and colleagues [1], only 24 instances of papillary muscle rupture were found in 546 autopsy cases of nonpenetrating trauma of the chest.

The timing of the rupture may be variable. Usually, mitral insufficiency after a chest trauma occurs immediately after the accident, and it is due to a damage of the subvalvular apparatus in early systole during isovolumetric contraction, when the force delivered by an impact grossly elevates the left ventricular pressure [2]. Therefore, traumatic papillary muscle rupture can result in severe acute mitral regurgitation. In our case, mitral regurgitation was not immediate, but it was delayed 24 hours after the trauma, and it can be attributed to the late rupture of the necrotic papillary muscle, contused and weakened by the initial trauma. Only a few reports describe delayed rupture hours after the accident [3, 4]. In these cases, the mechanism of rupture was the same. The bruised area transforms into necrosis at the insertion of the papillary muscle. The subsequent proteolytic process reaches its maximum during the 24 hours that account for the delayed presentation.

Many surgical approaches have been proposed for the treatment of post-traumatic mitral valve rupture; these vary from mitral valve repair [5] to replacement [6]. The ruptured papillary muscle may also be reimplanted into the left ventricular wall [7]. Although reconstruction of the subvalvular apparatus might be preferable, we believe that the choice to replace or to repair the native valve must be evaluated for each single patient, which must be based on the extent and location of the damage, accurate analysis of the mitral apparatus and the ventricular wall, and finally on the surgeon's technical expertise. In the current case, the extent of the damage was very large (Fig 2). Furthermore, the papillary muscle was noted to be necrotic and the ventricular wall was seriously contused. Therefore, we were discouraged from performing a conservative procedure, because we believe that there was a high possibility of failure.

In conclusion, a careful patient assessment is needed when diagnosing nonpenetrating traumatic cardiac injuries. The importance of transesophageal echocardiography in the rapid diagnosis of traumatic cardiac injuries is unquestionable. We suggest performing intraoperative coronary angiography to exclude a possible concomitant post-traumatic coronary artery lesion. Finally, this case shows how a chest trauma could generate a blowout mitral injury, even 24 to 48 hours after the event. Consequently, a careful observation of the patient is mandatory to timely intervene if a rapid clinical deterioration occurs.


    Acknowledgments
 Top
 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 
The authors are grateful to Paul Marcucci for his assistance in manuscript revision.


    References
 Top
 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 

  1. Parmley LF, Manion WC, Mattingly TVV. Nonpenetrating traumatic injury of the heart Circulation 1958;18:371-396.[Abstract/Free Full Text]
  2. Cuadros CL, Hutchinson 3d JE, Mogtader AH. Laceration of a mitral papillary muscle and the aortic root as a result of blunt trauma to the chest. Case report and review of the literature. J Thorac Cardiovasc Surg 1984;88:134-140.[Abstract]
  3. Larrea JL, Silvestre J, Oliver J, et al. Delayed papillary muscle rupture following mild chest trauma J Heart Valve Dis 1995;4:291-292.[Medline]
  4. Misfeld M, Ehlermann P, Sievers HH. Transaortic repair of blunt traumatic cardiac wall and papillary muscle rupture J Thorac Cardiovac Surg 2001;122:834-835.[Free Full Text]
  5. Halstead J, Hosseinpour A, Wells FC. Conservative surgical treatment of valvular injury after blunt chest trauma Ann Thorac Surg 2000;69:766-768.[Abstract/Free Full Text]
  6. Bruschi G, Agati S, Iorio F, Vitali E. Papillary muscle rupture and pericardial injury after blunt chest trauma Eur J Cardio Thorac Surg 2001;20:200-202.[Abstract/Free Full Text]
  7. McDonald ML, Orszulak TA, Bannon M, Zietlow SP. Mitral valve injury after blunt chest trauma Ann Thorac Surg 1996;61:1024-1029.[Abstract/Free Full Text]



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Alessandro Fabbri
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