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Late presentation of traumatic aortic regurgitation
International Journal of Cardiology 199 (2015) 389–390
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Late presentation of traumatic aortic regurgitation Miguel López-Garrido, Amalio Ruiz-Salas ⁎, Fernando Carrasco-Chinchilla, Isabel Rodriguez-Bailón, Eduardo Morillo, Juan José Gómez-Doblas, Eduardo de Teresa UGC del Corazón, Instituto de Biomedicina de Málaga (IBIMA), Hospital Universitario Virgen de la Victoria, Campus Teatinos s/n, Málaga, Spain
a r t i c l e
i n f o
Article history: Received 31 May 2015 Accepted 20 June 2015 Available online 21 July 2015 Keywords: Blunt chest trauma Aortic insufficiency Aortic valve prolapse
We describe a 66-year-old male who was referred for cardiac surgery because of symptomatic severe aortic regurgitation. The patient had dyspnea on moderate exertion and had presented progressive clinical deterioration over the last few months. He had a background history of uncontrolled hypertension and former smoking and was hospitalized two years earlier for a traffic accident with blunt chest trauma with pulmonary contusion. Examination revealed aortic diastolic and systolic murmur II/VI, apical holosystolic murmur IV/VI, gallop rhythm and bibasilar crackles. The blood test was normal except for NT-proBNP levels (985 pg/ml). Cardiomegaly and evidence of vascular redistribution were revealed in chest X-ray, and electrocardiogram presented signs of left ventricular hypertrophy. Severe mid-left anterior descending coronary disease with good distal caliber vessel was observed in coronariography. Transthoracic echocardiogram revealed normal dimensions of aortic root, tricuspid aortic valve with normal opening and severe regurgitation originated in the noncoronary cusp leaflet. Severe left ventricular dilation was observed, with eccentric hypertrophy and left ventricle ejection fraction of 47%. The mitral valve presented moderate to severe regurgitation originated by posterior leaflet restriction. These findings, confirmed with transesophageal echocardiogram (Fig. 1a and b), suggested that the mechanism of aortic regurgitation could be a traumatic tear in the noncoronary cusp leaflet. In the operating room the commissure disinsertion between right coronary cusp and noncoronary cusp was confirmed, with ⁎ Corresponding author. E-mail address: [email protected] (A. Ruiz-Salas).
http://dx.doi.org/10.1016/j.ijcard.2015.06.077 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
perforated right coronary leaflet and elongated and prolapsing noncoronary leaflet. Aortic valve repair was performed with commissure reimplantation, subcomisural plasty, central plication of the free edge of noncoronary leaflet and right coronary leaflet plasty with autologous pericardial patch. Furthermore, mitral valve annuloplasty and graft of internal mammary artery to left anterior descending were performed. After closing the aortotomy, the function of repaired aortic valve by transesophageal echocardiogram under beating heart conditions on cardiopulmonary bypass was assessed, presenting mild regurgitation (Fig. 2a and b). The postoperative course was uneventful, and one year later after surgery the patient is in good condition. The echocardiogram in the follow-up showed normal left ventricle size and recovery of left ventricle ejection fraction. Identifying the cause and mechanism of aortic regurgitation is one of the objectives of the echocardiographic assessment of this disease, especially if we consider the possibility of valve repair. Traumatic valve injury is a rare complication of blunt chest trauma, usually severe and of acute presentation [1–3]. However, it may have a late onset [4]. This case raises the convenience of considering the traumatic origin among the possible causes of aortic regurgitation. Although it often has an acute presentation with aortic wall injury [5], there are cases of isolated valve affectation with late presentation. Transesophageal echocardiography represents the most important tool for evaluating the nature and extent of such traumatic lesions. The most frequently affected is the noncoronary cusp; the reason is that if the injury occurs while the valve is closed, the overpressure cannot be dampened by coronary flow and tear or disinsert the leaflet [6]. The late and progressive manifestation is explained because the traumatism generates a small tear or disinsertion that progress with time, maybe favored by the presence of hypertension in our case. Moreover, the preoperative identification of this mechanism allows proposing a possible valve repair that prevents the implantation of a prosthesis.
Conflict of interest The authors report no relationships that could be construed as a conflict of interest.
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M. López-Garrido et al. / International Journal of Cardiology 199 (2015) 389–390
Fig. 1. Intraoperative transesophageal echocardiogram. Severe aortic regurgitation originated in the noncoronary cusp leaflet, observed in long axis (1a) and short axis (1b). Mild regurgitation after aortic valve repair (2a and 2b).
References [1] L. Cui, Y. Suo, L. Han, et al., Traumatic tricuspid regurgitation with ruptured chordae tendinae caused by a punch in the chest, Int. J. Cardiol. 182 (2015) 102–104. [2] M. Sochala, L. Aïssou, E. Sorbets, et al., Delayed cardiac tamponade following management of a massive hemothorax related to a penetrating thoracic trauma, Int. J. Cardiol. 172 (2014) 69–70. [3] hemothorax related to a penetrating thoracic trauma. C.D. Kan, Y.J. Yang, Traumatic aortic and mitral valve injury following blunt chest injury with a variable clinical course, Heart 91 (2005) 568–570.
[4] M. Matteucci, G. Rescigno, G. Altamura, M. Manfrin, D.L. Alfonso, G. Piccoli, G. Iacobone, Delayed traumatic aortic cusp detachment mimicking aortic dissection, Ann. Thorac. Surg. 82 (2006) 1093–1095. [5] S. Bartolome, M. Lázaro, J.E. Alcalá, L. Rodríguez-Padial, Traumatic aortic rupture, Rev. Esp. Cardiol. 62 (2009) 826–827. [6] S.M. Park, D.H. Kim, Y.T. Kwak, L.S. Sohn, Triple aortic root injury, Ann. Thorac. Surg. 87 (2009) 621–623.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Late presentation of traumatic aortic regurgitation Miguel López-Garrido, Amalio Ruiz-Salas ⁎, Fernando Carrasco-Chinchilla, Isabel Rodriguez-Bailón, Eduardo Morillo, Juan José Gómez-Doblas, Eduardo de Teresa UGC del Corazón, Instituto de Biomedicina de Málaga (IBIMA), Hospital Universitario Virgen de la Victoria, Campus Teatinos s/n, Málaga, Spain
a r t i c l e
i n f o
Article history: Received 31 May 2015 Accepted 20 June 2015 Available online 21 July 2015 Keywords: Blunt chest trauma Aortic insufficiency Aortic valve prolapse
We describe a 66-year-old male who was referred for cardiac surgery because of symptomatic severe aortic regurgitation. The patient had dyspnea on moderate exertion and had presented progressive clinical deterioration over the last few months. He had a background history of uncontrolled hypertension and former smoking and was hospitalized two years earlier for a traffic accident with blunt chest trauma with pulmonary contusion. Examination revealed aortic diastolic and systolic murmur II/VI, apical holosystolic murmur IV/VI, gallop rhythm and bibasilar crackles. The blood test was normal except for NT-proBNP levels (985 pg/ml). Cardiomegaly and evidence of vascular redistribution were revealed in chest X-ray, and electrocardiogram presented signs of left ventricular hypertrophy. Severe mid-left anterior descending coronary disease with good distal caliber vessel was observed in coronariography. Transthoracic echocardiogram revealed normal dimensions of aortic root, tricuspid aortic valve with normal opening and severe regurgitation originated in the noncoronary cusp leaflet. Severe left ventricular dilation was observed, with eccentric hypertrophy and left ventricle ejection fraction of 47%. The mitral valve presented moderate to severe regurgitation originated by posterior leaflet restriction. These findings, confirmed with transesophageal echocardiogram (Fig. 1a and b), suggested that the mechanism of aortic regurgitation could be a traumatic tear in the noncoronary cusp leaflet. In the operating room the commissure disinsertion between right coronary cusp and noncoronary cusp was confirmed, with ⁎ Corresponding author. E-mail address: [email protected] (A. Ruiz-Salas).
http://dx.doi.org/10.1016/j.ijcard.2015.06.077 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
perforated right coronary leaflet and elongated and prolapsing noncoronary leaflet. Aortic valve repair was performed with commissure reimplantation, subcomisural plasty, central plication of the free edge of noncoronary leaflet and right coronary leaflet plasty with autologous pericardial patch. Furthermore, mitral valve annuloplasty and graft of internal mammary artery to left anterior descending were performed. After closing the aortotomy, the function of repaired aortic valve by transesophageal echocardiogram under beating heart conditions on cardiopulmonary bypass was assessed, presenting mild regurgitation (Fig. 2a and b). The postoperative course was uneventful, and one year later after surgery the patient is in good condition. The echocardiogram in the follow-up showed normal left ventricle size and recovery of left ventricle ejection fraction. Identifying the cause and mechanism of aortic regurgitation is one of the objectives of the echocardiographic assessment of this disease, especially if we consider the possibility of valve repair. Traumatic valve injury is a rare complication of blunt chest trauma, usually severe and of acute presentation [1–3]. However, it may have a late onset [4]. This case raises the convenience of considering the traumatic origin among the possible causes of aortic regurgitation. Although it often has an acute presentation with aortic wall injury [5], there are cases of isolated valve affectation with late presentation. Transesophageal echocardiography represents the most important tool for evaluating the nature and extent of such traumatic lesions. The most frequently affected is the noncoronary cusp; the reason is that if the injury occurs while the valve is closed, the overpressure cannot be dampened by coronary flow and tear or disinsert the leaflet [6]. The late and progressive manifestation is explained because the traumatism generates a small tear or disinsertion that progress with time, maybe favored by the presence of hypertension in our case. Moreover, the preoperative identification of this mechanism allows proposing a possible valve repair that prevents the implantation of a prosthesis.
Conflict of interest The authors report no relationships that could be construed as a conflict of interest.
390
M. López-Garrido et al. / International Journal of Cardiology 199 (2015) 389–390
Fig. 1. Intraoperative transesophageal echocardiogram. Severe aortic regurgitation originated in the noncoronary cusp leaflet, observed in long axis (1a) and short axis (1b). Mild regurgitation after aortic valve repair (2a and 2b).
References [1] L. Cui, Y. Suo, L. Han, et al., Traumatic tricuspid regurgitation with ruptured chordae tendinae caused by a punch in the chest, Int. J. Cardiol. 182 (2015) 102–104. [2] M. Sochala, L. Aïssou, E. Sorbets, et al., Delayed cardiac tamponade following management of a massive hemothorax related to a penetrating thoracic trauma, Int. J. Cardiol. 172 (2014) 69–70. [3] hemothorax related to a penetrating thoracic trauma. C.D. Kan, Y.J. Yang, Traumatic aortic and mitral valve injury following blunt chest injury with a variable clinical course, Heart 91 (2005) 568–570.
[4] M. Matteucci, G. Rescigno, G. Altamura, M. Manfrin, D.L. Alfonso, G. Piccoli, G. Iacobone, Delayed traumatic aortic cusp detachment mimicking aortic dissection, Ann. Thorac. Surg. 82 (2006) 1093–1095. [5] S. Bartolome, M. Lázaro, J.E. Alcalá, L. Rodríguez-Padial, Traumatic aortic rupture, Rev. Esp. Cardiol. 62 (2009) 826–827. [6] S.M. Park, D.H. Kim, Y.T. Kwak, L.S. Sohn, Triple aortic root injury, Ann. Thorac. Surg. 87 (2009) 621–623.