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Cardiac contusion: Ending myocardial confusion in this capricious syndrome
International Journal of Cardiology 128 (2008) e107 – e110 www.elsevier.com/locate/ijcard
Letter to the Editor
Cardiac contusion: Ending myocardial confusion in this capricious syndrome Irene Riezzo a , Cristoforo Pomara a , Margherita Neri a , Giuseppina Rossi b , Vittorio Fineschi a,⁎ a
Department of Forensic Pathology, University of Foggia, Ospedali Riuniti, Via L. Pinto 1, 71100 Foggia, Italy b Department of Forensic Pathology, University of Siena, Italy Received 18 March 2007; accepted 26 May 2007 Available online 14 August 2007
Abstract Symptoms of cardiac contusion are very greatly and sometimes are non recognized or are masked by associated injury in severe chest trauma. Cardiac contusion clinically presents as a spectrum of signs and symptoms of varying severity, ranging from precordial pain, dyspnoea, and non specific ECG changes to increased serum activity of several enzymes, early severe rhythm abnormalities, severe conduction defects and death. We present a fatal case in which the definitive diagnosis of myocardial contusion has proved complex. All clinical data were suggestive of acute myocardial infarction, but the history of chest wall injury and gross and histological examination of the heart and coronary vessels led us to conclude for a cardiac contusion without myocardial infarction. In case of chest blunt trauma, the ECG should be interpreted within the context of the clinical situation, on history of chest wall injury, since a fatal myocardial contusion may occur after apparently mild injury. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Cardiac contusion; Blunt chest trauma; Acute myocardial infarct; Diagnosis; Troponins
1. Introduction Although the Cardiac Contusion (CC) is a well defined pathological entity, however the clinical diagnosis of this “capricious syndrome” is not easy. Symptoms of CC are very greatly and sometimes are non recognized or are masked by associated injury in severe chest trauma. Cardiac contusion clinically presents as a spectrum of signs and symptoms of varying severity, ranging from precordial pain, dyspnoea, and non specific ECG changes to increased serum activity of several enzymes, early severe rhythm abnormalities, severe conduction defects and death [1,2]. Therefore, frequently, the clinical signs of cardiac contusion are similar to those of an myocardial infarction.
⁎ Corresponding author. Tel.: +39 0881733834; fax: +39 0881732180. E-mail address: [email protected] (V. Fineschi). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.05.085
We report the case of a young man, with blunt chest trauma after a motorcycle crash, who died 8 h since his hospitalization after four episode of VF. The moderate trauma, the clinical symptoms and the ECG alterations led physicians to diagnose an AMI (acute myocardial infarct) as cause of death. The autopsy, instead, revealed the typical findings of a cardiac contusion. 2. Case report A 41 year old man after a motorcycle crash, was transported by emergency medical service to the Emergency Department. On admission (2:00 AM) the patient was awake and alert with GSC (Glasgow Coma Scale) 15/15, complaining of general and diffuse pain. The haemodynamic parameters were normal. On physical examination he presented only a frontal laceration, a second-degree burn at right leg and generalized pain. Blood samples for laboratory tests were taken.
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ECG was performed at admission, then every half an hour in the next 6 h. The first ECG (2:16 AM) showed no sustained ventricular tachycardia, right bundle branch block, atrial fibrillation and wide QRS with repolaritazion abnormality (Fig. 1A). 45 min after admission, suddenly the patient developed an episode of ventricular fibrillation. Resuscitative manoeuvres were successfully carry out. At 2:47 AM the second ECG showed a marked ST segment elevation in all peripheral leads and a complete right bundle branch block. (Fig. 1B). The third ECG (3:01 AM), performed after atropine administration, revealed sporadic P wave, close QRS with ST-segment elevation in the peripheral leads and a right axis deviation. Therefore the patient was transferred to intensive unit care, where a temporary Pace Maker was implanted. Computed tomography scan showed only a trifling frontal brain contusion, a moderate PNX and pneumomediastinum, and sternal fracture. No other trauma injuries were documented. In the next hours the patient developed three episodes of ventricular fibrillation, successfully treated, without regain consciousness. The last ECG showed a normal sinus rhythm with Q wave in D2-D3 aVF, suggesting
a myocardial infarction (Fig. 1C). Troponin I value was 0.3 ng/ml; troponin T was 0.6 ng/ml. On 8 h after admission the patient developed a sudden cardiac arrest and despite resuscitative manoeuvres he died. A diagnosis of acute inferior myocardial infarction with third AV conduction block was advanced. 2.1. Autopsy findings The autopsy was performed 24 h after death. The body was 168 cm in height and 70 kg in weight. The external examination of the body revealed only few contusions and abrasions, which one in sternal region. No others signs of injury. The internal examination revealed the sternal fracture and pericardium haemorrhages. All internal organs were macroscopically normal. The heart had a normal shape and was normal in size (12 cm × 12 cm × 6 cm) and weight (490 g). The left coronary artery arose normally. The right descending coronary artery showed for 1 cm from the right anterior sinus, an periadventitial concentric haemorrhagic cloak. No significant stenosis or thrombotic occlusion of the coronary
Fig. 1. (A) ECG demonstrating no sustained ventricular tachycardia, right bundle branch block, atrial fibrillation and wide QRS with repolaritazion abnormality. (B) ECG showed a marked ST segment elevation in all peripheral leads and a complete right bundle branch block. (C) ECG demonstrating a normal sinus rhythm with Q wave in D2–D3 aVF, suggesting a myocardial infarction.
I. Riezzo et al. / International Journal of Cardiology 128 (2008) e107–e110
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Fig. 2. (A) The myocardium showed mild myofiber eosinophilia and elongation of sarcomeres and nuclei, with interstitial haemorrhages (H&E, ×40). (B) Right coronary artery: histological cross section showed periadventitial and adventitial haemorrhages (Masson's trichrome, ×60). (C) The immunohistochemical examination of the myocardial samples (right sample, anterior and lateral left samples) revealed a higher degree of depletion (light colour) of Troponin I (Ab antiTnI) and (D) Troponin C in contrast with the normal fibres (brown colour) (Ab anti-TnC).
segment were detected. The atrio-ventricular and semilunar valves were normal. The myocardium showed a dark area (intramural haemorrhages) (7.5 cm × 0.7 cm) that extended from apex to posterior–inferior left ventricular wall and also to posterior right ventricular wall. The histological examination of the heart, performed with routine haematoxylin-eosin and Azan, Mallory and Van Gieson stains, revealed in the superficial myocardial layers, numerous foci of contraction band necrosis. Segmentation of the myocardial cells and widening of intercalated discs and bundles of contracted myocardium alternating with bundles of distended myocardium with granular disruption of the myocytes in all myocardial sections were noted. The examination of right samples, showed subepicardial adipose haemorrhages and interstitial haemorrhages with foci of necrosis with contraction bands localized, limited in their extension and sharp delimitated from the surrounding undamaged myocardium. In other field the myocardium showed mild myofiber eosinophilia and elongation of sarcomeres and nuclei, with interstitial haemorrhages (Fig. 2A). No infarct necrosis was detected. In the samples taken from the right coronary artery (1 cm from the right anterior sinus), histological cross section showed periadventitial and adventitial haemorrhages (Fig. 2B). The immunohistochemical examination of the samples (right sample,
anterior and lateral left samples) revealed a higher degree of depletion of Troponin I and Troponin C and low degree of depletion of myoglobin (Fig. 2C, D). The remainder of the histological examination was unremarkable. The diagnosis of cardiac contusion was established as cause of death. 3. Discussion Cardiac contusion can be defined as cellular damage that result from non penetrating chest or abdominal trauma. It's frequently associated with blunt chest trauma, and the traffic accidents are the most frequent cause of cardiac contusion in these patients. However, the exact incidence of myocardial contusion in patients with blunt chest injury is not well known. It varies among 0% an 76% [3] and depending on the criteria used for establishing the diagnosis. Postmortem incidence in cases of immediate fatalities from blunt injury is 14% [4]. Blunt chest trauma may result in various cardiac injuries including pericardial injury, cardiac injury (cardiac concussion and contusion, cardiac rupture), valvular injury, great vessel injury, cardiac conduction system injury cardiac rhythm disturbances, coronary artery injury, and acute
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myocardial infarction (with or without coronary artery dissection) [1,5,6]. Cardiac injuries result from main mechanisms: a direct blow to the chest, in which the heart is compressed between the sternum and the thoracic vertebrae, sudden deceleration, striking compression of the abdomen, and secondarily from sternal or rib fractures. The right ventricular wall is the area most vulnerable [7]. CC may be diagnosed by serial electrocardiogram, serum determination of biochemical cardiac markers, echocardiogram, radionuclide imaging and coronary angiography. These patients have an increased serum activity of several enzymes such as CK-MB, Troponin I, troponin T, LDH [8]. Elevated cTnI is a marker of myonecrosis and does not necessarily imply myocardial infarction. It may arise as a result of direct myocardial damage or as a result of mismatch between myocardial oxygen supply and consumption [9]. ECG findings included non specific ST-segment-T-wave changes, ST segment elevation and depression, T-wave abnormalities, right bundle branch block and atrioventricular blocks, tachycardia including nodal tachycardia, atrial fibrillation and flutter, ventricular tachycardia and ventricular fibrillation, [10] whereas Q-waves are rarely observed [11]. However there is no a gold standard and a consensus on the best indicator of cardiac damage, and which of these examinations may accurately predict the outcome in terms of myocardial cell loss [11,12]. The described clinical and instrumental signs are similar to those of an infarction, and although relative uncommon, myocardial infarction can result from blunt chest trauma (5%) [3]. In our case the definitive diagnosis of myocardial contusion has proved complex. All clinical data were suggestive of acute myocardial infarction, but the history of chest wall injury and gross and histological examination of the heart and coronary vessels led us to conclude for a cardiac contusion: pericardial haemorrhages, peri-adventitial and adventitial right coronary haemorrhage, absent of trombotic stenosis, intramyocardial haemorrhages and sharp transition from normal to damaged myocardial tissue,
associated with an high degree of troponins' depletion [1,13]. In case of chest blunt trauma, the ECG should be interpreted within the context of the clinical situation, on history of chest wall injury, since a fatal myocardial contusion may occur after apparently mild injury. References [1] Fineschi V, Baroldi G, Silver MD. Pathology of the heart and sudden death in forensic medicine. Boca Raton, FL: CRC Press; 2006. p. 309–10. [2] Sybrandy KC, Cramer MJ, Burgersdijk C. Diagnosing cardiac contusion: old wisdom and new insights. Heart 2003;89:485–9. [3] Maenza RL, Seaberg D, D'Amico F. A meta-analysis of blunt cardiac trauma: ending myocardial confusion. Am J Emerg Med 1996;14:237–41. [4] Kaye P, O'Sullivan I. Myocardial contusion: emergency investigation and diagnosis. Emerg Med J 2002;19:8–10. [5] Sato Y, Matsumoto N, Komatsu S, et al. Coronary artery dissection after blunt chest trauma: Depiction at multidetector-row computed tomography. Int J Cardiol 2007;118:108–10. [6] Vougiouklakis T, Peschos D, Doulis A, Batistatou A, Mitselou A, Agnantis NJ. Sudden death from contusion of the right atrium after blunt chest trauma: case report and review of the literature. Injury 2005;36:213–7. [7] Darok M, Beham-Schmid C, Gatternig R, Roll P. Sudden death from myocardial contusion following an isolated blunt force trauma to the chest. Int J Leg Med 2001;115:85–9. [8] Baum VC. The patient with cardiac trauma. J Cardiothorac Vasc Anesth 2000;14:71–81. [9] Mahajan N, Mehta Y, Rose M, Shani J, Lichstein E. Elevated troponin level is not synonymous with myocardial infarction. Int J Cardiol 2006;111:442–9. [10] Plautz CU, Perron AD, Brady WJ. Electrocardiographic ST-segment elevation in the trauma patient: acute myocardial infarction vs myocardial contusion. Am J Emerg Med 2005;23:510–6. [11] Holanda MS, Dominguez MJ, Lopez-Espadas F, Lopez M, DiazReganon J, Rodriguez-Borregan JC. Cardiac contusion following blunt chest trauma. Eur J Emerg Med 2006;13:373–6. [12] Bernardis V, Kette F, Blarasin L, Pegoraro C, Coassin R. Isolated myocardial contusion in blunt chest trauma. Eur J Emerg Med 2004;11:287–90. [13] Peter J, Kirchner A, Kuhlisch E, Menschikowski M, Neef B, Dressler J. The relevance of the detection of troponins to the forensic diagnosis of cardiac contusion. Forensic Sci Int 2006;160:127–33.
Letter to the Editor
Cardiac contusion: Ending myocardial confusion in this capricious syndrome Irene Riezzo a , Cristoforo Pomara a , Margherita Neri a , Giuseppina Rossi b , Vittorio Fineschi a,⁎ a
Department of Forensic Pathology, University of Foggia, Ospedali Riuniti, Via L. Pinto 1, 71100 Foggia, Italy b Department of Forensic Pathology, University of Siena, Italy Received 18 March 2007; accepted 26 May 2007 Available online 14 August 2007
Abstract Symptoms of cardiac contusion are very greatly and sometimes are non recognized or are masked by associated injury in severe chest trauma. Cardiac contusion clinically presents as a spectrum of signs and symptoms of varying severity, ranging from precordial pain, dyspnoea, and non specific ECG changes to increased serum activity of several enzymes, early severe rhythm abnormalities, severe conduction defects and death. We present a fatal case in which the definitive diagnosis of myocardial contusion has proved complex. All clinical data were suggestive of acute myocardial infarction, but the history of chest wall injury and gross and histological examination of the heart and coronary vessels led us to conclude for a cardiac contusion without myocardial infarction. In case of chest blunt trauma, the ECG should be interpreted within the context of the clinical situation, on history of chest wall injury, since a fatal myocardial contusion may occur after apparently mild injury. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Cardiac contusion; Blunt chest trauma; Acute myocardial infarct; Diagnosis; Troponins
1. Introduction Although the Cardiac Contusion (CC) is a well defined pathological entity, however the clinical diagnosis of this “capricious syndrome” is not easy. Symptoms of CC are very greatly and sometimes are non recognized or are masked by associated injury in severe chest trauma. Cardiac contusion clinically presents as a spectrum of signs and symptoms of varying severity, ranging from precordial pain, dyspnoea, and non specific ECG changes to increased serum activity of several enzymes, early severe rhythm abnormalities, severe conduction defects and death [1,2]. Therefore, frequently, the clinical signs of cardiac contusion are similar to those of an myocardial infarction.
⁎ Corresponding author. Tel.: +39 0881733834; fax: +39 0881732180. E-mail address: [email protected] (V. Fineschi). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.05.085
We report the case of a young man, with blunt chest trauma after a motorcycle crash, who died 8 h since his hospitalization after four episode of VF. The moderate trauma, the clinical symptoms and the ECG alterations led physicians to diagnose an AMI (acute myocardial infarct) as cause of death. The autopsy, instead, revealed the typical findings of a cardiac contusion. 2. Case report A 41 year old man after a motorcycle crash, was transported by emergency medical service to the Emergency Department. On admission (2:00 AM) the patient was awake and alert with GSC (Glasgow Coma Scale) 15/15, complaining of general and diffuse pain. The haemodynamic parameters were normal. On physical examination he presented only a frontal laceration, a second-degree burn at right leg and generalized pain. Blood samples for laboratory tests were taken.
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ECG was performed at admission, then every half an hour in the next 6 h. The first ECG (2:16 AM) showed no sustained ventricular tachycardia, right bundle branch block, atrial fibrillation and wide QRS with repolaritazion abnormality (Fig. 1A). 45 min after admission, suddenly the patient developed an episode of ventricular fibrillation. Resuscitative manoeuvres were successfully carry out. At 2:47 AM the second ECG showed a marked ST segment elevation in all peripheral leads and a complete right bundle branch block. (Fig. 1B). The third ECG (3:01 AM), performed after atropine administration, revealed sporadic P wave, close QRS with ST-segment elevation in the peripheral leads and a right axis deviation. Therefore the patient was transferred to intensive unit care, where a temporary Pace Maker was implanted. Computed tomography scan showed only a trifling frontal brain contusion, a moderate PNX and pneumomediastinum, and sternal fracture. No other trauma injuries were documented. In the next hours the patient developed three episodes of ventricular fibrillation, successfully treated, without regain consciousness. The last ECG showed a normal sinus rhythm with Q wave in D2-D3 aVF, suggesting
a myocardial infarction (Fig. 1C). Troponin I value was 0.3 ng/ml; troponin T was 0.6 ng/ml. On 8 h after admission the patient developed a sudden cardiac arrest and despite resuscitative manoeuvres he died. A diagnosis of acute inferior myocardial infarction with third AV conduction block was advanced. 2.1. Autopsy findings The autopsy was performed 24 h after death. The body was 168 cm in height and 70 kg in weight. The external examination of the body revealed only few contusions and abrasions, which one in sternal region. No others signs of injury. The internal examination revealed the sternal fracture and pericardium haemorrhages. All internal organs were macroscopically normal. The heart had a normal shape and was normal in size (12 cm × 12 cm × 6 cm) and weight (490 g). The left coronary artery arose normally. The right descending coronary artery showed for 1 cm from the right anterior sinus, an periadventitial concentric haemorrhagic cloak. No significant stenosis or thrombotic occlusion of the coronary
Fig. 1. (A) ECG demonstrating no sustained ventricular tachycardia, right bundle branch block, atrial fibrillation and wide QRS with repolaritazion abnormality. (B) ECG showed a marked ST segment elevation in all peripheral leads and a complete right bundle branch block. (C) ECG demonstrating a normal sinus rhythm with Q wave in D2–D3 aVF, suggesting a myocardial infarction.
I. Riezzo et al. / International Journal of Cardiology 128 (2008) e107–e110
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Fig. 2. (A) The myocardium showed mild myofiber eosinophilia and elongation of sarcomeres and nuclei, with interstitial haemorrhages (H&E, ×40). (B) Right coronary artery: histological cross section showed periadventitial and adventitial haemorrhages (Masson's trichrome, ×60). (C) The immunohistochemical examination of the myocardial samples (right sample, anterior and lateral left samples) revealed a higher degree of depletion (light colour) of Troponin I (Ab antiTnI) and (D) Troponin C in contrast with the normal fibres (brown colour) (Ab anti-TnC).
segment were detected. The atrio-ventricular and semilunar valves were normal. The myocardium showed a dark area (intramural haemorrhages) (7.5 cm × 0.7 cm) that extended from apex to posterior–inferior left ventricular wall and also to posterior right ventricular wall. The histological examination of the heart, performed with routine haematoxylin-eosin and Azan, Mallory and Van Gieson stains, revealed in the superficial myocardial layers, numerous foci of contraction band necrosis. Segmentation of the myocardial cells and widening of intercalated discs and bundles of contracted myocardium alternating with bundles of distended myocardium with granular disruption of the myocytes in all myocardial sections were noted. The examination of right samples, showed subepicardial adipose haemorrhages and interstitial haemorrhages with foci of necrosis with contraction bands localized, limited in their extension and sharp delimitated from the surrounding undamaged myocardium. In other field the myocardium showed mild myofiber eosinophilia and elongation of sarcomeres and nuclei, with interstitial haemorrhages (Fig. 2A). No infarct necrosis was detected. In the samples taken from the right coronary artery (1 cm from the right anterior sinus), histological cross section showed periadventitial and adventitial haemorrhages (Fig. 2B). The immunohistochemical examination of the samples (right sample,
anterior and lateral left samples) revealed a higher degree of depletion of Troponin I and Troponin C and low degree of depletion of myoglobin (Fig. 2C, D). The remainder of the histological examination was unremarkable. The diagnosis of cardiac contusion was established as cause of death. 3. Discussion Cardiac contusion can be defined as cellular damage that result from non penetrating chest or abdominal trauma. It's frequently associated with blunt chest trauma, and the traffic accidents are the most frequent cause of cardiac contusion in these patients. However, the exact incidence of myocardial contusion in patients with blunt chest injury is not well known. It varies among 0% an 76% [3] and depending on the criteria used for establishing the diagnosis. Postmortem incidence in cases of immediate fatalities from blunt injury is 14% [4]. Blunt chest trauma may result in various cardiac injuries including pericardial injury, cardiac injury (cardiac concussion and contusion, cardiac rupture), valvular injury, great vessel injury, cardiac conduction system injury cardiac rhythm disturbances, coronary artery injury, and acute
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myocardial infarction (with or without coronary artery dissection) [1,5,6]. Cardiac injuries result from main mechanisms: a direct blow to the chest, in which the heart is compressed between the sternum and the thoracic vertebrae, sudden deceleration, striking compression of the abdomen, and secondarily from sternal or rib fractures. The right ventricular wall is the area most vulnerable [7]. CC may be diagnosed by serial electrocardiogram, serum determination of biochemical cardiac markers, echocardiogram, radionuclide imaging and coronary angiography. These patients have an increased serum activity of several enzymes such as CK-MB, Troponin I, troponin T, LDH [8]. Elevated cTnI is a marker of myonecrosis and does not necessarily imply myocardial infarction. It may arise as a result of direct myocardial damage or as a result of mismatch between myocardial oxygen supply and consumption [9]. ECG findings included non specific ST-segment-T-wave changes, ST segment elevation and depression, T-wave abnormalities, right bundle branch block and atrioventricular blocks, tachycardia including nodal tachycardia, atrial fibrillation and flutter, ventricular tachycardia and ventricular fibrillation, [10] whereas Q-waves are rarely observed [11]. However there is no a gold standard and a consensus on the best indicator of cardiac damage, and which of these examinations may accurately predict the outcome in terms of myocardial cell loss [11,12]. The described clinical and instrumental signs are similar to those of an infarction, and although relative uncommon, myocardial infarction can result from blunt chest trauma (5%) [3]. In our case the definitive diagnosis of myocardial contusion has proved complex. All clinical data were suggestive of acute myocardial infarction, but the history of chest wall injury and gross and histological examination of the heart and coronary vessels led us to conclude for a cardiac contusion: pericardial haemorrhages, peri-adventitial and adventitial right coronary haemorrhage, absent of trombotic stenosis, intramyocardial haemorrhages and sharp transition from normal to damaged myocardial tissue,
associated with an high degree of troponins' depletion [1,13]. In case of chest blunt trauma, the ECG should be interpreted within the context of the clinical situation, on history of chest wall injury, since a fatal myocardial contusion may occur after apparently mild injury. References [1] Fineschi V, Baroldi G, Silver MD. Pathology of the heart and sudden death in forensic medicine. Boca Raton, FL: CRC Press; 2006. p. 309–10. [2] Sybrandy KC, Cramer MJ, Burgersdijk C. Diagnosing cardiac contusion: old wisdom and new insights. Heart 2003;89:485–9. [3] Maenza RL, Seaberg D, D'Amico F. A meta-analysis of blunt cardiac trauma: ending myocardial confusion. Am J Emerg Med 1996;14:237–41. [4] Kaye P, O'Sullivan I. Myocardial contusion: emergency investigation and diagnosis. Emerg Med J 2002;19:8–10. [5] Sato Y, Matsumoto N, Komatsu S, et al. Coronary artery dissection after blunt chest trauma: Depiction at multidetector-row computed tomography. Int J Cardiol 2007;118:108–10. [6] Vougiouklakis T, Peschos D, Doulis A, Batistatou A, Mitselou A, Agnantis NJ. Sudden death from contusion of the right atrium after blunt chest trauma: case report and review of the literature. Injury 2005;36:213–7. [7] Darok M, Beham-Schmid C, Gatternig R, Roll P. Sudden death from myocardial contusion following an isolated blunt force trauma to the chest. Int J Leg Med 2001;115:85–9. [8] Baum VC. The patient with cardiac trauma. J Cardiothorac Vasc Anesth 2000;14:71–81. [9] Mahajan N, Mehta Y, Rose M, Shani J, Lichstein E. Elevated troponin level is not synonymous with myocardial infarction. Int J Cardiol 2006;111:442–9. [10] Plautz CU, Perron AD, Brady WJ. Electrocardiographic ST-segment elevation in the trauma patient: acute myocardial infarction vs myocardial contusion. Am J Emerg Med 2005;23:510–6. [11] Holanda MS, Dominguez MJ, Lopez-Espadas F, Lopez M, DiazReganon J, Rodriguez-Borregan JC. Cardiac contusion following blunt chest trauma. Eur J Emerg Med 2006;13:373–6. [12] Bernardis V, Kette F, Blarasin L, Pegoraro C, Coassin R. Isolated myocardial contusion in blunt chest trauma. Eur J Emerg Med 2004;11:287–90. [13] Peter J, Kirchner A, Kuhlisch E, Menschikowski M, Neef B, Dressler J. The relevance of the detection of troponins to the forensic diagnosis of cardiac contusion. Forensic Sci Int 2006;160:127–33.