This article has Open Peer Review reports available.
Coronary artery rupture in blunt thoracic trauma: a case report and review of literature
© The Author(s). 2016
Received: 26 January 2016
Accepted: 28 July 2016
Published: 2 August 2016
Blunt thoracic trauma can rarely result in coronary artery injury. Blunt trauma can result in occlusion of any of the coronary arteries or can lead to its rupture and bleeding. Traumatic coronary artery occlusion can lead to myocardial infarction, while its rupture and bleeding can result in hemopericardium and cardiac tamponade, and can be rapidly fatal. Survival after coronary artery rupture in blunt thoracic trauma is exceedingly rare.
We present a case of a young male who sustained a blunt thoracic trauma in a motor vehicle collision, that resulted in rupture of the left anterior descending (LAD) coronary artery and subsequent cardiac tamponade. Prompt surgical intervention with pericardiotomy and ligation of the artery has resulted in survival of the patient.
In cases of traumatic coronary artery rupture, early surgical intervention is crucial to avoid mortality. Ligation of the injured coronary is a viable option in selected cases, and can be the most expeditious option in patients in extremis.
Coronary artery injury in blunt chest trauma is uncommon yet potentially fatal. Autopsy studies reveal an incidence of around 2 % of all cardiac injuries caused by blunt chest trauma [1, 2]. The mechanical energy from trauma transmitted to coronaries can result in intimal tears, wall dissection, dislodgement or rupture of a pre-existing atherosclerotic plaque, coronary artery spasm, or coronary artery rupture [1, 3–5]. Fractured ribs from blunt trauma can result in coronary laceration [6, 7]. Lesions that result in subsequent occlusion of the involved coronary artery (like intimal tears, wall dissection, rupture of a pre-existing atheromatous plaque, and coronary artery spasm) can culminate in myocardial infarction, which can be immediate or delayed . On the other hand, coronary rupture can result in precipitous development of hemopericardium and cardiac tamponade, and is thought to be universally fatal .
Few case reports exist on coronary artery rupture in blunt chest trauma. In cases were the pericardium remains intact, rapid development of cardiac tamponade makes survival improbable after such injuries. We present a rare case of left anterior descending (LAD) coronary artery rupture in a young male following blunt chest trauma in a motor vehicle collision. The patient survived despite developing cardiac tamponade and circulatory arrest, and was treated by emergency thoracotomy and ligation of the distal LAD.
A 26-year-old male, who was not known to have any risk factors for coronary artery disease, presented to the emergency department after a head-on motor vehicle collision as unrestrained driver. The patient complained of chest pain and shortness of breath. His GCS was 15/15. He was tachypneic (RR: 45 breaths/min) and tachycardic (HR: 134 beats/min). He was found to be hypotensive upon arrival (BP: 87/54 mmHg), but his blood pressure normalized following the rapid infusion of two liters of lactated Ringer’s solution. Auscultation of lung fields revealed reduced breath sounds on the right side. Chest x-ray (CXR) revealed a large right-sided hemothorax. A thoracostomy tube was inserted on the right side resulting in the immediate drainage of two liters of blood. Initial focused assessment with sonography in trauma (FAST) exam was negative, but the patient became hypotensive again soon after (BP: 60/40 mmHg). Repeated FAST revealed a moderate amount of fluid in the pericardial space. The patient was rushed into the operating room for thoracotomy and pericardiotomy. Induction of anesthesia was accompanied by progressive bradycardia that degenerated rapidly into asystole. A resuscitative thoracotomy (left anterolateral) revealed hemopericardium and cardiac tamponade. The pericardium was intact. Pericardiotomy and evacuation of more than 200 ml of blood from the pericardium, followed by internal cardiac massage, resulted in restoration of heart activity after 3 min. With restoration of spontaneous circulation, bleeding was noticed from a small perforation in the distal LAD near the apex. The distal LAD was ligated proximal to the site of perforation. The left anterolateral thoracotomy was extended across the midline to the right side into a clamshell thoracotomy to allow for proper exploration of the right hemithorax. The bleeding was found to arise from multiple injured intercostal vessels, and hemostasis was secured. The blood pressure started to improve, and the patient was sent to the intensive care unit on mechanical ventilation.
Cardiac markers were all elevated at presentation (CK: 4,267 U/L, Ref. Range 30–200. CK-MB: 226 U/L, Ref. Range <25 U/L. Troponin I: 19.29 ng/ml, Ref. Range 0.04 ng/ml), and continued to rise to reach a peak at 48 h (CK: 32,109 U/L. CK-MB: >1000 U/L. Troponin I: 19.43 ng/ml), after which they started to decline. A standard 12 lead ECG showed sinus tachycardia with left axis deviation, and a down sloping ST segment depression of anterolateral leads (V1-V6) with T wave inversion. A transthoracic echocardiogram (TTE) was done on the first postoperative day. It showed a normal left ventricular (LV) function with an ejection fraction (EF) of 60 %. The echocardiogram did not show any wall motion abnormalities at that point, and there was no significant valvular pathology.
There was considerable difficulty in liberating the patient from mechanical ventilation due to underlying pulmonary edema and bilateral lung contusions. The patient was extubated after 14 days of mechanical ventilation. A follow up TTE done 4 weeks later showed a moderate LV systolic dysfunction with an EF of 35 %, and wall motion abnormalities involving the apical and anterolateral regions. The patient was discharged from hospital few days later on anti-heart failure medication.
Albeit rare, blunt chest trauma may result in the occlusion of any of the coronary arteries or may lead to its rupture and bleeding. Each of these two patterns of injury is associated with a distinct corresponding patient population, clinical presentation, management, and outcome.
Intimal tears, wall dissection, disruption of atherosclerotic plaque, coronary artery spasm, and epicardial hematomas can result in partial or complete occlusion of the coronary artery and subsequent myocardial ischemia. Depending on the severity of the occlusion and the rapidity by which it develops, patients may present with angina pectoris, myocardial infarction, or even heart failure many years after the injury. Christensen et al. conducted a review on cases of myocardial ischemia following blunt chest trauma . The review showed that 82 % of the 77 studied patients were below the age of 45. All of the reported patients developed myocardial infarction due to occlusive lesions of the coronary arteries, except for one patient who had angina pectoris without evidence of infarction. The LAD was the most common coronary involved. Only 5 of the 77 (6.5 %) reported cases died secondary to the coronary artery injury and ischemia. The favorable prognosis was attributed to the patients’ young age, and to the involvement of a single vessel. Percutaneous transluminal coronary angioplasty (PTCA) and stenting is thought to be the most suitable treatment in these cases .
Summary of reported cases of coronary artery rupture in blunt thoracic trauma
Age & gender
Mechanism of injury
Associated cardiac injuries
Coronary artery disease
Goffin et al. 1974 .
Dyspnea, chest pain, shock.
CXR: Multiple rib fractures. Slight enlargement of the heart.
ECG changes of inf. MI and AV block.
Moderately elevated CPK and SGOT.
Aortic tear. Intimal tear in LCX
Trotter et al. 1998 .
Chest wall contusion. Continuous murmur. Initially stable vital signs, then worsening dyspnea and cardiogenic shock.
CXR: widened cardiac silhouette. RBB on ECG.
Suzuki et al. 2000 .
Severe dyspnea and chest pain 14 h after the incident. CXR: fractures of left 7th and 8th ribs with left pleural effusion.
Dimopoulos et al. 2003 .
Anemia. Massive left pleural effusion on CXR.
Atrial fibrillation and LBBB. Echocardiogram: 700 ml of pericardial effusion with normal ejection fraction.
Straub et al. 2003 .
No visible chest wall lesions. Cardiogenic shock.
CXR: normal. Elevated cardiac enzymes.
Echocardiography: pericardial effusion, no wall motion disturbances. CT scan: hemorrhagic pericardial effusion and para-aortic contrast fluid extravasation.
Sugimoto et al. 2003 .
Unconscious and in severe shock.
Echocardiogram: massive hemopericardium.
ER thoracotomy with attempted ligation of the RCA. Interval ACB three weeks later.
Dueholm et al. 2009 .
Chest pain. Normal exam.
ECG: Acute MI. CXR: Fractures in left 6th and 7th ribs.
Arrhythmia, followed by cardiogenic shock.
Tyson et al. 2010 .
Breath sounds decreased on the left. CXR: left hemothorax and widened mediastinum. CT scan: minimal pericardial fluid. Fractures in left 2nd -7th ribs. Tube thoracostomy drained 2 L of blood.
Posterior cardiac vein
Anterolateral thoracotomy and ligation of bleeding vessels.
Burcar et al. 2013 .
Chest wall hematomas. GCS 5/15. Hypotension. ST segment depression. Troponin I & CPK elevation. Bilateral lung contusions on CT scan.
Intimal tear in MPA
Pericardiotomy. LIMA to LAD. SVG to LCX.
Unlike cases of coronary occlusion that has been reported after apparently trivial trauma, the amount of energy needed to rupture a coronary artery is high and is usually associated with high-speed motor vehicle collisions. The clinical picture is variable and patients may complain of chest pain and might be hemodynamically unstable. The injury is rarely suspected and the clinical picture is usually attributed to more common causes of chest pain in blunt chest trauma. ECG changes are non-specific and are usually attributed, along with elevated cardiac enzymes, to cardiac contusion. CXR may show fractured ribs but coronary artery rupture may occur with an intact thoracic skeleton . The heart shadow may appear enlarged due to hemopericardium, but a traumatic communication between the pericardial and pleural cavities can result in the appearance of pleural effusion in its place [6, 7]. Similarly, pericardial effusion, which is the principal manifestation of coronary artery rupture, can be undetectable or absent on FAST exam if the pericardium is not intact. In addition, bleeding from the ruptured coronary can seep beneath the epicardium and become contained in the form of an epicardial hematoma that could be missed on FAST examination or mistaken for chamber dilatation. This phenomenon can also result in failed attempts at pericardiocentesis or subxiphoid pericardiotomy . Rarely, spasm in the severed coronary artery can result in absence of pericardial effusion despite an intact pericardium .
Contrary to popular belief that such injuries are usually instantly fatal, accounts of coronary artery rupture report a time window ranging from 2 to 56 h [Table 1]. This time window could theoretically be sufficient to avoid mortality when timely management is provided. Patients with pericardial effusion or hemodynamic instability should undergo prompt exploratory surgery. As discussed above, pericardiocentesis might be of limited utility in these cases since it has been observed that blood can accumulate in the form of epicardial hematoma instead of collecting in the pericardial space. In addition, despite the presence of pericardial effusion, coronary injury was only identified intraoperatively or at autopsy and was not suspected preoperatively in most reported cases [Table 1]. Therefore, a low threshold for timely thoracotomy and exploration should be kept in patients with blunt chest trauma and pericardial effusion or hemodynamic instability. More stable patients, in absence of pericardial effusion, who continue to complain of chest pain or other cardiac symptoms, and those who show evidence of myocardial ischemia on electrocardiogram or elevated cardiac enzymes, can undergo formal echocardiogram followed by coronary angiogram to detect any coronary injury.
Operative options in the management of coronary artery rupture include ligation or revascularization. The choice of incision is dictated by the clinical situation. A left anterolateral thoracotomy incision is used in patients who need an emergency department or resuscitative thoracotomy, while median sternotomy is preferred in the more stable patient. The left anterolateral incision can be extended across the midline to the right side into a clamshell thoracotomy for better exposure if needed. The decision to ligate or revascularize the injured coronary artery depends on the amount of ventricular mass that would be affected by the interruption of the artery, and on the physiologic status of the patient. Distal injuries in main coronary arteries, and most injuries in secondary coronary arteries such as the diagonal, obtuse marginal, or acute marginal coronary arteries, can be treated by ligation. Ligation in such injuries might result in a small area of infarction that does not usually lead to significant cardiac dysfunction . In contrast, ligation of proximal injuries in main coronary arteries might result in a widespread infarct, with consequent intractable heart failure and fatal arrhythmias. Revascularization is typically indicated in these injuries. However, it is theorized that the majority of patients with significant proximal coronary artery injuries suffer widespread cardiac ischemia, fibrillate, and die earlier in their course of injury, such that survival to care is an implicit indicator that ligating the injured coronary artery is likely to be tolerated by the patient . In patients with severe physiologic derangements and a proximal coronary artery injury, who are unlikely to tolerate an immediate revascularization procedure, it is appropriate to use a damage control approach by ligating the artery, resuscitating and rewarming the patient, correcting coagulopathy, and performing revascularization on a later date if needed. Intra-aortic balloon pump can be used as a temporary measure in patients who develop cardiac dysfunction after coronary artery ligation .
Coronary artery rupture is a rare occurrence in blunt trauma, and high index of suspicion is needed to identify these injuries. Low threshold for exploratory surgery should be kept in patients manifesting pericardial effusion or hemodynamic instability. These injuries are compatible with a short period of survival, and may be survivable with proper resuscitation and timely surgery.
Many of these injuries can be safely treated by ligation.
ACB, aortocoronary bypass; CABG, coronary artery bypass grafting; CXR, chest x-ray; EF, ejection fraction; FAST, focused assessment with sonography in trauma; FD, falling down; IABP, intra-aortic balloon pump; ICM, intermediate coronary artery; LAD, left anterior descending artery; LCX, circumflex artery; LIMA, left internal mammary artery; LM, left main coronary artery; LV, left ventricular; MPA, main pulmonary artery; MVC, motor vehicle collision; OM, obtuse marginal artery; OPCAB, off –pump coronary artery bypass; PTCA, percutaneous transluminal coronary angioplasty; RCA, right coronary artery; SVG, saphenous vein graft; TTE, transthoracic echocardiogram
We would like to thank Elizabeth Alverson for helping us in the revision of the final draft of the manuscript.
JHA, AIA, RSY, SA, YMK treated the patient. JHA, SA, YMK collected the patient’s data. JHA, HHA, AMA, AAA, MHA, MIA, NRA performed the literature review. JHA wrote the manuscript and RSY revised and edited the manuscript. All authors read and approved the final manuscript.
The authors declare that they have no competing interests.
Consent for publication
Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
- Parmley LF, Manion WC, Mattingly TW. Nonpenetrating traumatic injury of the heart. Circulation. 1958;18(3):371–96.View ArticlePubMedGoogle Scholar
- Turan AA, Karayel FA, Akyildiz E, et al. Cardiac injuries caused by blunt trauma: an autopsy based assessment of the injury pattern. J Forensic Sci. 2010;55(1):82–4. doi:10.1111/j.1556-4029.2009.01207.x.View ArticlePubMedGoogle Scholar
- Heyndrickx G, Vemdre P, Goffin Y, Van den Bogaert P. Rupture of the Right Coronary Artery Due to Nonpenetrating Chest Trauma. CHEST J. 1974;65(5):577. doi:10.1378/chest.65.5.577.View ArticleGoogle Scholar
- Neiman J, Hui WKK. Posteromedial papillary muscle rupture as a result of right coronary artery occlusion after blunt chest injury. Am Heart J. 1992;123(6):1694–9. doi:10.1016/0002-8703(92)90827-I.View ArticlePubMedGoogle Scholar
- Hugar BS, Shetty HS, Yajaman GCP, Rao AS. Death due to coronary artery insufficiency following blunt trauma to the chest. J Forensic Sci. 2014;59(3):830–2. doi:10.1111/1556-4029.12371.View ArticlePubMedGoogle Scholar
- Suzuki I, Sato M, Hoshi N, Nanjo H. Coronary arterial laceration after blunt chest trauma. N Engl J Med. 2000;343(10):742–3. doi:10.1056/NEJM200009073431017.View ArticlePubMedGoogle Scholar
- Tyson GH, Anderson CA, Rodriguez E, Kypson AP. Blunt coronary injury presenting as massive left-sided hemothorax. Asian Cardiovasc Thorac Ann. 2010;18(1):71–3. doi:10.1177/0218492309354219.View ArticlePubMedGoogle Scholar
- Christensen MD, Nielsen PE, Sleight P. Prior blunt chest trauma may be a cause of single vessel coronary disease; hypothesis and review. Int J Cardiol. 2006;108(1):1–5. doi:10.1016/j.ijcard.2005.04.010.View ArticlePubMedGoogle Scholar
- Trotter TH, Knott-Craig CJ, Ward KE. Blunt injury rupture of tricuspid valve and right coronary artery. Ann Thorac Surg. 1998;66(5):1814–6. doi:10.1016/S0003-4975(98)00919-9.View ArticlePubMedGoogle Scholar
- Straub A, Beierlein W, Küttner A, Hahn U, Raygrotzki S, Ziemer G. Isolated coronary artery rupture after blunt chest trauma. Thorac Cardiovasc Surg. 2003;51(2):97–8. doi:10.1055/s-2003-38980.View ArticlePubMedGoogle Scholar
- Goffin Y, Heyndrickx G. Traumatic rupture of the right coronary artery with nine hours survival a clinical, histopathological and enzymologic study. Forensic Sci. 1974;4:135–44. doi:10.1016/0300-9432(74)90094-6.View ArticlePubMedGoogle Scholar
- Dueholm S, Fabrin J. Isolated coronary artery rupture following blunt chest trauma: a case report. Scand J Thorac Cardiovasc Surg. 2009;20(2):183–4.View ArticleGoogle Scholar
- Wall MJ, Mattox KL, Chen CD, Baldwin JC. Acute management of complex cardiac injuries. J Trauma. 1997;42(5):905–12.View ArticlePubMedGoogle Scholar
- Raja SG. Pump or no pump for coronary artery bypass: current best available evidence. Tex Heart Inst J. 2005;32(4):489–501.PubMedPubMed CentralGoogle Scholar
- Mangoush O, Purkayastha S, Haj-Yahia S, et al. Heparin-bonded circuits versus nonheparin-bonded circuits: an evaluation of their effect on clinical outcomes. Eur J Cardiothorac Surg. 2007;31(6):1058–69. doi:10.1016/j.ejcts.2007.01.029.View ArticlePubMedGoogle Scholar
- Dimopoulos K, Angelini A, Mencarelli R, Thiene G. Multiple coronary rupture after blunt chest trauma. Heart. 2003;89(6):594.View ArticlePubMedPubMed CentralGoogle Scholar
- Sugimoto S, Yamauchi A, Kudoh K, Hayakawa M, Igarashi Y, Tanaka T. A successfully treated case of blunt traumatic right coronary ostium rupture. Ann Thorac Surg. 2003;75(3):1001–3. doi:10.1016/S0003-4975(02)04562-9.View ArticlePubMedGoogle Scholar
- Burcar I, Petricevic M, Gasparovic H, Coric V, Biocina B. Blunt chest trauma caused rupture of the left main coronary artery in a 15 year old motocross rider. J Cardiothorac Surg. 2013;8 Suppl 1:25. doi:10.1186/1749-8090-8-S1-P25.View ArticleGoogle Scholar