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Acute Coronary Occlusion and Myocardial Infarction Secondary to Blunt Chest Trauma from an Automobile Airbag Deployment
CASE REPORTS:
Acute Coronary Occlusion and Myocardial Infarction Secondary to Blunt Chest Trauma from an Automobile Airbag Deployment

- Alan Zajarias, MD, Srihari Thanigaraj, MD, Megumi Taniuchi, MD, PhD

Automobile airbags have been universally installed to save lives in motor vehicle accidents, but have also been linked with facial and thoracic burns and chest trauma during rapid deployment. Blunt trauma to the chest may result in electrical and mechanical injuries to the heart and great vessels. We report a case of a 19-year-old man who presented with acute myocardial infarction following a blunt chest trauma from an automobile airbag deployment. Although mechanical complications resulting from airbag injury have been reported in the past, this is the first report of an acute thrombotic coronary occlusion triggered by the rapid airbag deployment. The case underscores the importance of systematic clinical evaluation to guide management in patients with confounding clinical presentation.


       Non-penetrating thoracic trauma has been associated with multiple structural and electrical cardiac injuries and complications with a mortality rate of up to 15%.1 The mechanisms for non-penetrating cardiac injury include: direct trauma, rapid deceleration, myocardial compression between the thoracic spine and the sternum, or sudden increase in the aortic pressure.2 Airbags have become standard equipment in all automobiles and are generally assumed to improve driver and passenger safety in the event of a crash. However, there are reported examples where airbag deployment has resulted in significant injuries. We present the case of a young man who sustained acute thrombotic occlusion of the first diagonal artery following blunt chest trauma from an airbag deployment during an automobile accident.

       Case report and clinical presentation. A 19-year-old male was brought to the emergency room following a motor vehicle accident. The accident involved a head-on collision with a roadside fire hydrant that occurred while the patient was driving intoxicated. He was restrained by a seat belt, and reportedly was driving at a speed of 40 mph. The impact triggered the deployment of the driver-side airbag, resulting in a blunt injury to patient’s face and chest. Following a transient loss of consciousness, the patient complained of severe chest pain at the scene of the accident, which continued on arrival to the emergency room. Vital signs were as follows: temperature = 37.40º C, blood pressure = 110/70 mmHg, heart rate = 70/minute regular and respiratory rate = 16/minute and unlabored. The physical examination was otherwise unremarkable except for mild precordial chest wall tenderness. No pericardial rub, murmur or neurological
Figure 1
Electrocardiogram taken upon arrival to the emergency room showing, 3 mm ST-segment elevation in I and aVL, hyperacute T-waves with J-point elevation in leads V4–V5, reciprocal ST-segment depression and T-wave inversion in leads III, aVF and V1–V3.
deficits were noted. An electrocardiogram (ECG) showed 3 mm ST-segment elevation in leads I and aVL, hyperacute T-waves with J-point elevation in leads V4–V5, and associated ST-segment depression and T-wave inversion in leads III, aVF and V1–V3 (Figure 1). The patient denied any prior history of cardiac disease. He admitted to smoking 3 cigarettes per day for less than 4 years and occasional alcohol consumption, but denied cocaine or intravenous drug abuse.
       CT scans of the head, chest, and abdomen were noted to be normal, ruling out cerebral hemorrhage and aortic dissection. Initial laboratory data showed a myoglobin of 328 ng/mL, troponin I of 1.0 ng/mL, and a blood alcohol level of 105 mg/dl. Urine drug screen was negative, serum electrolytes and other hematological values were within normal limits. The patient’s symptoms and ECG changes were attributed to myocardial contusion or coronary vasospasm. He was managed with intravenous nitroglycerin and metoprolol, with
Figure 2
Coronary angiogram in the LAO cranial view of the left coronary artery depicting complete occlusion of the first diagonal artery immediately after its origin (arrow).
marked improvement his chest pain and ST-segment elevation. Over the next 6 hours the patient experienced recurrence of chest pain and ST-segment elevation on the ECG. A transthoracic echocardiogram revealed akinesis of the anterior wall. Repeat laboratory data were as follows: troponin I = 49.1 ng/mL, total creatinine kinase = 3,389 IU/L, with an MB fraction of 186 ng/mL.
       The patient immediately underwent emergency cardiac catheterization, which showed complete occlusion of the proximal part of the first diagonal artery (Figure 2 – arrow). All other coronaries were noted to be patent and free of significant lesions. A left ventriculogram demonstrated anterior wall akinesis with a preserved overall ejection fraction. Immediate percutaneous transluminal coronary angioplasty with placement of a 3 mm x 16 mm NIR stent in the proximal first diagonal branch was performed with restoration of TIMI 3 flow (Figure 3). The patient’s creatinine kinase peaked at 5,018 IU/L (MB of 208 ng/mL). His fasting lipid panel, serum homocysteine levels and tests for hypercoagulable state were noted to be normal. The rest of
Figure 3
Coronary angiogram in the LAO cranial view after successful stent placement in the diagonal artery. Note full vessel patency (arrow).
the hospital course was uneventful and he was discharged home on the fourth day of hospitalization in stable condition with prescriptions for 75 mg of clopidogrel daily for 6 weeks, daily aspirin, 25 mg of atenolol, and 2.5 mg of lisinopril.
       Six months after discharge, he was readmitted to the hospital with chest pain and a positive stress test in the antero-lateral wall. He underwent repeat cardiac catheterization, which only revealed 30% in-stent restenosis in the diagonal artery. The left ventriculogram documented lateral wall akinesis, with an ejection fraction of 55%. He was discharged on the same medical regimen and has been asymptomatic since. The patient is able to perform his daily activities without limitations.


       Discussion. Blunt chest trauma has been associated with myocardial contusion, aortic dissection, aortic avulsion, and acute tricuspid insufficiency. Acute coronary artery occlusion is a very rare complication of non-penetrating chest trauma. This complication has been reported after trauma of various types and severity, including sport activities and crush injury associated with motor vehicle accidents.3,4 It has been postulated that traumatic coronary artery occlusion may result from vascular spasm, intimal tear with thrombus formation, atheromatous plaque rupture and hemorrhage or external compression by an epicardial hematoma. The vessel most commonly involved is the left anterior descending artery, although involvement of the right coronary artery and the left main coronary artery have also been documented. To our knowledge, the involvement of the diagonal arteries has never been reported with blunt chest trauma.
       Automobile airbags are designed to deploy instantaneously in the event of a collision and are controlled by electronic deceleration sensors. Airbags inflate at a rate of 6 liters/millisecond, generating a velocity that ranges from 98 to 211 mph (average 144 mph).5 A variety of thoracic injuries including aortic transection,6 aortic valve avulsion,7 right atrial rupture8 and rib fractures9 resulting from airbag deployment have been reported previously. Although myocardial infarction associated with other types of chest trauma has been described in the literature, to our knowledge this is the first case where a blunt injury from an airbag deployment resulted in an acute thrombotic coronary occlusion and myocardial infarction. The localized nature of the occlusion and absence of other internal or external thoracic injuries makes this case unique.
       The diagnosis of coronary artery occlusion following blunt chest trauma requires a strong clinical suspicion. Chest pain is a common complaint in these patients and may be easily mistaken for musculoskeletal pain, but may reflect an evolving myocardial infarction or major injuries such as aortic dissection or esophageal rupture. Myocardial contusion and coronary spasm are known to precipitate chest pain, ECG changes and arrhythmias, all of which may easily confound the diagnosis of myocardial infarction, as in the case presented here. The combination of dynamic ST-segment changes, clinical instability and wall motion abnormalities in the absence of acute aortic dissection or transection merits prompt evaluation with coronary angiography to exclude acute coronary thrombosis or occlusion. Delays in performing coronary angiography may limit the therapeutic benefit of revascularization and result in significant morbidity. Due to the frequency of concomitant musculoskeletal injuries, the use of thrombolytics may be contraindicated, thus favoring mechanical revascularization.
       Conclusions and clinical implications. Airbags have been shown to decrease morbidity and mortality associated with motor vehicle accidents when used in conjunction with seat belts. However, airbag deployment has been implicated in several clinically significant injuries. The case presented herein underscores the importance of considering acute coronary occlusion in the differential diagnosis of chest pain following blunt trauma related to airbag deployment, even in young patients. With the increasing number of airbag-equipped automobiles, and with the rising incidence of motor vehicle accidents, such occurrences are likely to become more common.


1. Shackford SR. Blunt chest trauma: The intensivist perspective. J Intens Care Med 1986;1:25–36.
2. Chirtwood WR, Austin EH. Cardiac trauma: Penetrating and blunt. In: Moylan JA (ed). Trauma Surgery. Philadelphia: Lipincott. 1988, pp. 123–181.
3. Voyce SJ, Ball S, Gore JM, et al. Angiographically documented thrombotic coronary artery occlusion secondary to mild non-penetrating thoracic trauma. Cathet Cardiovasc Diagn 1991;24:179–181.
4. Unterberg C, Buchwals A, Wiegand. Traumatic thrombosis of the left main coronary artery and myocardial infarction caused by blunt chest trauma. Clin Cardiol 1989;12:672–674.
5. Yoganandan N, et al. Mechanisms of thoracic injury in frontal impact. J Biomechanical Eng 1996;118:595–597.
6. deGuzman BJ, Morgan AS, Pharr WF. Aortic transection following air-bag deployment [letter]. N Engl J Med 1997;337:573–574.
7. Hanna KM. Aortic valve injury secondary to blunt trauma from an airbag [comments]. Tennessee Med 1997;90:195–196.
8. Lancaster GI, DeFrance JH, Borruso JJ. Air-bag-associated rupture of the right atrium [letter]. N Engl J Med 1993;328:358.
9. Daniels RJ, Fulcher RA. An unusual cause of rib fracture following a road traffic accident. J Accident Emer Med 1997;14:113–114.

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