Driver side air bags are meant to provide protection during the rapid deceleration that occurs after accidents, particularly in those involving frontal collision.¹ These have been shown to decrease the morbidity and mortality associated with high speed injuries when used in conjunction with lap and shoulder belts.^2–4 Air bags inflate at a rate of 6 l/ms, generating a velocity that has been measured at 157.7–339.6 km/h (98–211 miles/h; average 21.7 km/h or 144 miles/h).⁵

In some instances air bags have been implicated as the direct cause of the injuries, most of which are usually minor. However, three major cardiovascular problems, aortic transection,^6,7 tricuspid valve injury,⁸ and delayed cardiac rupture,⁹ have been reported. We present a patient who experienced reversible myocardial injury following air bag deployment.

CASE REPORT

A 62 year old lady was driving at a speed of about 32 km/h (20 miles/h) when her car was hit on the side by another car travelling at about the same speed (the patient could not recollect which side it was). She was wearing her seat belt, and her air bag deployed almost instantaneously. She felt a crushing anterior chest pain radiating to her left arm immediately after the accident, but denied loss of consciousness, shortness of breath, or palpitations. She had no significant past medical history, was not currently on any medication, and had never smoked. There was no significant family history of ischaemic heart disease.

On examination she was well oriented with a Glasgow Coma Scale score of 15/15. She was haemodynamically stable with a pulse of 96/min and blood pressure 40/80 mm Hg. Jugular venous pressure was not elevated and auscultation of her heart revealed normal heart sounds with no murmurs. The anterior chest wall was tender on palpation. Her respiratory rate was 15/min with 98% oxygen saturations on room air. Auscultation of the chest revealed no abnormalities. Abdomen and nervous system examinations were essentially normal.

A chest x ray revealed normal cardiac contours, clear lung fields, and no bony injuries. The initial electrocardiogram (ECG) revealed ventricular bigemini but no other abnormality (fig 1). Another ECG, one and half hours after admission revealed 1 mm ST segment elevation in leads V2 and V3 (fig 2). Troponin I (TnI) level, measured six hours after admission, was elevated at 23.9 ng/l (normal<0.3 ng/l). Echocardiogram recorded within 12 hours of the accident revealed akinesia of the mid-septum and apex with mild left ventricular impairment but no pericardial effusion. We did not consider thrombolysis due to preceding history of trauma and the risk of cardiac tamponade. Her symptoms were controlled with opioid analgesia, and she was started on aspirin, atenolol, and ramipril.

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Figure 1

 Initial electrocardiogram of a 62 year old woman involved in a car accident showing ventricular bigemini.

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Figure 2

 Electrocardiogram done one and a half hours after admission showing ST segment elevation in leads V2 and V3.

A repeat ECG 36 hours after the accident revealed T wave inversion in the anterolateral leads (fig 3). She underwent cardiac catheterisation one week after admission. The ventriculogram confirmed mild anterior left ventricular impairment; selective coronary arteriography revealed normal coronary arteries. She was discharged on an angiotensin converting enzyme inhibitor and β-blocker. She was symptom free when seen in clinic three months later. An ECG at that time revealed no evidence of previous anterior myocardial injury (fig 4). An echocardiogram six months following the accident was normal with no evidence of wall motion abnormality. She remained well and symptom free 12 months after the accident, with normal ECG.

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Figure 3

 Electrocardiogram done 36 hours after admission showing T wave inversion in the anterolateral leads.

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Figure 4

 Electrocardiogram three months after accident.

DISCUSSION

There have been previous reports of acute myocardial infarction following blunt chest wall trauma, specially in association with sternal or rib fractures,^10,11 but acute reversible myocardial injury following air bag deployment has not been reported.

In our patient, a diagnosis of acute anterior myocardial infarction was made on the basis of the ECG changes, elevated TNI and left ventricular changes on echocardiography and left ventriculography. Interestingly, she had no rib fractures and selective coronary arteriography revealed normal coronary arteries. However, two normal ECGs (at three and 12 months) and a normal echocardiogram six months following the accident led us to revise our initial diagnosis and suggest that she underwent cardiac contusion rather than a myocardial infarction.

Even though we diagnosed acute myocardial infarction at the time of admission, we felt the patient was not suitable for thrombolysis for three reasons. Firstly, her ECG on admission did not fulfil the criteria for thrombolysis. Secondly, any cardiac damage which she suffered would have been due to transient occlusion of the left anterior coronary artery caused by chest trauma, not by occlusion of the artery by plaque rupture followed by thrombus formation on the denuded plaque. Therefore there was no reason to suppose that she had occlusive thrombus in the coronary artery and consequently no reason to suppose that she would benefit from thrombolysis. Lastly, given the fact that she had experienced chest trauma, even though there were no rib fractures, thrombolysis could have led to haemorrhage into thoracic structures such as the pleural cavity and/or the pericardium with potentially grave consequences.

The current case highlights the facts that (a) myocardial injury can occur even in the absence of rib fractures or chest wall injury as has previously been reported¹⁰ and (b) the diagnosis of myocardial infarction should be made with extreme caution in cases involving chest wall trauma including air bag injuries as it is difficult to differentiate it from myocardial contusion. These patients should therefore have a coronary angiogram to determine the coronary anatomy. In the presence of normal coronary arteries, this should be followed up with repeat investigations to assess the extent of myocardial damage because ECG changes and left ventricular wall abnormalities seen on echocardiography may reverse with time.