A blunt chest trauma causing left anterior descending artery dissection and acute myocardial infarction treated by deferred angioplasty.

Traumatic coronary artery dissection is an uncommon cause of acute myocardial infarction (AMI). We report a case of blunt chest trauma resulting from a motorcycle collision causing ostial dissection of the left anterior descending (LAD) artery in a 31-year-old previously healthy male. The patient also suffered from compound comminuted fractures of the humerus and ulna and severe liver laceration, which hampered both percutaneous and surgical acute revasularization. After a stormy hospital course, a bare metal stent was implanted to seal the LAD artery dissection. The patient was discharged in a stable condition and was followed-up for rehabilitation. This case report underscores the multidisciplinary approach in facing challenges encountered after rare sequelae of chest trauma.

INTRODUCTION

Blunt chest trauma might lead to various cardiac injuries ranging from simple arrhythmias to fatal cardiac rupture. Only a few reports in the literature for coronary injuries proven by coronary angiography highlighted therapeutic percutaneous or surgical revascularization modalities.[1] We report a case of blunt chest trauma creating dissection causing subtotal occlusion of the LAD artery culminating in AMI and treated by deferred angioplasty. The challenges encountered in the management are discussed.

CASE PRESENTATION

A 31-year-old, previously healthy man sustained a blunt chest trauma after a motorcycle collision. The patient was conscious but with multiple bruises. Heart rate was 88 per minute, blood pressure 103/53 mmHg and pulse oximetry 97%. An electrocardiogram (ECG) showed 3-mm ST-segment elevation in leads I, aVL and V1-2 [Figure 1]. X-rays showed humerus shaft and ulnar olecranon compound comminuted fractures. Chest computed tomography (CT) revealed thin-rimmed left-sided pneumothorax, bilateral pulmonary contusion and fractures of the left 1st and 6th ribs. Abdominal CT demonstrated right hepatic lobe focal contusion of 4.0 cm × 3.0 cm, with adjacent laceration of 5.0 cm length (grade III hepatic injury). Transthoracic echocardiogram (TTE) demonstrated akinetic apex, hypokinetic anterior septum and anterior wall segments with left ventricular ejection fraction (LVEF) of 42%. Initial creatine kinase-MB was 32 ng/mL and troponin-T was 0.35 ng/mL. The condition was diagnosed as coronary artery injury secondary to cardiac contusion causing anterolateral AMI.

Figure 1

An electrocardiogram obtained in the emergency room showed normal sinus rhythm with 3-mm ST-segment elevation in leads I, aVL and V1-2

A multidisciplinary plan involving a cardiologist, anesthesiologist, cardiac, orthopedist and general surgeon was initiated. The arm fractures were stabilized with a cast. In view of the findings of acute severe liver injury and compound fractures, fibrinolytic therapy was abandoned and the patient was treated conservatively with B-blocker and nitrate and, also, a decision was made to avoid antithrombotic treatment, including antiplatelets and heparin because of the risk of bleeding. However, aspirin was started when the patient was in stable condition.

On the third hospital day, repeat TTE demonstrated a highly mobile echogenic mass in the right ventricular outflow tract (RVOT). A transesophageal echocardiogram confirmed the presence of a 1.1 cm x 1.2 cm mass just below the posterior leaflet of the pulmonary valve prolapsing into RVOT during systole, raising the possibility of thrombus. A chest CT with contrast confirmed the diagnosis of pulmonary embolism, and intravenous unfractionated heparin was initiated. The following day, the patient progressed to respiratory failure and was put on assisted mechanical ventilation. Coronary angiogram revealed a subtotal ostial occlusion and filling defect with clot in the mid-segment of the LAD artery while the other coronaries were normal [Figure 2a]. The cardiology team elected to continue managing him conservatively in view of the need for planned orthopedic surgery of the wound and compound comminuted fractures of the arm and to repeat angiography with possible Percutaneous coronary intervention (PCI) after surgery.

Figure 2

(a) Coronary angiogram revealing a subtotal ostial occlusion and filling defect with clot in the mid segment of the left anterior descending coronary artery (arrow). (b) Post angioplasty and stent angiogram

On the fourteenth hospital day, while the patient was still on mechanical ventilation, he developed hypotension and compromised peripheral circulation followed by fever with leucocytosis and severe pulmonary edema. The patient was managed with central monitoring, inotropes, diuretic, heparin and empiric combination antibiotics. The hemodynamics improved and he was weaned off the ventilator after 11 days.

Abdominal ultrasound showed no evidence of liver contusion after 10 days of trauma. A repeat TTE showed no intracardiac masses, but there was a significant drop in LVEF from 42% to 26%. During this period of deterioration, the orthopedic surgeon elected conservative therapy, following up the patient's open wound closely. Thereafter, a repeated coronary angiogram was performed and a 3.0 mm × 23 mm bare metal stent was successfully implanted, sealing the dissection and maintaining normal flow distally [Figure 2b]. He was discharged in stable condition on aspirin, clopidogrel, diuretic, B-blocker and an angiotensin-converting enzyme inhibitor and followed for rehabilitation.

DISCUSSION

The causative mechanisms of coronary artery injuries after blunt chest trauma are hypothesized to be vascular spasm, dissection, and intimal tear or rupture of an existing plaque with thrombus formation.[2] Recently, several reports described coronary artery dissection following blunt chest trauma, which might reflect the previous underestimation of this sequale.[1-5] Chest pain might be masked by other injuries; nevertheless, a strong clinical suspicion is warranted.

Our case was easily recognized within the first hour of trauma because of chest pain and significant ECG. The first challenge prompted was the reperfusion management. In our opinion, if coronary angiography and revascularization are performed early after the onset of ischemia, myocardial tissue may be significantly salvaged. PCI, both with or without stent implantation, has been performed with successful revascularization and reversal of ST-elevations.[16] However, in view of acute severe liver lacerations and arm compound fractures in this patient, both percutaneous and surgical interventional procedures were avoided to minimize potential bleeding hazard with antiplatelet and heparin. However, cases adapting this strategy have reported a post-infarction sequelae with reduced ejection fraction.[7] Although fibrinolytic therapy has been given to certain patients after mild chest trauma,[8] we were prudent not to use such strategy in patient for the same reasons, i.e., the potential for bleeding.

We believe that severe liver lacerations were an obstacle against early intervention of the infarct-related artery, and waiting for a more suitable time may lead to unpredicted complications.

Another challenge that we faced three days post trauma was when, the patient had pulmonary embolism complicated by respiratory compromise. This was when we opted to use heparin to reduce the risk of further thrombosis along with aspirin, which was started earlier. Anticoagulation to manage acute pulmonary embolism was a two-edged-sward in this particular patient. Nevertheless, uneventful anticoagulation might encourage PCI. The diagnostic coronary angiogram revealed dissection causing subtotal ostial LAD occlusion, but conservative treatment continued in view of a planned orthopedic surgery and possible PCI was deferred.

Despite meticulous conservative care, we believe that patients with traumatic coronary artery dissection associated with multiple traumatic injuries, such as in our patients, should have the opportunity of PCI as long as patient is in a favorable clinical status to prevent further deterioration in LV function and occurrence of unpredicted complications.

CONCLUSION

Blunt cardiac injury caused primarily by motor vehicle collisions encompasses a spectrum of pathology ranging from clinically silent, transient dysrhythmia to deadly free wall rupture. It carries a high mortality rate, yet no reliable diagnostic test exists to identify those patients at greatest risk for an adverse outcome. A high index of suspicion is mandatory in combination with electrocardiogram, troponin, and echocardiography as well as appropriate coronary angiography to improve diagnosis and risk stratification. In addition, we believe that a multidisciplinary approach to the management of complicated cases of blunt cardiac injury with coronary dissection, as in our patient, led to a successful outcome. This case highlights the management challenges in this subset of patients.