Acute Myocardial Infarction Following Right Coronary Artery Dissection due to Blunt Trauma.

Despite the frequent occurrence of blunt chest trauma, associated cardiac injuries are relatively rare. The most common presentation of blunt cardiac injury is benign arrhythmia (e.g., sinus tachycardia), followed in decreasing frequency by increasingly severe arrhythmias and finally physically evident injuries to the heart muscle, the conducting system, cardiac valves, and/or coronary vessels. Here we present an unusual case of a patient who sustained a right coronary artery dissection and associated acute myocardial infarction following a motor vehicle crash.

INTRODUCTION

Blunt chest trauma is among the most commonly seen problems in traumatology.[1] In addition to the ubiquitous musculoskeletal thoracic injuries (i.e., rib fractures, spine fractures, pulmonary contusions), a number of less common injuries that clinicians must be aware of, have been reported.[2345] Among those are blunt cardiac injuries which can present as a spectrum that spans from cardiac “concussion” and contusion to acute posttraumatic valvular and coronary artery changes.[356]

Manifestations and patterns of more severe cardiac injuries may include myocardial contusion, hemorrhage, simple or complex arrhythmias, myocardial infarction, septal and/or free wall ruptures, valvular pathologies, ventricular aneurysm, and even coronary artery thrombosis.[235789] Ischemic heart disease due to coronary artery dissection following blunt trauma is extremely rare.[891011] After ruling out preexisting coronary disease as the primary cause, myocardial infarction associated with blunt trauma should raise the suspicion of coronary artery injury.[3510] Here we present a case of a young man who was diagnosed with acute myocardial infarction due to right coronary artery (RCA) dissection after blunt chest trauma sustained during a motor vehicle crash.

CASE REPORT

A 25-year-old male, an unrestrained driver, was involved in a motor vehicle crash. He denied the loss of consciousness. He did not require dedicated extrication procedures at the scene. Upon arrival to the trauma resuscitation area, he was hemodynamically stable (blood pressure of 148/93 mmHg, heart rate 70 beats/min), and alert, with Glasgow Coma Scale of 15. His primary trauma survey was unremarkable. The secondary trauma survey revealed a complex parietal scalp laceration with a degloving component, as well as a right knee complex laceration. Upon further questioning, the patient admitted that he is a poly-substance user, including alcohol, marijuana, and cocaine. His initial hemoglobin value was 16.2 g/dL (lowest hemoglobin during entire hospitalization was 11.2 on day 3).

The patient was subsequently taken to the computed tomography (CT) scanner where images of his head, cervical spine, chest, abdomen, and pelvis were obtained. He also underwent plain film imaging of his right knee. Examination of CT images showed that he had an unstable sixth cervical vertebral fracture as well as a second lumbar vertebral fracture associated with significant canal stenosis. Despite these injuries, the patient was neurologically intact and moving all extremities. His qualitative urine drug screen was positive for cocaine metabolites and tetrahydrocannabinol. The remainder of his imaging and laboratory workup was unremarkable.

His scalp laceration was closed in the Emergency Department. His right knee laceration was primarily closed after it was determined that there was no associated fracture or joint violation. Neurological surgery evaluated the patient for this C6 and L2 fractures, with a preliminary plan made for an operative intervention the next morning. In the interim, the patient was admitted to the surgical Intensive Care Unit (SICU) for close neurologic monitoring. Approximately 12 h following his SICU admission, the patient complained of acute mid-sternal chest pain. A 12-lead electrocardiogram (EKG) [Figure 1] and serum troponin (Tn) levels were obtained.

Figure 1

An 12-lead electrocardiogram showing acute ST-segment changes in leads II, III, and VF (shaded in light blue)

The patient's EKG showed acute ST-segment elevations in leads II, III, and AVF [Figure 1]. He was also noted to have elevated initial Tn-I, at 0.16 ng/mL, which subsequently trended higher (5.36 ng/mL at 6 h). Given the above findings, the patient was diagnosed with an acute ST-elevation myocardial infarction (STEMI). Cardiology service was consulted, and the initial attribution of the STEMI was given to a possible coronary vasospasm phenomenon associated with cocaine use. A transthoracic echocardiogram was obtained, demonstrating a left ventricular ejection fraction of 65%. However, hypokinesis was noted in the mid-inferior lateral wall of the right ventricle. In the interim, his Tn-I began to normalize (5.22 ng/mL at 12 h and 2.00 ng/mL at 24 h). Given the above findings, combined with the contraindication to anticoagulation (due to significant spinal injuries) and the concurrent contraindication for beta blocker use (due to very recent cocaine use), it was decided that spinal fixation should be the first management step.

During the subsequent 24 h, the patient's chest pain had resolved, and a repeat EKG showed resolution of the ST segment elevations. The patient underwent fixation of the sixth cervical vertebral fracture and fixation/decompression of the fifth lumbar vertebral fracture. He tolerated the procedures very well. Given an uneventful immediate postoperative period, the patient underwent cardiac catheterization at 48 h following his neurosurgical spinal procedure. The catheterization demonstrated that the patient's proximal RCA developed a focal dissection [Figure 2], with preserved distal right coronary flow. This was deemed to be the proximal cause of the patient's acute chest pain and STEMI. Since more than 48 h had passed since his neurological surgery, it was decided that aspirin use was safe at this point. Because the patient remained asymptomatic, it was felt that coronary stenting was not necessary. Consequently, he was placed on oral aspirin 325 mg daily, and beta blockers were initiated with the caveat that the patient would not be continuing to use cocaine.

Figure 2

Cardiac catheterization images showing selective angiograms of the right coronary artery. Circled areas of the right coronary artery correspond to different images of the right coronary artery dissection (middle image, inset, and arrow). There was no evidence of associated right coronary artery thrombosis, and the distal right coronary artery was patent, with no evidence of stenosis or filling defects

The patient was discharged from the hospital on postinjury day 8, symptom-free from a cardiac standpoint, and recovering well from neurosurgical perspective. His predischarge assessment also cleared him for release to home with a regimen of outpatient physical therapy. He subsequently underwent a follow-up cardiac catheterization at 6 weeks postdischarge. Findings included complete resolution of his RCA dissection, without any evidence of thrombosis or other residual abnormality [Figure 3]. In addition, his follow-up on left ventricular ejection fraction was 70%, with no residual hypokinesis observed.

Figure 3

Follow-up cardiac catheterization demonstrates complete resolution of the right coronary artery dissection (areas corresponding to acute abnormalities noted on the initial cardiac catheterization – see Figure 2 – are circled)

The patient also denied any acute cardiovascular symptoms. He had abstained from drugs, alcohol, and tobacco. The final therapeutic plan, following the second cardiac catheterization, was to continue the aspirin for another month and follow-up with cardiology as needed. Beta blockers were also discontinued at this point.

DISCUSSION

The incidence of coronary artery dissection is very low.[12] Coronary artery dissection following blunt thoracic injury is seen even less frequent.[13] Traumatic coronary artery dissection is most commonly seen in the left anterior descending distribution (76%), followed by the RCA (12%), and rarely in the circumflex (6%) distribution.[1415] The mechanism, while not well understood, probably involves intimal tearing secondary to injury from deceleration, compression of the artery between the heart and sternum, or coronary spasm.[16] Similar to other rare types of arterial pathology, the diagnosis of coronary dissection is often delayed due to limited practitioner awareness combined with very low incidence.[1718] In the current case, it was initially believed that the patient experienced a STEMI secondary to cocaine abuse. However, this line of reasoning actually delayed the correct diagnosis.

Typically, a traumatic coronary artery dissection will manifest on EKG as hyperacute T-waves in the distribution of the affected territory.[19] This subsequently evolves into ST-segment elevation.[19] The management of traumatic coronary artery dissection remains controversial and there is no clearly established standard of care. Procedural intervention is indicated if pathologic findings are severe, including aneurysm formation, ventricular septal defect, or complete arterial occlusion associated with the dissection.[20] While the definitive diagnosis is made via cardiac catheterization, the decision to place a stent must be made on a case-by-case basis. In the current case, the decision was made not to stent the patient's RCA, and conservative management was elected with close follow-up. As demonstrated on follow-up coronary angiography, there was a complete angiographic resolution of the traumatic coronary dissection with combined aspirin/beta blocker combination therapy. The nonoperative/noninterventional approach in selected arterial injury cases is now well-established and generally accepted.[21]

CONCLUSIONS

Coronary artery dissection, although very rare, must be considered after blunt force trauma to the thorax that is accompanied by ischemic EKG changes, chest pain, and elevated troponins. The current case is unique because it highlights the management of this unusual finding in the context of other competing priorities (e.g., preinjury cocaine use and severe spinal trauma). Finally, this report illustrates very well the natural history of traumatic coronary artery dissection, including its complete resolution within 6 weeks of acute presentation with combined aspirin and beta blocker therapy.

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Conflicts of interest

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