Case Report. A 35-year-old healthy male with no significant previous medical illness presented to the emergency room with 24 hours of dull constant pain across his chest. Prior to the onset, he had collided with another player during a competitive soccer game, sustaining a blow from the other player’s elbow to his chest that knocked him to the ground. He experienced transient dyspnea, but was able to return to the game. He developed chest pain while driving home, approximately 40 minutes after the collision during the soccer game. It was not exertional or positional, did not radiate, and had no associated dyspnea. The chest pain persisted over the next 24 hours and was associated with intermittent diaphoresis, nausea, and small emesis. The patient’s only cardiac risk factor was smoking. The patient ultimately presented to the emergency room at the insistence of his wife approximately 24 hours after the chest pain began. On examination, he appeared relaxed and was in no acute distress. His pulse was regular at 66 beats per minute, with an occasional premature beat, and his blood pressure was 136/82 mmHg. There was no ecchymosis or swelling over his chest. He was mildly tender to palpation over his sternum and left anterior chest wall. There was no palpable bony deformity or crepitus. The patient had distinct first and second heart sounds with no gallops, murmurs, or rubs. The lungs were clear to auscultation bilaterally. His chest x-ray was normal and revealed no rib fractures or cardiomegaly. His electrocardiogram showed persistent anterior ST-segment elevation in leads V1-V4, Q-waves in leads V1-V2, and transient accelerated idioventricular rhythm consistent with acute anterior myocardial infarction (Figure 1). Troponin-I was elevated at 32.4. The patient underwent emergent coronary angiography which revealed a right dominant system and a 100% thrombotic occlusion of the proximal left anterior descending artery with distal filling from the left circumflex and right coronary arteries (Figure 2). No evidence of atherosclerotic disease was seen in any of the coronary vessels or the aorta. Coronary intervention was performed using an AngioJet rheolytic thrombectomy device. Following extraction of the thrombus, repeat angiography showed a spiral dissection of the proximal left anterior descending artery (Figure 3). The residual stenosis was then pre-dilated with a 2.5 mm x 15 mm Cross-Sail balloon (Guidant, Santa Clara, California), stented with a 3.0 mm x 33 mm Velocity stent (Cordis, Miami, Florida) and post-dilated with a 3.0 mm x 18 mm non-compliant Power-Sail balloon. Excellent results were achieved with 0% stenosis and TIMI-3 flow (Figure 4). An intra-aortic balloon pump was placed for 12 hours. The patient tolerated the procedure well, and his chest pain was relieved completely. He was placed on abciximab for twelve hours and started on clopidogrel, metoprolol, lisinopril, and lovastatin. An echocardiogram done post-procedure revealed mild to moderate decreased left ventricular function with an estimated ejection fraction of 40% and a moderate region of hypokinesis involving the anterior, septal, and apical segments. He was transferred to the intensive care unit for 24 hours of observation and then to the telemetry unit. Troponin-I peaked at 41.2. The remainder of his hospital course was uneventful. He underwent in-patient cardiac rehabilitation and was discharged from the hospital three days later. On follow-up four months after his discharge, the patient was doing well with no recurrence of his symptoms. He began to play soccer again without any difficulties. A repeat echocardiogram at one year showed recovery of normal left ventricular function with a small area of mild septal hypokinesis. Discussion. Cardiac injury secondary to trauma has been well described and has been reported to occur in an estimated 15% of patients with blunt chest trauma.1 In patients who sustain severe chest trauma, the rate has been shown to be as high as 55%.2 Injuries include arrhythmia, myocardial contusion, valvular damage, vessel aneurysm or dissection, pericarditis, septal damage, and ventricular wall rupture.3 Myocardial infarction secondary to blunt chest trauma is a rare event. A review of the literature since 1970 reveals 58 reported cases of coronary artery dissection and/or occlusion resulting from blunt chest trauma. Greater than 50% of the reported cases of myocardial infarction secondary to blunt chest trauma involved a motor vehicle collision.4 As this case and three other cases involving contact sports illustrate, the presence of myocardial infarction cannot be excluded based on the nature of the trauma.5–7 The differential diagnosis for sudden cardiac death among patients who suffer blunt chest trauma should include both ventricular arrhythmia (commotio cordis) and myocardial infarction secondary to coronary dissection and thrombotic occlusion. Greenberg et al. describe a case in which a 35-year-old woman was evaluated at two different emergency rooms over two days for chest pain following mild chest trauma from waterskiing and diagnosed with musculoskeletal pain. The next day she went into cardiopulmonary arrest and was declared brain-dead eight days later. Autopsy confirmed acute dissection of the circumflex coronary artery presumed secondary to blunt chest trauma.8 The left anterior descending artery is the most frequently injured vessel (76%), followed by the right coronary artery (12%), and the circumflex coronary artery (6%).9 This is explained by the anatomic location of the arteries in relation to direct chest trauma.10 Initially, it was thought that occlusion of the artery occurred secondary to the traumatic rupture of a pre-existing atherosclerotic plaque. Further reports and post-mortem studies suggest it is possible for a normal coronary artery to become occluded secondary to intimal or subintimal tears with or without the presence of dissection.11 These tears frequently occur in the proximal portion of vessels which are the most susceptible to acceleration and deceleration forces.10 It is proposed that given this patient’s young age, only one cardiac risk factor, and otherwise normal coronaries, his acute myocardial infarction was secondary to thrombus formation resulting from traumatic intimal tearing and dissection. Management of patients with myocardial infarction secondary to trauma remains controversial due to its rare incidence and its frequent association with other traumatic injuries. Conservative management has been suggested to result in aneurysmal disease in 30% of patients.9 In one case report of proximal left anterior descending artery obstruction secondary to chest trauma from a motor vehicle accident, conservative management was chosen due to the presence of other severe injuries. The patient survived the event, but later developed severe congestive heart failure and is being considered for a heart transplant.4 Thrombolytic therapy in the setting of blunt trauma has been attempted but is controversial, as it could lead to significant bleeding in the presence of other non-cardiac injuries. Two cases reported successful use of thrombolytic therapy in patients with blunt chest trauma, one systemically and one with intracoronary delivery.5,12 Other cases using thrombolytic therapy have been unsuccessful and it is argued that this may be due in part to the frequent presence of an associated dissection with the thrombus.6 It is difficult to know the true failure rate of thrombolytics since the cases are presumably under-reported. Two cases have demonstrated the successful use of coronary angioplasty and stenting in the setting of an occlusive dissection of a right coronary artery after blunt chest trauma.9,13 The case we present expands support for this treatment modality. To the best of our knowledge, this is the first reported successful use of both rheolytic thrombectomy and coronary stenting to reperfuse a vessel in this setting. Although rarely reported, myocardial infarction secondary to injury of the coronary arteries may be under-diagnosed and should be considered in patients with blunt chest trauma and signs of ischemia. Troponins and creatinine kinase concentrations may be unreliable in this setting, as they are frequently elevated secondary to contusion of the myocardium.14,15 Coronary angiography remains the gold standard to confirm the diagnosis if concern is high. As shown by this case and those discussed above, primary coronary angioplasty and stenting, with possible combination of rheolytic thrombectomy in the setting of blunt chest trauma, may be more beneficial than conservative management or thrombolytic therapy.
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