Acute myocardial infarction and coronary artery dissection following rugby-related blunt chest trauma in France.

Coronary artery (CA) dissection following blunt chest trauma is a life-threatening and rare event. Its occurrence in the setting of a contact sport like rugby is even less common. We report on two cases of young adult presenting with segment elevation myocardial infarction related to CA dissection following rugby game. Both were successfully treated with stent implantation. We discuss the mechanism, diagnosis, and optimal management of blunt chest trauma-induced CA dissection.

Coronary artery (CA) dissection following blunt chest trauma is a life-threatening and rare event. Its occurrence in the setting of a contact sport like rugby is even less common. We report on two cases of young adult presenting with acute myocardial infarction related to CA dissection following rugby game.

CASE REPORTS

Case 1

A 31-year-old nonprofessional rugby player, with no medical history experienced acute substernal chest pain with dyspnea, shortly after a rugby game. Lungs were clear to auscultation and cardiac examination was normal without murmurs, rubs or gallops. Chest examination revealed no external sign of injury. Initial electrocardiogram (ECG) revealed sinus rate with segment (ST) elevation in V2 to V6 leads with inferior mirror image. Shortly after ECG recording, he presented a sudden cardiac arrest related to ventricular fibrillation, successfully treated by external defibrillation (200J then 300J). Emergency cardiac catheterization showed a proximal left anterior descending (LAD) artery dissection extending into mid-artery, with thrombolysis in myocardial infarction (TIMI) 1 flow. A CYPHER® (Cordis Corporation, Warren, NJ) drug-eluting stent (3.5 mm × 28 mm) was successfully implanted at the proximal LAD and TIMI 3 flow was immediately achieved. Time from initial symptoms to stenting was 2 h 15. Initial high sensitivity troponine T level was normal, but subsequently increased and peaked at 4700 IU/L (normal <14) with creatine phosphokinase (CPK) peak of 3550 IU (normal 39-308). Echocardiography showed moderate hypokinesis of the septum and the anterior wall, with left ventricular ejection fraction (LVEF) of 55%. Right ventricular and valvular functions appeared normal, with no pericardial effusion. He was discharged home 8 days later and remained event-free at 12 months follow-up.

Case 2

A 33-year-old amateur rugby player, without medical history, was admitted for dizziness, nausea with vomiting within 2 h following a rugby game. During this game, he had been struck sharply in the mid-sternum by an opponent's shoulder. At initial examination, the patient denied any chest pain except at anterior costal palpation. Blood pressure was 95/57 and heart rate 55. Cardiac and lung examination was normal. Initial ECG revealed sinus rate with ST elevation in inferior leads with lateral mirror image [Figure 1]. Emergency cardiac catheterization with radial access revealed a proximal right coronary artery (RCA) dissection extending to mid-RCA with TIMI 3 flow [Figure 2]. A PROMUS ELEMENT® (Boston Scientific Corporation, Natick, MA), drug-eluting stent (3.5 mm × 38 mm) was successfully placed in the artery. The time from initial symptoms to stenting was 5 h 45. High sensitivity troponine T level peaked at 6300 IU/L (normal <14) with CPK peak of 4750 IU (normal 39–308). Echocardiography showed moderate hypokinesis of the inferior wall, with LVEF of 58%. Right ventricular and valvular functions appeared normal with no pericardial effusion. He was discharged home 7 days later and referred for enrollment in a cardiac rehabilitation program. He remained event-free at 6 months follow-up.

Figure 1

inferior segment elevation myocardial infarction with antero-lateral mirror image

Figure 2

Right coronary artery dissection from proximal to mid-segment

DISCUSSION

Coronary artery injury resulting in myocardial infarction is an extremely rare complication of blunt chest trauma and is mostly observed in high-speed motor vehicle accidents.[1]

Suspected mechanism of CA dissection is shearing of the coronary vessel wall, caused by dramatic acceleration/deceleration forces, producing intimal tearing. Platelet aggregation and intraluminal thrombosis then follow, explaining possible delayed symptoms.

The LAD CA is most commonly affected (76%), followed by the RCA (12%) and circumflex artery (6%).[2] The higher incidence of LAD CA involvement may relate to its proximity to the chest wall. The RCA may be more prone to injury when blunt chest trauma occurs during ventricular systole, a time when this vessel lies in a more vulnerable anterior position.

The recognition of traumatic CA dissection may be difficult since symptoms can be wrongly attributed to chest wall pain. Blunt chest trauma with myocardial contusion may also produce ECG changings (as ST elevation or depression, Q waves), myocardial enzyme elevation or wall motion abnormalities on echocardiography. Moreover, a significant delay (up to 7 days) between blunt trauma and dissection can be observed and may result from gradual enlargement of the false lumen.

Cases of sports-related traumatic CA dissection are very unusual and have been reported following waterskiing, bicycle accidents and after collisions during basketball, soccer[3] or rugby games.[45]

Prognosis in survivors of CA dissection varies according to the amount of ischemic myocardium and the residual LVEF. Cases of sudden death in sports-related blunt chest trauma that are attributed to commotio cordis (ventricular arrhythmia induced by blunt chest trauma) may, in fact, represent cases of coronary dissection and myocardial infarction.

As with any myocardial infarction, timing is critical in establishing early reperfusion. However, optimal management of traumatic CA dissection is uncertain, most likely because of the rare incidence of the condition. Emergency transfer to the cath lab is pivotal to confirm CA and rule out myocardial contusion. Management options include medical therapy with anticoagulation and antiplatelet agents, angioplasty (with or without stenting) and CA bypass surgery. Thrombolytic therapy should be avoided in the setting of wall chest trauma because of potential catastrophic consequences. Thrombolysis has also been associated with the extension of the dissection by promoting hemorrhage into the false lumen.