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Case Report

Traumatic Total Occlusion of Left Main Coronary Artery Caused by Blunt Chest Trauma

Omer Goktekin, MD, Ahmet Unal?r, MD, Bulent Gorenek, MD, Gulmira Kudaiberdieva, MD, Yuksel Cavusoglu, MD, Mehmet Melek, MD, Recep Aslan, MD, Bilgin Timuralp, MD
August 2002
Myocardial infarction is a rare complication that can occur immediately after a blunt chest trauma. We report a 36-year-old male who experienced a fatal anterolateral myocardial infarction after a nonpenetrating chest injury sustained in a car accident. The electrocardiogram showed ST elevation in leads D1, avL and V1–V6, right bundle branch block and left anterior hemiblock. Coronary angiography confirmed a total occlusion of the left main coronary artery. The patient showed signs of cardiogenic shock. Although the patient underwent emergency surgical revascularization, he died immediately after the operation. Cardiac trauma resulting from traffic accidents is a cause of death for people involved in such accidents. The incidence rate may be as high as 15% of all blunt chest traumas.1 The spectrum of post-traumatic cardiac lesions varies greatly. Among the recorded consequences are cardiac arrhythmias, septal damage, valve damage, coronary fistulae, coronary artery damage, ventricular aneurysm, cardiac rupture and myocardial infarction.2 Traumatic occlusions and dissections of normal coronary arteries are rare but important complications of blunt chest trauma.3 Injuries of the coronary arteries associated with blunt chest trauma predominantly affect the left anterior descending artery.4 We report the first case of traumatic complete occlusion of the left main coronary artery (LMCA) demonstrated by coronary angiography. Case Report.A previously asymptomatic and healthy 36-year-old male was admitted to our emergency department after a car accident. Upon arrival, the patient appeared tachypneic, restless and diaphoretic. He was fully conscious and complained of severe retrosternal pain. On examination, his periphery was cool, pulse was regular, heart rate was 96 bpm, and blood pressure was 85/50 mmHg. Cardiac examination revealed normal heart sounds and no murmurs were audible. An area of contusion was detectable over the chest wall, and there was tenderness from the second to fourth left ribs. There was right radial and ulnar open fracture and right femoral fracture. The electrocardiogram showed an extensive anterolateral wall myocardial infarction (ST elevation noted in leads avL, D1, V1–V6), right bundle branch and left posterior hemiblock (Figure 1). Thorax roentgenogram detected fractures of the second and third ribs. The patient was put on intravenous heparin, nitroglycerin and analgesics. Thrombolytic therapy was not initiated due to a high bleeding risk after the accident. Considering the persisting severe pain in the chest, which was resistant to intravenous analgesics and nitroglycerin, and signs of hypotension (blood pressure, 70/40 mmHg), emergency coronary angiography was performed within half an hour of admission to the hospital. On angiography, there was a total occlusion of the LMCA (Figure 2), while the large dominant right coronary artery was normal (Figure 3). The patient was taken to the operating room for urgent surgical coronary revascularization. An intraaortic balloon pump was inserted into the aorta just before the operation. The patient developed ventricular fibrillation and was successfully resuscitated, which lasted for 2 minutes. Coronary revascularization was performed under cardiopulmonary bypass through a midsternal splitting incision. On inspection of the operating field right ventricular wall, motions were determined to be normal, and entire anterior, lateral walls and apex of the left ventricle were noncontracting. The site of injury was visible over the left main artery, along with the hematoma formation. No obvious injury along the course of other vessels was detectable. Saphenous venous conduits were grafted to the well-developed first diagonal and left circumflex arteries. Grafting to the left descending artery could not be performed due to its deep intramyocardial course. Although the revascularization procedure was completed successfully, the patient died due to cardiogenic shock. Discussion. Coronary artery occlusion and acute myocardial infarction secondary to blunt chest trauma have been assumed to be a rare occurrence. Blunt chest trauma may cause coronary artery injury, which results in thrombosis,5 dissection,6 laceration,7 fistulas,8 and aneurysm.9 Other mechanisms involved in coronary occlusions are localized spasm over a pre-existing arterosclerotic plaque3 and the appearance of focal myocardial contusion that may compress adjacent areas.10 Findings based on post mortem studies have shown the existence of thrombosis in the coronary artery supplying the infarction area, the intimal tear, and even the rupture of the coronary artery.11 Angiographic findings range from normal to dissection and complete occlusion of the coronary artery, by way of varying degrees of stenosis.12 Traumatic thrombosis and dissection are more common in the left descending artery4 and have also been reported to occur in the right coronary artery.13 Traumatic left main stem lesions seem to be exceptionally rare. Only four cases of traumatic LMCA lesions have been reported. First, Baker et al. reported a case of LMCA thrombosis following mechanical closed chest resuscitation, which ended fatally.14 Untenberg et al. demonstrated a nonocclusive thrombi in the LMCA and distal occlusion of the left anterior descending coronary artery 3 days post-accident.5 Recently, aneurysm and dissection of the left main coronary artery of the LMCA were reported.6,15 To the best of our knowledge, this is the first report of total LMCA occlusion following a blunt chest trauma associated with fatal acute anterolateral myocardial infarction. Coronary angiogram showing a total occlusion of the LMCA was performed immediately after the accident. However, angiogram showed a very large dominant normal right coronary artery, which may have been the reason he survived for some time. Considering the possibility of coronary artery rupture, transluminal revascularization was not undertaken. Thrombolytic therapy was not applied due to the increased bleeding risk after the accident. During the operation, local hematoma was blatantly obvious over the LMCA, which led us to believe that a mechanical trauma occurred in the coronary artery during the impact. We also concluded that this impact may have produced a tear of the intima with subsequent thrombosis. Because we believe that thorough knowledge and clear appearance of the coronary arteries may facilitate a better selection of convenient therapeutic approach, we suggest that an early coronary angiography be considered before any therapy is instituted.
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