Spontaneous coronary artery dissection following low-intensity blunt chest trauma: a case report and review of current treatment options

Spontaneous coronary artery dissection is the non-iatrogenic, clinical occurrence of acute separation of the arterial media from the intima by hemorrhage. Impingement of the false lumen into the true lumen can cause myocardial ischemia or infarction.1 In women the left anterior descending or left main coronary artery is most commonly involved, while in men the right coronary artery is most commonly involved.1 Although it is a rare cause of acute coronary syndromes, there seem to be several associated risk factors (Table 1). We report a case of dissection of the second obtuse marginal branch of the circumflex artery following minimal chest trauma in a middle-aged, otherwise healthy male. Review of the literature regarding trauma-induced coronary artery dissection describes high-impact injuries, such as motor vehicle accidents, as the preceding insult. To our knowledge, this is the first reported case of coronary artery dissection associated with relatively low-intensity chest trauma. Additionally, we review the current treatment strategies for this rare event. Case Report. A 49-year-old man presented to an outside institution with the chief complaint of a brief but severe episode of left shoulder pain, preceded earlier in the day by an episode of presyncope, nausea and diaphoresis. The patient had a history significant for treated non-familial hyperlipidemia. He had no history of known coronary artery disease or other identifiable atherosclerotic risk factors, i.e., smoking, hypertension, diabetes, or first-degree relatives with a history of premature coronary or vascular disease, and no use of cocaine or other unprescribed drugs. Two days prior to presentation, he was involved in a physical altercation during which he was “grabbed around the chest”. He reported that another individual used his arms to restrain him from entering a room. He was not struck with a fist or other object. This resulted in a visible bruise on his left chest. Approximately 36 hours following this event, while at work, he experienced the sudden onset of profound lightheadedness, nausea and diaphoresis. He immediately rested and the symptoms spontaneously resolved in 15–20 minutes. Later that evening, he experienced severe left shoulder pain, which resolved spontaneously in one to two minutes. This prompted the patient to present to the emergency department of an outside institution, where he was asymptomatic and hemodynamically stable. His cardiovascular and pulmonary exams were normal and he did not demonstrate any signs of congestive heart failure. Of note, there was an approximately 6 x 4 cm ecchymotic bruise centered near the left midaxillary line without hematoma. His electrocardiogram demonstrated normal sinus rhythm with Q-waves in the inferior leads as well as prominent R-waves in leads V1 and V2, without significant ST-segment deviation, consistent with an inferoposterior myocardial infarction, which was not seen on prior ECG. The chest x-ray was normal with a normal cardiac silhouette and no rib fractures. His cardiac enzymes were markedly abnormal with a troponin of 26.3 ng/ml and a creatine kinase of 831 mg/dl. He was transferred to our institution and treated with aspirin, clopidogrel, metoprolol, nitroglycerin, enoxaparin and atorvastatin as treatment of acute coronary syndrome. During the initial portion of his hospitalization, he had a short run of non-sustained ventricular tachycardia. He subsequently underwent coronary angiography and left ventriculography. This demonstrated a 3-cm long dissection of the mid portion of the second obtuse marginal branch of the circumflex artery, with total occlusion distal to the dissection (Figures 1 and 2). No other epicardial coronary disease was noted. The left ventricle demonstrated moderate hypokinesis of the diaphragmatic wall; the remaining segments were all mildly hypokinetic. The fact that he had been asymptomatic and hemodynamically stable over the prior 36 hours, with decreasing troponin levels, suggested that the dissection was stable and not evolving. The distal location of the lesion, the relatively small area of myocardium supplied by this vessel and the involvement of only one vessel favored a conservative approach with medical management. This consisted of aspirin, beta-blocker, HMG CoA reductase inhibitor and angiotensin-converting enzyme inhibitor. The remainder of his hospital course was uneventful. On clinical follow-up, approximately three months after his hospitalization, he returned to his normal active lifestyle without any recurrence of symptoms compatible with angina or congestive heart failure. The pathophysiology of coronary dissection attributed to blunt chest trauma is presumed to be related to deceleration injury. Delay in onset of symptoms may be related to the time to development of false lumen impingement into the true lumen. The type of traumatic insult as described in this case is relatively minor to the degree of trauma which has been previously described as resulting in coronary artery dissection. Examples from the literature include motor vehicle accidents, a water-skiing accident and a horseback riding injury. Table 1. Etiologic factors in spontaneous coronary artery dissection • Middle aged, female sex • Peri or post partum state • Oral contraceptive use2,3 • Presence of atherosclerotic coronary disease4–7 • Presence of multiple risk factors for atherosclerotic vascular disease3,8 • Intense physical exertion6,9 • Connective tissue disorders (Ehlers-Dahnlos syndrome and alpha-1 antitypsin deficiency10,11 • Cocaine abuse12,13 • High-impact blunt chest trauma14–18 Discussion. Treatment options for coronary artery dissection include medical therapy (which has included thrombolytics, antithrombin and antiplatelet agents), angioplasty with or without stenting, bypass surgery and in extreme cases, cardiac transplantation. There are no trials designed to evaluate and compare these strategies, and given the uncommon nature of this event, such trials are unlikely to be performed. As a result there are no established guidelines for treatment of such patients. Sudden cardiac death is a common mode of presentation and early mortality is at least 50%.19–21 Fortunately, previous case reports demonstrate favorable mortality for patients who survive to time of angiographic diagnosis, regardless of subsequent treatment, although this may reflect the bias of the reported literature. Upon presentation, differentiating acute coronary syndrome resulting from an atherothrombotic etiology from coronary dissection is not usually possible, although it may be suspected in certain situations, particularly in young, pregnant or peripartum females without traditional cardiovascular risk factors. Consequently, there are several reports of such patients receiving traditional medical therapy for acute coronary syndrome, including thrombolytic and glycoprotein IIb/IIIa antagonist therapy.9,22–26 Diagnosis of dissection was subsequently made angiographically when patients failed to clinically reperfuse or showed signs of ongoing ischemia. There are some reports, which describe good outcomes in cases in which these agents were used.9,25,26 However, it would seem advisable to avoid thrombolytics and glycoprotein IIb/IIIa antagonists if there is suspicion for coronary dissection, as thrombosis is not the pathophysiologic mechanism and there is a risk of propagation of the dissection with these agents.22,24 Rather, if there is suspicion for coronary dissection, one should have a low threshold to proceed to urgent coronary angiography. Generally, treatment modality is dictated by the clinical scenario. Important factors to consider when establishing a therapeutic plan should include location and extent of dissection, resolution or continuation of symptoms, recurrence of symptoms following initial event, hemodynamic stability and resultant left ventricular function. Factors which would favor a more aggressive treatment strategy include evidence of ongoing ischemia, left main or proximal left anterior descending coronary artery involvement, or jeopardy of a large area of myocardium. In many situations, if these features are not present, a conservative treatment strategy is favored, and complete healing may in fact be observed on follow-up angiography.9,18,28 Revascularization is complicated by the usual rates of graft disease and restenosis.6 The reported rate of recurrence of conservatively managed patients ranges from 3–20%.3,6,19

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