Acute Myocardial Infarction in a Young Male While Playing Paintball

Case description. A 25-year-old Filipino male without any prior medical history presented to an outside hospital 1 hour after the acute onset of severe substernal chest pain that developed while playing a vigorous game of professional paintball. The pain increased with sitting up and leaning forward, and was associated with shortness of breath and nausea. The patient denied chest trauma, fevers or chills. Initial electrocardiogram (Figure 1) revealed 2 to 4 mm ST-segment elevation in leads I, II, V2-V6. He was treated with aspirin, heparin and nitroglycerin with resolution of his chest pain. Due to the resolution of his chest pain and the concern over possibility of chest trauma, fibrinolytic therapy was not administered and the patient was transferred to our facility for further management. He had no past medical history and was not taking prescription medications. He was a current smoker with a 5-pack/year history of exposure. He had minimal alcohol use and denied illicit drug use. He was a student, and his family resided in Hawaii, where he had been born and raised. His family history was remarkable only for a grandmother who had had a stroke in her 60s. Review of systems was otherwise negative. In addition, his temperature was 37.6, pulse was 67 beats/minute and regular, blood pressure was 137/65 mmHg in the right arm and 131/60 mmHg in the left arm. Respirations were 10/minute, and oxygen saturation was 97% on room air. He was a well-developed male in mild distress. His lungs were clear to auscultation bilaterally. Cardiovascular examination revealed a normal point of maximal impulse and normal S1 and S2, without murmurs, rubs, or gallops. His pulses were normal throughout. There were no ecchymoses or other overt signs of trauma. The remainder of the physical examination was unremarkable. Laboratory studies at an outside hospital showed a cardiac troponin-I of 0.36 ng/L (normal 0.0–1.5), and creatine phosphokinase of 180 U/L (normal 55–170) with an MB fraction of 5.3 ng/mL (normal 0.0–4.9). Creatinine was 1.0 mg/dl and hematocrit was 46. On arrival at our facility, he was hemodynamically stable without chest pain. Repeat ECG revealed 1 mm ST-segment elevation in leads V2-V5 (Figure 2). Echocardiography revealed akinesis of the anterior wall and apex, with an ejection fraction of 45%. Patient management. The patient was continued on intravenous heparin and was also treated with intravenous nitroglycerin and eptifibatide. He was taken urgently to the cardiac catheterization laboratory. Selective coronary angiography revealed a normal left main coronary artery. The right coronary artery and left circumflex artery were normal. The left anterior descending artery (LAD) contained a large filling defect in the mid segment (Figure 3). Aortic root angiography was normal without evidence of dissection. He developed several episodes of nonsustained ventricular tachycardia during the procedure. He was treated with a bolus of intravenous lidocaine and was hemodynamically stable thereafter. An intra-aortic balloon pump (IABP) was inserted. Because of the large thrombus burden, the presence of TIMI 3 anterograde coronary blood flow, and resolution of his chest pain, it was decided to defer percutaneous intervention at the time of his diagnostic angiography. He was given a half dose of tenecteplase and his intravenous eptifibatide was continued. He had no further chest pain. His creatine phosphokinase level peaked at 1587 ng/ml with a peak MB fraction of 167 ng/ml. Thirty-six hours after treatment with half-dose fibrinolytic therapy and eptifibatide, he was taken back to the cardiac catheterization laboratory for a repeat selective coronary angiography. This revealed a dissection of the LAD with near complete resolution of the thrombus (Figure 4). The first diagonal branch had slow angiographic filling. Due to the absence of a significant stenosis and concern over extending the dissection plane, it was elected not to perform a percutaneous intervention, but instead to treat him medically. He therefore received aspirin, clopidogrel, beta-blocker and enoxaparin. His IABP was weaned and he had no further recurrence of chest pain. He underwent a hypercoagulablity workup which showed no evidence for a hypercoagulable state. The etiology of his spontaneous coronary artery dissection (SCAD) with resultant thrombosis was felt to be extreme physical exertion. He was discharged 5 days after admission. Discharge medications included aspirin, clopidogrel for 6 months, enoxaparin for 5 days, and a beta-blocker. He was counseled to avoid physically strenuous activities for 6 months. The patient did well after discharge and had no further recurrence of his chest pain. He tolerated a cardiac rehabilitation program without limitation. Six months after discharge, his clopidrogel was discontinued, and he resumed playing professional paintball. Repeat echocardiogram revealed akinesis of the apex and hypocontractility of the anterior wall, with an EF of 50%. How Would You Manage This Case? Joshua De Leon, MD Winthrop University Hospital Mineola, New York The management of SCAD is a difficult one, and the authors should be commended for their thoughtful management. While SCAD is a rare cause of acute MI, especially in men, it should be considered in an otherwise healthy patient without clinical risk factors for CAD. Successful treatment is controversial. There are case reports of thrombolytic, surgical, and percutaneous approaches to treatment with varying results. Systemic thrombolysis has been attempted with some success, the concept being that thrombolytic therapy might lyse the thrombus in the false lumen to release the pressure effect on the true lumen. However, there are reports of extension of the dissection with this approach. CABG for SCAD has generally been considered technically difficult, as a result of the need to graft into a dissected coronary artery, and is associated with a high mortality rate and complications occurring with acute MI. This approach is generally for symptomatic patients, who would otherwise benefit from CABG based on usual criteria. Stenting for SCAD has been used successfully, but often presents difficult technical issues, and increased frequency of post-stent thrombotic events have been reported. Conservative management of SCAD has been more widely reported, and outcomes have been favorable in those that have survived the acute phase of the illness. In reviewing the angiographic studies, the initial images suggest dissection distal to the large thrombus in the mid-portion of the LAD. We agree with the authors regarding their concern for a significant clot burden, but given the likelihood of SCAD as the etiology of the presentation and the possibility of extension with thrombolytic therapy, we propose treatment with a GP IIb/IIIa receptor antagonist and heparin for 24–48 hours, followed by repeat coronary angiography and possible intervention. Half-dose tenecteplase would not have been employed. It should be stated that, while debulking the thrombus intuitively makes sense (and is advocated here in one form), this strategy has not been compared to the more conventional one that does not include debulking. Presumably, the IABP was placed for the dysrhythmia occurring during the procedure, and we would probably have done the same for that indication; otherwise the pump would not have been employed. As clearly no specific protocol exists for SCAD, direct intracoronary stenting may have been successful in this instance, extending from the principle that balloon-induced dissections are routinely treated in this manner. However, concerns regarding “unroofing” the dissection, extending the plane, or traumatizing a non-involved portion of the artery are relevant. The same concerns exist for direct stenting after pre-treatment with a distal protection device, and to some extent with mechanical thrombectomy devices. However, given his lack of symptoms and the presence of TIMI grade III flow, conservative management as described, with prolonged aspirin, clopidogrel and close observation after identification of dissection would likely have been our approach. In summary, a conservative, symptom-based management of SCAD is probably best, and our approach to this patient would be quite similar to that of the authors. This case presents the additional dilemma of extreme clot burden in a SCAD patient. Jeffrey A. Werner, MD Mercy Health Systems of Northwest Arkansas Rogers, Arkansas The case submitted is, of course, fascinating. While an acute coronary occlusion due to direct chest trauma is well described, this particular set of circumstances and activities is unique. The rise of enthusiasm for this sport, however, could bring additional cases. Whether the precipitating agent is a paintball gun, baseball or volleyball (all previously described), in my view, the considerations for treatment and prognosis should be similar. Due to the patient’s age and low risk factors for atheroscerotic coronary disease, it would seem that the natural history of CAD, including subsets with an anterior wall infarction would not apply. The long-term prognosis would depend more on the severity of the resulting left ventricular dysfunction and the presence or absence of coexistent ventricular arrythmias. As has been well shown, the risk of untoward events, specifically, sudden cardiac death due to ventricular fibrillation following acute MI, are highest in the first year and drop dramatically in subsequent years. With regard to the specific management applied here, the choices of the clinicians seem very reasonable. Most interventionists would wonder about the advisability of placing 1 or more coronary stents on the day 2 after lowering the thrombus burden. I agree, however, with this patients managing physicians in withholding stenting at this time. The primary reason being the possibility of placing a guidewire in the false lumen which, in looking at these angiograms, would definitely be a risk. Because of the unique nature of this clinical situation, it is virtually impossible to feel firm about a “right” course of action. It may seem reasonable, however, to wait a month or so and do an exercise myocardial perfusion study. Were significant reversible ischemia to be present, the possibility of stenting could be reconsidered on a more elective basis and include the use of IVUS as well as the technique of distal contrast injection through the dilatation balloon to assure that the true lumen has been chosen before placing a stent. Andrey Espinoza, MD and Zoltan G. Turi, MD Drexel University College of Medicine Philadelphia, Pennsylvania This patient presents significant challenges in diagnosis and clinical management. Besides SCAD, there is a long list of important differential diagnoses in this previously healthy patient, including aortic dissection, anomalous coronary origin and other congenital abnormalities, thrombosis secondary to hypercoagulable state, thrombotic or malignant embolic disease, pericarditis, coronary spasm, hematological abnormalities, valvular and other structural heart disease, and a variety of metabolic, connective tissue and inflammatory disorders. Further, although the patient denied chest trauma and illegal drug use, we do not believe the clinician is well served in immediately accepting history alone. One could envision a scenario in which blunt trauma during vigorous physical activity was overlooked, and the authors were right to defer thrombolytic therapy initially. With regard to cocaine, we have seen a nearly identical presentation, including coronary dissection, in a young cocaine abuser. The caveat in that setting is the avoidance of beta blockers: since cocaine causes alpha-adrenergically mediated vasoconstriction, unopposed alpha adrenergic activity may potentiate vasospasm as well as systemic hypertension. With regard to therapy for SCAD, there is little guidance, although a recent review appeared in this Journal.1 Thrombolytic therapy is appealing for thrombus, but potentially life-threatening extension of perivascular hemorrhage has been described.2 GP IIb/IIIa inhibitors have been effective anecdotally. CABG was more commonly recommended a decade ago, although surgeons have reported difficulty identifying the true lumen (leaving a guidewire in place has been suggested, but finding the true lumen has been occasionally impossible). Similarly, coronary stenting has been reported to be successful, particularly since it can seal the proximal origin of the dissection, but identification of the true lumen is still a problem. The algorithm used in this patient was elegant and reasonable, although the effect of intraaortic balloon pumping on coronary dissection in the setting of TIMI 3 flow is unknown. One could hope that the spike in augmented diastolic pressure had no deleterious effect on the dissection plane while potentially decreasing myocardial oxygen demand. Since this patient was asymptomatic, had resolving EKG findings, unimpaired distal flow and good hemodynamics, we would not have chosen this option. Experimental invasive approaches, including the use of distal protection with simultaneous clot extraction, may allow for earlier and possibly safer intervention in this setting. Finally, it is worth commenting on long-term management. First, the histopathologic changes that account for spontaneous coronary dissection have varied in description with the exact mechanism unknown. Vessel wall inflammation, medial degeneration, spontaneous plaque rupture, and ruptured vasa vasorum have been proposed. The important common element is that these involve chronic pathology. Also, two-thirds of patients had persistent or new coronary artery dissections within 6 months (albeit in a post-partum population)3 and recurrent infarction within the first 2 months has been reported. Thus, this patient not only had a life-threatening event, but in our opinion is at risk of recurrence. We would loathe to allow him to return to any professional sport involving intense physical activity, and would keep him on some form of chronic antiplatelet therapy indefinitely.

1. Velusamy M, Fisherkeller M, Keenan ME, et al. Spontaneous coronary artery dissection in a young woman precipitated by retching. J Invas Cardiol 2002;14:198–201. 2. Almahmeed WA, Haykowski M, Boone J, et al. Spontaneous coronary artery dissection in young women. Cathet Cardiovasc Diagn 1996;37:201–205. 3. Koller PT, Cliffe CM, Ridley DJ. Immunosuppressive therapy for peripartum-type spontaneous coronary artery dissection: Case report and review. Clin Cardiol 1998;21:40–46.