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Traumatic Coronary Artery Dissection : Potential Cause of Sudden Death in Soccer
Nicolas M. Van Mieghem, Sander van Weenen, Gijs Nollen, Jurgen Ligthart, Evelyn Regar and
Robert-Jan van Geuns
Circulation. 2013;127:e280-e282
doi: 10.1161/CIRCULATIONAHA.112.119982
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Images in Cardiovascular Medicine
Traumatic Coronary Artery Dissection
Potential Cause of Sudden Death in Soccer
Nicolas M. Van Mieghem, MD; Sander van Weenen, BSc; Gijs Nollen, MD; Jurgen Ligthart, BSc;
Evelyn Regar, MD, PhD; Robert-Jan van Geuns, MD, PhD
A
33-year-old male soccer player started to experience
chest discomfort briefly after taking a blow from an
opponent’s knee into his chest during a dribbling maneuver
on the pitch. He completed the game but then consulted a
referring hospital because of waxing and waning chest
complaints irradiating to his left arm. The ECG demonstrated
ST-T–segment changes compatible with inferoposterior ischemia (Figure 1). Cardiac enzyme markers were elevated.
Echocardiography confirmed inferior wall hypokinesis.
The patient was loaded with aspirin and clopidogrel. He
Figure 1. ECG at baseline.
Figure 2. Selective right coronary angiography in left anterior oblique (right) and
anteroposterior superior projection (left).
Arrow indicates suspect region for dissection and thrombus.
From the Department of Interventional Cardiology, Thoraxcenter, Erasmus Medical Center, Rotterdam, the Netherlands (N.M.V.M., S.v.W., J.L., E.R.,
R.-J.v.G.); and Department of Cardiology, Ikazia Ziekenhuis, Rotterdam, the Netherlands (G.N.).
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIRCULATIONAHA.
112.119982/-/DC1
Correspondence to Nicolas M. Van Mieghem, MD, Department of Interventional Cardiology, Thoraxcenter, ErasmusMC, Room Bd 171, Gravendijkwal
230 3015 CE Rotterdam, The Netherlands. E-mail [email protected]
(Circulation. 2013;127:e280-e282.)
© 2013 American Heart Association, Inc.
Circulation is available at http://circ.ahajournals.org
DOI: 10.1161/CIRCULATIONAHA.112.119982
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e280
Van Mieghem et al
Traumatic Coronary Artery Dissection
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Figure 3. Optical coherence tomography. Top, Longitudinal reconstruction, labels a to d correspond with the cross-sectional panels A
to D below. A shows the atrial side branch (sb) at 7 o’clock and illustrates predominantly lipid-rich plaque from 7 o’clock to 3 o’clock. B
shows red and white thrombus compromising the lumen. C is 5 mm proximal from the thrombus and shows a plaque rupture (arrow). D,
near the ostium of the right coronary artery, shows an intimal dissection (arrow).
subsequently underwent transradial invasive coronary angiography, which demonstrated Thrombolysis In Myocardial
Infarction (TIMI) 2 flow in the right coronary artery and a
dissection-suspect lesion in its proximal segment (onlineonly Data Supplement Movie I and Figure 2). Invasive imaging of the right coronary artery by means of optical coherence
tomography confirmed mild atherosclerotic disease and
unequivocally pointed toward dissection in the proximal segment surrounded by significant thrombus burden (Figure 3
and online-only Data Supplement Movie II). It is noteworthy
that the size of the right coronary artery exceeded 5 mm in
diameter.
Figure 4. Thrombotic debris (arrow) extracted from the right
coronary artery with thrombectomy catheter.
The patient’s young age, his active lifestyle, the large vessel caliber precluding regular stent sizes, and the pathophysiology of trauma rather than atherosclerosis were considered
to proceed with thrombectomy followed by implantation of a
3.5 to 4.5 self-expanding nitinol bare metal STENTYS stent
(STENTYS SA, Paris, France), which is believed to accommodate up to 6-mm vessels (online-only Data Supplement
Movie III). Figure 4 shows the extracted thrombus material.
The final angiographic result was satisfactory (Figure 5 and
online-only Data Supplement Movie IV). Intravascular ultrasound after stent deployment confirmed adequate stent expansion and perfect apposition resulting in a final diameter of 5.5
mm (Figure 6 and online-only Data Supplement Movie V).
The patient was discharged from the hospital with a regimen
of dual-antiplatelet therapy (aspirin and clopidogrel) for 1
Figure 5. Final right coronary angiogram after stenting.
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Circulation
January 22, 2013
Underlying structural or electric cardiovascular disease is
the predominant substrate for sudden cardiac death in athletes.
In a large registry on sudden death in US competitive athletes
covering a 27-year period, preexisting cardiovascular disease
was present in 56%, blunt trauma causing bodily injury of
the head or neck was present in 22%, and precordial blows
leading to commotio cordis was present in 3%.1 High-impact
chest trauma during contact sports can cause traumatic proximal right coronary artery dissection, which can provoke coronary ischemia, myocardial infarction, malignant ventricular
arrhythmias, and even sudden cardiac death. Traumatic coronary artery injury has been reported occasionally, but arguably
is underreported.2,3 A high index of suspicion should trigger
prompt cardiovascular workup including electrocardiography,
echocardiography, evaluation of serial cardiac enzymes, and,
when deemed appropriate, invasive coronary angiography.
Disclosures
None.
References
Figure 6. Intravascular ultrasound examination with confirmation of excellent stent apposition to the vessel wall.
month and low-dose aspirin indefinitely thereafter. In view of
the documented coronary atherosclerosis by invasive coronary
imaging, the patient was also instructed regarding appropriate
lifestyle changes, and statin therapy was initiated.
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in young competitive athletes: analysis of 1866 deaths in the United
States, 1980–2006. Circulation. 2009;119:1085–1092.
2. Hobelmann A, Pham JC, Hsu EB. Case of the month: Right coronary
artery dissection following sports-related blunt trauma. Emerg Med J.
2006;23:580–581.
3. Hazeleger R, van der Wieken R, Slagboom T, Landsaat P. Coronary dissection and occlusion due to sports injury. Circulation.
2001;103:1174–1175.
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