A 22-year-old man was admitted to our emergency department with recent-onset chest pain and dyspnea. The patient had experienced chest pain 42 days earlier, and it had lasted 2 days. He smoked cigarettes, 1 pack per day for 4 years, but had no other risk factors for atherosclerosis. His electrocardiogram revealed pathologic Q waves and 2-mm ST elevations in leads V1 through V6—findings that are consistent with subacute myocardial infarction and possible aneurysm formation. Transthoracic echocardiography showed left ventricular regional wall motion abnormalities (akinesia of the apical, septal, and anterior segments), severely reduced global ejection fraction (0.20 by the Simpson method), mild ischemic mitral regurgitation, and a restrictive-type diastolic filling pattern. Coronary angiography showed a linear image consistent with coronary dissection between the proximal left anterior descending coronary artery (LAD) and the 3rd diagonal artery, with Thrombosis in Myocardial Infarction (TIMI)-III flow (Fig. 1A). The left main coronary artery (LMCA), left circumflex coronary artery (LCx), and right coronary artery were normal (Fig. 1B). Positron emission tomography showed a lack of perfusion and metabolism in the apical, anteroseptal, and septal segments and hypometabolism in the basal segments (Fig. 2). Multislice computed tomographic (MSCT) coronary angiography, which was performed to determine whether the dissection extended to the LMCA or the proximal LCx, revealed that the intimal dissection originated from the proximal LAD and continued to the level of the 3rd diagonal artery (Fig. 3A). No dissection was observed in the LMCA or the LCx (Fig. 3B). Rheumatology consultation confirmed no connective tissue disorders. The patient was discharged from the hospital on medical treatment for heart failure, and he was placed on the waiting list for cardiac transplantation.
Fig. 1 Coronary angiography shows A) a linear image consistent with coronary dissection (arrows) between the proximal left anterior descending coronary artery and the 3rd diagonal artery, with Thrombosis in Myocardial Infarction (TIMI)-III flow. B) Another view of the dissection (arrows) shows normal left main coronary and left circumflex arteries.
Fig. 2 Positron emission tomography with 18fluorodeoxyglucose reveals a lack of perfusion and metabolism in the A) apical, septal, and anterolateral segments and hypometabolism in the basal segments. Additional views show nonviable myocardial tissue in the B) anterior segment and C) anteroseptal and anterior segments.
Fig. 3 Multislice computed tomographic coronary angiography reveals A) the intimal dissection (arrows) originating from the proximal left anterior descending coronary artery and continuing to the level of the 3rd diagonal artery. B) Another view of the dissection (arrows) shows that the left main coronary artery and the left circumflex coronary artery are not involved.
Comment
Spontaneous coronary artery dissection is an uncommon cause of acute coronary syndrome and sudden death. Oral contraceptive use, heavy exercise, sexual intercourse, isolated fibromuscular dysplasia, blunt chest trauma, drug use (cocaine), immunosuppression (cyclosporine), Marfan and Ehlers-Danlos syndromes, and some inflammatory diseases (for example, sarcoidosis, Kawasaki, and systemic lupus erythematosus) have been shown to be associated with spontaneous coronary artery dissection.1,2 Coronary angiography is crucial in the diagnosis of spontaneous coronary artery dissection. Intravascular ultrasonography and MSCT are other diagnostic methods. Conservative treatment is suggested for managing stable, asymptomatic patients. Stents have been implanted successfully in selected cases where the true and false lumens were clearly distinguishable and the dissection flap did not involve a long segment.3 Coronary artery bypass surgery is recommended when the dissection involves the LMCA or multiple vessels or when percutaneous intervention fails.4 In our patient, a diagnosis of idiopathic spontaneous coronary artery dissection was established by coronary angiography. The patient was treated conservatively due to the length of the dissection and the absence of myocardial viability in the affected areas, as confirmed by positron emission tomography.
Footnotes
Address for reprints: Emre Gurel, MD, Canbaziye Mh., Abdullahdede Sk., Yuvam Apt. 10/3, 34107 Kocamustafapasa, Istanbul, Turkey
E-mail: emregurelctf@yahoo.com
References
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- 2.Capuano C, Sesana M, Predolini S, Leonzi O, Cuccia C. Literature review: spontaneous coronary artery dissections. Cardiovasc Revasc Med 2006;7(4):231–3. [DOI] [PubMed]
- 3.Roig S, Gomez JA, Fiol M, Guindo J, Perez J, Carrillo A, et al. Spontaneous coronary artery dissection causing acute coronary syndrome: an early diagnosis implies a good prognosis. Am J Emerg Med 2003;21(7):549–51. [DOI] [PubMed]
- 4.Mohamed HA, Eshawesh A, Habib N. Spontaneous coronary artery dissection–a case report and review of the literature. Angiology 2002;53(2):205–11. [DOI] [PubMed]



