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A Woman With Multiparity Experiencing Chest Pain in Her Early 60s

Educational Objective
Based on this clinical scenario and the accompanying image, understand how to arrive at a correct diagnosis.
1 Credit CME

A woman in her early 60s with a medical history of chest pain requiring a coronary angiogram (which demonstrated only mild luminal irregularities) approximately 1 year prior to presentation, hypertension, long-standing dyslipidemia, and multiparity presented to the emergency department with a sudden onset of dull, pressurelike chest pain radiating to the left arm. The pain started at rest, was 10 of 10 in severity, and was not alleviated by changing position. She also experienced concomitant nausea and diaphoresis. Her family history was notable for hypertension, and no other systemic diseases were reported. On physical examination, her blood pressure was 115/76 mm Hg, heart rate was regular at 72 beats per minute, respiratory rate was 20 breaths per minute, and oxygen saturation level was 98% on room air. The patient was afebrile. Physical examination also revealed mild bibasilar crackles and jugular venous distention, and no murmurs or lower extremity edema. Laboratory test results demonstrated an elevated troponin, and the 12-lead electrocardiogram showed marked ST-segment elevations in leads V2 to V5 (Figure, A). The ST-segment elevation myocardial infarction (STEMI) pager was activated, and the patient was transferred urgently to the catheterization laboratory. Coronary angiography of the patient’s left anterior descending coronary artery was performed, and the findings are depicted in the Figure, B.

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Spontaneous coronary artery dissection

C. Treat medically with aspirin, β-blocker, clopidogrel, and a statin

Spontaneous coronary artery dissection (SCAD) is a nontraumatic and noniatrogenic separation of the coronary arterial wall, typically leading to the formation of a false lumen, in the presence or absence of significant obstructive coronary artery disease.1 While the precise pathophysiological mechanism remains unclear, a tear in the intima of a coronary vessel or the development of an intramural hematoma due to bleeding from the rupture of the vasa vasorum have been suggested as possibilities.2,3 The disease process tends to affect women, particularly young women, with underlying fibromuscular dysplasia or other connective tissue disease (such as Marfan syndrome, Loeys-Dietz syndrome, and Ehlers-Danlos syndrome type 4).4 Hormonal therapy and postpartum or multiparous state are also known risk factors. Without early detection and treatment, SCAD can be life-threatening.3,5,6

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Article Information

Corresponding Author: Prakriti Gaba, MD, Department of Internal Medicine, Columbia University Medical Center, 622 W 168th St, New York, NY 10032 (prg9025@nyp.org).

Published Online: June 12, 2019. doi:10.1001/jamacardio.2018.4511

Conflict of Interest Disclosures: Dr Parikh reported receiving nonfinancial support from Abbott Vascular, Medtronic, Boston Scientific, Philips, and CSI Inc. He has also reported serving as a paid consultant for Terumo, Asahi, Siemens, Heartflow, and Merrill LifeSciences and receiving grants and institutional support from Shockwave Medical, TriReme Medical, and Surmodics Inc outside the submitted work. No other disclosures were reported.

References
1.
Saw  J, Mancini  GBJ, Humphries  KH.  Contemporary review on spontaneous coronary artery dissection.  J Am Coll Cardiol. 2016;68(3):297-312. doi:10.1016/j.jacc.2016.05.034PubMedGoogle ScholarCrossref
2.
Alfonso  F.  Spontaneous coronary artery dissection: new insights from the tip of the iceberg?  Circulation. 2012;126(6):667-670. doi:10.1161/CIRCULATIONAHA.112.122093PubMedGoogle ScholarCrossref
3.
Vrints  CJ.  Spontaneous coronary artery dissection.  Heart. 2010;96(10):801-808. doi:10.1136/hrt.2008.162073PubMedGoogle ScholarCrossref
4.
Hayes  SN, Kim  ESH, Saw  J,  et al; American Heart Association Council on Peripheral Vascular Disease; Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Genomic and Precision Medicine; Stroke Council.  Spontaneous coronary artery dissection: current state of the science: a scientific statement from the American Heart Association.  Circulation. 2018;137(19):e523-e557. doi:10.1161/CIR.0000000000000564PubMedGoogle Scholar
5.
Michelis  KC, Olin  JW, Kadian-Dodov  D, d’Escamard  V, Kovacic  JC.  Coronary artery manifestations of fibromuscular dysplasia.  J Am Coll Cardiol. 2014;64(10):1033-1046. doi:10.1016/j.jacc.2014.07.014PubMedGoogle ScholarCrossref
6.
Saw  J, Humphries  K, Aymong  E,  et al.  Spontaneous coronary artery dissection: clinical outcomes and risk of recurrence.  J Am Coll Cardiol. 2017;70(9):1148-1158. doi:10.1016/j.jacc.2017.06.053PubMedGoogle ScholarCrossref
7.
Saw  J, Aymong  E, Sedlak  T,  et al.  Spontaneous coronary artery dissection: association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes.  Circ Cardiovasc Interv. 2014;7(5):645-655. doi:10.1161/CIRCINTERVENTIONS.114.001760PubMedGoogle ScholarCrossref
8.
Saw  J.  Coronary angiogram classification of spontaneous coronary artery dissection.  Catheter Cardiovasc Interv. 2014;84(7):1115-1122. doi:10.1002/ccd.25293PubMedGoogle ScholarCrossref
9.
Amsterdam  EA, Wenger  NK, Brindis  RG,  et al; ACC/AHA Task Force Members; Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons.  2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines  [published correction appears in Circulation. 2014;130(25):e431-e432].  Circulation. 2014;130(25):2354-2394. doi:10.1161/CIR.0000000000000133PubMedGoogle ScholarCrossref
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