Author + information
- Received April 7, 2014
- Accepted April 10, 2014
- Published online October 1, 2014.
- Muhammad Rizwan Sardar, MD∗,†∗ (, )
- Lauren M. Pieczynski, MD‡,
- Wajeeha Saeed, MD§,
- Steven M. Domsky, MD†,
- Timothy A. Shapiro, MD† and
- Paul Coady, MD†
- ∗Department of Cardiology, Cooper University Hospital, Cooper Medical School of Rowan University, Camden, New Jersey
- †Department of Cardiology, Lankenau Medical Center, Thomas Jefferson University, Wynnewood, Pennsylvania
- ‡Department of Anesthesia, Hospital of the University of Pennsylvania, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania
- §Department of Medicine, Albert Einstein College of Medicine, Bronx-Lebanon Hospital Center, Bronx, New York
- ↵∗Reprint requests and correspondence:
Dr. Muhammad Rizwan Sardar, Department of Cardiology, Cooper University Hospital, Cooper Medical School of Rowan University, 3rd Floor Dorrance, One Cooper Plaza, Camden, New Jersey 08103.
- coronary artery disease
- myocardial infarction
- spontaneous coronary artery dissection
- ST-segment elevation myocardial infarction
A 35-year-old woman, 12 days post-partum presented to the emergency department from her physician's office with chest discomfort that started the previous night. She described the chest discomfort discomfort “on-and-off”, occurring at rest, and located in the central chest with radiation to the left arm lasting a maximum of 5 min. Initial electrocardiogram showed sinus rhythm left axis deviation with non-specific ST-T wave changes in the inferior leads. Her physical exam showed equal blood pressures in both arms (140/75 mm Hg), a pulse of 77 beats/min, and pulse oximetry of 95% on room air. There were no obvious Marfanoid features, no murmurs or gallops, and normal jugular venous distention. She underwent a computed tomography scan of her chest, which showed a low probability of pulmonary embolism. She had normal basic labs besides the first set of troponin (0.11 ng/ml) and was kept in the hospital for observation. Three hours later, she had a sudden onset of similar chest discomfort with diaphoresis and 12-lead electrocardiogram revealed ST-segment elevations in leads V2 and aVL, with ST-segment depressions in the inferior leads (Figure 1A, red arrows). Cardiac catheterization was performed; it showed spontaneous coronary artery dissection in the left anterior descending artery, second diagonal branch, left circumflex, and right coronary artery (RCA). She had complete proximal occlusion of her RCA with no collaterals (Figures 1B, 1D, 1F, black arrows, Online Video 1). Percutaneous coronary intervention of the RCA was performed (Figure 1G, black arrow). For the remaining affected vessels, a conservative approach was employed with dual antiplatelet therapy, in addition to intravenous heparin and Eptifibatide for 24 h. During her RCA intervention, wire presence in true lumen was confirmed using intravascular ultrasound. Transthoracic echocardiogram showed an ejection fraction of 40% with moderate area of apical, inferior, and inferolateral wall hypokinesis. The patient remained asymptomatic with stable levels of cardiac biomarkers. At day 3, computed tomography coronary calcium score revealed a calcium score of 0, and renal and carotid ultrasound demonstrated no evidence of fibromuscular dysplasia. At day 5, repeat cardiac catheterization showed stable and healed left anterior descending artery, second diagonal, and left circumflex lesions (Figures 1C, 1E, yellow arrows, Online Video 2) with a patent stent in the RCA. She was discharged on dual antiplatelet and beta-blockers. The patient remained asymptomatic, and a follow-up echocardiogram 1 month later showed a normal ejection fraction with no wall motion abnormalities. Multivessel spontaneous coronary artery dissection is rare (1) and can be fatal (2). Our case demonstrates the employment of conservative therapy might still be enough for treating a patient with extensive multivessel spontaneous coronary artery dissection.
For accompanying videos, please see the online version of this paper.
Dr. Sardar has received speaker's fees from the Atrial Fibrillation Education Program, North American Center for Continuing Medical Education. Dr. Shapiro receives speaker's fees from AstraZeneca. All other authors have reported that they have no relationships relevant to this paper to disclose.
- Received April 7, 2014.
- Accepted April 10, 2014.
- American College of Cardiology Foundation
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