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A 38 year-old nulliparous woman with no cardiac risk factors abruptly developed chest discomfort during a routine exercise run. The discomfort recurred with minimal exertion for the next three days, after which she presented to the emergency department for evaluation.
Her physical examination and ECG were unremarkable but troponin I was 0.25 ng/ml (Normal <0.04 ng/ml). Pharmacologic nuclear stress imaging demonstrated a medium sized, severe ischemic defect of the anterolateral wall with corresponding hypokinesis (Fig. 1a ). Left ventricular function was normal. Coronary angiography demonstrated a 99% complex stenosis of the second diagonal branch from the left anterior descending artery that extended from the ostium to a second branching point with linear contrast dye staining in the wall of the vessel (Fig. 1b, asterisks). There was TIMI grade 2 flow (partial reperfusion) into the distal aspect of the vessel (Fig. 1c, arrows). All other epicardial vessels were angiographically normal.
Fig. 1(a) Nuclear perfusion stress images demonstrate a medium sized, severe reversible defect in the anterolateral wall consistent with ischemia, marked by the arrows. (HLA: Horizontal long axis; VLA: Vertical long axis).
(b) Linear contrast dye staining within the arterial wall of the second diagonal branch from the left anterior descending artery, marked by the asterisks, is consistent with a coronary artery dissection. The focal dissection corresponds with the perfusion defect seen in the anterolateral wall on nuclear imaging.
(c) There was partial reperfusion of the distal diagonal branch and slow clearance of the contrast dye, also consistent with a coronary artery dissection.
(d) Repeat coronary angiography one month later showed resolution of the dissection (see arrow) with no other angiographic abnormalities.
The clinical and angiographic information were consistent with spontaneous coronary artery dissection (SCAD). She had no risk factors for premature coronary artery disease and no angiographic evidence of atherosclerosis.
In SCAD, hemorrhage into the media of the coronary artery creates a hematoma which can compress the true arterial lumen and propagate along the vessel. An intimal tear creating a false lumen within the vessel wall is seen on angiography as a linear contrast dye staining within the wall of the vessel with a radiolucent true lumen and slow clearing of the contrast, as was seen in this case [
This patient was treated conservatively with aspirin, clopidogrel, and metoprolol with no recurrent symptoms. One month later repeat angiography showed resolution of the dissection with no other angiographic abnormalities (Fig. 1d, arrow). One year after her initial presentation she remained symptom free with normal functional capacity.
Optimal management for patients presenting with SCAD is uncertain and should be individualized based on the severity of the clinical presentation and the coronary anatomy by angiography [
SCAD is an uncommon cause of myocardial infarction but should be considered in patients without cardiac risk factors presenting with an acute coronary syndrome, especially in young women. Clinical management that refrains from mechanical intervention may be appropriate in patients who are clinically stable.
Funding source
None
Conflicts of interest
The authors state that they have no conflicts of interest.
Authorship
Both authors had access to the data and contributed to writing the manuscript.
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