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During embryonic life, events may alter the normal growth and fusion of the endocardial tube, the paired dorsal aortae, and the vitelline plexus leading to anomalies and variants of the mature axial arterial system 1. Many of these are well known, especially those associated with the aorta, heart, and umbilical artery 1,2. Vitelline variants have also been found which are either associated with Meckel’s diverticulum or caudal regression syndrome 3,4. We present a case of anomalous intercostal arterial supply, which to our knowledge has not been reported previously. The aberrant intercostal trunk is associated with aberrant descending thoracic aorta position, a replaced common hepatic artery from the superior mesenteric artery and an isolated splenic artery origin from the aorta.
A 27 year old male with past medical history of irritable bowel syndrome and stage I hypertension presented for renal vasculature evaluation. A renal arterial MR angiogram (not shown) and subsequent thoracoabdominal CT angiogram (64-row MDCT, 1.0 mm section thickness following intravenous injection of 600 mgI/kg Isovue 370) demonstrated normal renal arteries and an anomalous branch artery arising from the posterior aspect of the aorta at the level of T12 with median ascension, terminating at T3. The artery gradually tapered from its 7-mm diameter origin to its terminus and supplied the third through twelfth intercostal arteries bilaterally (Figure 1). This “anomalous intercostal trunk” coursed between the thoracic spine and the descending thoracic aorta, which was elevated 23 mm anterior to the thoracic vertebral bodies and was in close association with the esophagus (Figure 2). An additional posterior trunk arose at the level of T6 and ascended superiorly to supply the first and second intercostals spaces. Associated with this anomaly was an isolated splenic artery arising from the aorta at the level of T11 (Figure 3) and a replaced common hepatic artery arising from the proximal superior mesenteric artery, which arose from the anterior aspect of the aorta at the T11-12 level (Figure 4). In addition, the patient had an anomalous trunk arising from the posterior aspect of the aorta supplying the lumbar arteries at L2 and L3 levels. The remainder of the lumbar segments was supplied by the expected lumbar arteries from the aorta.
We speculate that this constellation of findings may represent a manifestation of anomalous development of the aorta and the vitelline arterial plexus. Possible anomalies may include: 1) an interrupted aortic arch where the vitelline plexus connects with the aortic arch to develop into the aorta while the native aorta atrophies but retains supply to the segmental somites or 2) lack of expected vitelline atrophy that leads to a dominant ventral arterial supply with aortic fusion to the vitelline arteries. Regardless of the mechanism of this anomaly, it is intriguing to consider how the reported intercostal arterial supply could facilitate spinal arterial revascularization in the setting of descending aortic replacement and also place the spinal cord at risk should the single arterial trunk become occluded.
Sources of Funding: No external sources of funding was applicable to this work.
Disclosures: The authors have no conflicts germane to this material to disclose.