(J Vasc Surg 2009;50:1255-64 )”
“Calcitonin gene-related pep

(J Vasc Surg 2009;50:1255-64.)”
“Calcitonin gene-related peptide (CGRP) is expressed throughout the central and peripheral nervous systems, consistent with control of vasodilatation, nociception, motor function, secretion, and olfaction. alpha CGRP is prominently localized in primary spinal afferent C and A Delta fibers of sensory ganglia, and beta CGRP is the main isoform in the enteric nervous system. In the CNS there is a wide distribution of CGRP-containing neurons, with the highest levels occurring in striatum, amygdala, colliculi, and cerebellum. The peripheral projections are involved in

neurogenic LDK378 concentration vasodilatation and inflammation, and central release DAPT clinical trial induces hyperalgesia. CGRP is released from trigeminal nerves in migraine. Trigeminal nerve activation results in antidromic release of CGRP to cause non-endothelium-mediated vasodilatation. At the central synapses

in the trigeminal nucleus caudalis, CGRP acts postjunctionally on second-order neurons to transmit pain signals centrally via the brainstem and midbrain to the thalamus and higher cortical pain regions. Recently developed CGRP receptor antagonists are effective at aborting acute migraine attacks. They may act both centrally and peripherally to attenuate signaling within the trigeminovascular pathway.”
“Background: Successful repair of the ruptured (non-traumatic) descending thoracic aorta (rTA) remains a formidable clinical challenge. Although effective for rTA, traditional open repair (DTAR) has significant associated morbidity. With expanding indications for thoracic endovascular aortic repair (TEVAR), we describe our experience with TEVAR and DTAR in this high-risk setting to elucidate their evolving roles.

Methods: Since the inception of our thoracic aortic endovascular program in 1993, 69 patients underwent DTAR (34)

or TEVAR (35) for rTA. Patients underwent TEVAR if they were considered nonoperative for candidates because of extensive comorbidities (n = 31; 88.6%) or had extremely favorable anatomy for endovascular repair (eg, mid-descending saccular aneurysm, n = 4). Aortic pathology causing rupture was fusiform aneurysm (18), saccular aneurysm/ulcer (22), and dissection (29). Associated aortobronchial fistulae (12) and aortoesophageal (1) fistulae were also present in 18.8%. Arch repair was needed in 46; total descending repair was needed in 33. Follow-up was 100% complete (mean 37.4 months).

Results: Mean age was 65.9 years (DTAR 60.3 year vs TEVAR 71.3 years, P = .005). In-hospital or 30-day mortality was seen in 13 patients (TEVAR n = 4; 11.4% vs DTAR it = 9; 26.5%, P = .13). Median length of stay was shorter after TEVAR (8 days vs DTAR 15 days, P = .02). Mean Kaplan-Meier survival was similar between groups (TEVAR 67.4 months vs DTAR 65.0 months, P = .7).

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