itored consecutive patients with MRI-proven sCAD by duplex ultrasound imaging daily in the hospital, monthly for the first 6 months after discharge, and every 6 months thereafter.The authors studied 105 sCADs in 76 patients. The mean follow-up was 58 months (range, 28-96 months). Of the 105 dissections in this study, 61 (58.1%) involved the internal carotid artery and 44 (41.9%) involved the vertebral artery. Four patients had multiple sCADs. Follow-up was available for 74 (103 vessels) of the 76 patients (97.3%). Complete and hemodynamically significant (Ͻ50% stenosis) recanalization rates were 51.4% and 20.4%. All but one of the complete recanalizations occurred within the first 9 months after the initial event. Early recurrences (in-hospital recurrence) were common, with a second sCAD occurring in 20 previously unaffected arteries. There were only two late recurrences (2.7%) at a site of a previous sCAD. Six patients had a family history of arterial dissection and all had a sCAD recurrence. Recurrence rate in patients without a family history of arterial dissection was much less, with only 16 arteries (22.8%) affected (P Ͻ .001).Comment: There are several interesting points here. First, although recurrence of sCAD is reasonably uncommon, it generally occurs early after the initial event and in a different cervical artery. The authors' early recurrence of 25% is much higher than previously suspected and may relate to the rigorous follow-up protocol in the study. The fact that late sCAD recurrence can happen in previously affected artery suggests recurrence after sCAD in the early and late periods may have different pathologies. Perhaps, as the authors point out, early recurrences are correlated with a transient arterial disorder, such as a vasculitis, while late recurrences may be indicative of underlying persistent connective tissue weakness. The high early recurrence rate suggests that aggressive treatment of sCADs, including control of double product and lowering blood pressure within the constraints imposed by the neurologic pathology, should be implemented.
Cardiopulmonary bypass (CPB) causes a systemic inflammatory response syndrome (SIRS), which can progress to an acute lung inflammation known as postperfusion syndrome. We developed a two-phase hypothesis: first, that SIRS, as indicated by elevated cytokines post-CPB, would be correlated with postoperative pulmonary dysfunction (Phase I), and second, that the cytokine interleukin-6 (IL-6) is predominantly released from the heart in CPB patients (Phase II). Blood samples were collected from patients undergoing CPB for elective cardiac surgery. In seven patients (Phase I), arterial samples were drawn before, during (5 minutes and 60 minutes), and after CPB. In 14 patients (Phase II), samples were collected from the coronary sinus, superior vena cava, and a systemic artery at the times indicated previously. Samples were analyzed with enzyme-linked immunosorbent assay: IL-1, IL-6, IL-8, IL-10, and tumor necrosis factor-α were assessed in Phase I and IL-6 assessed in Phase II. In Phase I, IL-6, IL-8, and IL-10 were elevated after CPB, but only IL-6 concentrations correlated with lung function. In summary, Phase I data demonstrate that increased IL-6 levels at the end of CPB correlate with reduced lung function postoperatively. In Phase II, IL-6 elevation was similar at all sample sites suggesting that the heart is not the major source of IL-6 production. We suggest that IL-6 be implemented as a prognostic measure in patient care, and that patients with elevated IL-6 after CPB be targeted for more aggressive anti-inflammatory therapy to protect lung function.
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