Perivascular application of NO-releasing self-assembling nanofiber gels is an effective and simple therapy to prevent neointimal hyperplasia after arterial injury. Our study demonstrates that the PROLI/NO nanofiber gel most effectively prevented neointimal hyperplasia and resulted in less inflammation than the DPTA/NO nanofiber gel. This therapy has great clinical potential to prevent neointimal hyperplasia after open vascular interventions in patients.

Nitric oxide (NO)-based therapies effectively inhibit neointimal hyperplasia in animal models of arterial injury and bypass grafting, but are not available clinically. We created a simple, effective, locally-applied NO-eluting therapy to prevent restenosis following vascular procedures. We investigated the efficacy of perivascular delivery of two different distinctly different diazeniumdiolate NO donors, 1-[2-(carboxylato)pyrrolidin-1-yl]diazen-1-ium-1,2-diolate (PROLI/ NO), (short half-life) and diazeniumdiolated poly(acrylonitrile) (PAN/NO), (long half-life), in powder or gel form (30% poloxamer 407), at inhibiting neointimal hyperplasia using the rat carotid artery injury model. Two weeks post-injury, all of the NO-eluting therapies successfully reduced neointimal hyperplasia. However, most dramatically, PROLI/NO powder reduced intimal area by 91.2% (P<0.05) versus injury alone. PROLI/NO powder was noted to reduce the medial area (40.2% vs. injury alone, P<0.05), while other groups showed no such effect. Three days post-injury, each NO treatment group significantly reduced cellular proliferation. However, inflammatory markers revealed a distinct pattern: PAN/NO groups displayed increased leukocyte infiltration (P<0.05) whereas PROLI/NO groups displayed less macrophage infiltration (P<0.05). In conclusion, perivascular delivery of diazeniumdiolate NO donors in powder or gel form effectively inhibits neointimal hyperplasia. Application of short-acting PROLI/NO powder most effectively inhibited neointimal hyperplasia and inflammation and may represent a simple, clinically applicable NOeluting therapy to prevent neointimal hyperplasia and restenosis following open vascular interventions.

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Background: Cyclops syndrome is characterized by a symptomatic extension deficit attributed to impingement of a cyclops lesion within the intercondylar notch. The syndrome is an important cause of reoperation after anterior cruciate ligament reconstruction (ACLR). It has been suggested that remnant-preserving ACLR techniques may predispose to cyclops syndrome, but there is very limited evidence to support this. In general terms, risk factors for cyclops syndrome are not well-understood. Purpose: To determine the frequency of and risk factors for reoperation for cyclops syndrome in a large series of patients after ACLR. Study Design: Case-control study; Level of evidence, 3. Methods: A retrospective analysis of prospectively collected data was performed, including all patients who underwent primary ACLR between January 2011 to December 2017. Patients undergoing major concomitant procedures were excluded. Demographic data, intraoperative findings (including the size of preserved remnants), and postoperative outcomes were recorded. Those patients who underwent reoperation for cyclops syndrome were identified, and potential risk factors were evaluated in multivariate analysis. Results: A total of 3633 patients were included in the study, among whom 65 (1.8%) underwent reoperation for cyclops syndrome. Multivariate analysis demonstrated that preservation of large remnants did not predispose to cyclops lesions (odds ratio [OR], 1.11; 95% CI, 0.63-1.93). The most important risk factor was extension deficit in the early postoperative period. If present at 3 weeks postoperatively, it was associated with a >2-fold increased risk of cyclops syndrome (OR, 2.302; 95% CI, 1.268-4.239; P < .01), which was increased to 8-fold if present 6 weeks after ACLR (OR, 7.959; 95% CI, 4.442-14.405; P < .0001). None of the other potential risk factors evaluated were found to be significantly associated with an increased frequency of cyclops syndrome. Conclusion: Failure to regain full extension in the early postoperative period was the only significant risk factor for cyclops syndrome after ACLR in a large cohort of patients. Other previously hypothesized risk factors, such as preservation of a large anterior cruciate ligament remnant, did not predispose to the development of this debilitating postoperative complication.