Benefits of First Pass Recanalization in Basilar Strokes Based on Initial Clinical Severity.

PURPOSE: Randomized trials demonstrating the benefits of thrombectomy for basilar artery occlusions have enrolled an insufficient number of patients with a National Institutes for Health Stroke Scale (NIHSS) score < 10 and shown discrepant results for patients with an NIHSS > 20. Achieving a first pass recanalization (FPR) improves clinical outcomes in stroke. We aimed to evaluate the effect of the FPR on outcomes among basilar artery occlusion patients, characterized by prethrombectomy initial NIHSS score. METHODS: We retrospectively analyzed the Endovascular Treatment in Ischemic Stroke (ETIS) registry of 279 basilar artery occlusion patients treated with thrombectomy from 6 participating centers. We compared the 90-day clinical outcomes of achieving a FPR versus no FPR, categorized by initial clinical severity: mild (NIHSS < 10), moderate (NIHSS 10-20) and severe (NIHSS > 20). We used Poisson regression with robust error variance to determine the effect of the NIHSS score on the association between FPR and outcomes. RESULTS: The FPR patients with NIHSS < 10 or NIHSS 10-20 were more likely to have a favorable clinical outcome (modified Rankin scale, mRS 0-3) than non-FPR patients (relative risk, RR = 1.32, 95% confidence interval, CI: 1.04, 1.66, p-value = 0.0213, and RR = 1.79, 95% CI: 1.26, 2.53, p-value = 0.0011, respectively). A similar benefit was not found in patients with severe symptoms. We found a significantly lower risk of poor clinical outcome (mRS 4-6) in FPR patients with NIHSS 10-20, but not among patients with an NIHSS > 20. CONCLUSION: Achieving a FPR in basilar artery occlusion patients with mild (NIHSS < 10) or moderate (NIHSS 10-20) symptoms is associated with better clinical outcomes, but not in patients with severe symptoms. These results support the importance of further clinical trials on the benefits of thrombectomy in severe strokes.

Comparison of ventilation defects quantified by Technegas SPECT and hyperpolarized 129Xe MRI.

Introduction: The ideal contrast agents for ventilation SPECT and MRI are Technegas and 129Xe gas, respectively. Despite increasing interest in the clinical utility of ventilation imaging, these modalities have not been directly compared. Therefore, our objective was to compare the ventilation defect percent (VDP) assessed by Technegas SPECT and hyperpolarized 129Xe MRI in patients scheduled to undergo lung cancer resection with and without pre-existing obstructive lung disease. Methods: Forty-one adults scheduled to undergo lung cancer resection performed same-day Technegas SPECT, hyperpolarized 129Xe MRI, spirometry, and diffusing capacity of the lung for carbon monoxide (DLCO). Ventilation abnormalities were quantified as the VDP using two different methods: adaptive thresholding (VDPT) and k-means clustering (VDPK). Correlation and agreement between VDP quantified by Technegas SPECT and 129Xe MRI were determined by Spearman correlation and Bland-Altman analysis, respectively. Results: VDP measured by Technegas SPECT and 129Xe MRI were correlated (VDPT: r = 0.48, p = 0.001; VDPK: r = 0.63, p < 0.0001). A 2.0% and 1.6% bias towards higher Technegas SPECT VDP was measured using the adaptive threshold method (VDPT: 23.0% ± 14.0% vs. 21.0% ± 5.2%, p = 0.81) and k-means method (VDPK: 9.4% ± 9.4% vs. 7.8% ± 10.0%, p = 0.02), respectively. For both modalities, higher VDP was correlated with lower FEV1/FVC (SPECT VDPT: r = -0.38, p = 0.01; MRI VDPK: r = -0.46, p = 0.002) and DLCO (SPECT VDPT: r = -0.61, p < 0.0001; MRI VDPK: r = -0.68, p < 0.0001). Subgroup analysis revealed that VDP measured by both modalities was significantly higher for participants with COPD (n = 13) than those with asthma (n = 6; SPECT VDPT: p = 0.007, MRI VDPK: p = 0.006) and those with no history of obstructive lung disease (n = 21; SPECT VDPT: p = 0.0003, MRI VDPK: p = 0.0003). Discussion: The burden of ventilation defects quantified by Technegas SPECT and 129Xe MRI VDP was correlated and greater in participants with COPD when compared to those without. Our observations indicate that, despite substantial differences between the imaging modalities, quantitative assessment of ventilation defects by Technegas SPECT and 129Xe MRI is comparable.

Lipid hydroperoxide formation regulates postnatal rat lung cell apoptosis and alveologenesis.

An acute increase in oxygen tension after birth imposes an oxidative stress upon the lung. We hypothesized that the resultant increase in reactive oxygen species, specifically lipid hydroperoxides, would trigger postnatal alveologenesis and physiological lung cell apoptosis in the neonatal rat. Neonatal rats were either untreated or treated daily with subcutaneous vehicle or diphenyl phenyl diamine, a scavenger of lipid hydroperoxides and inhibitor of lipid peroxidation, from day 1 to 6 of life. Alveolar formation and physiological lung cell apoptosis were assessed by morphometry, immunohistochemistry, and Western blot analyses on day 7 samples. Substitution experiments were conducted using the prototypic lipid hydroperoxide t-butylhydroperoxide. At a minimum effective dose of 15µg/g body wt, treatment with diphenyl phenyl diamine resulted in a significant increase in tissue fraction and mean linear intercept and significant reductions in small peripheral blood vessels, secondary crest formation, lung and secondary crest cell DNA synthesis, and estimated alveolar number. Decreased numbers of apoptotic type II pneumocytes and mesenchymal cells, and decreased contents of proapoptotic cleaved caspase-3 and -7 and cytoplasmic cytochrome c, and an increase in antiapoptotic Bcl-xL were found in lungs treated with diphenyl phenyl diamine. A prevention of selected changes induced by diphenyl phenyl diamine was observed with concurrent treatment with intraperitoneal t-butylhydroperoxide, at a minimally effective dose of 187µg/g body wt. We conclude that oxidative stress after birth induces lipid hydroperoxide formation, which, in turn, triggers postnatal alveologenesis and physiological lung cell apoptosis in the neonatal rat.