PurposeThe purpose of this study was to: (1) test the hypothesis that HTO improves articular cartilage composition in the medial compartment without adversely affecting the lateral compartment and patella, and; (2) explore associations between knee alignment and cartilage composition after surgery. Methods3T MRI and standing radiographs were obtained from 34 patients before and 1‐year after HTO. Articular cartilage was segmented from T2 maps. Mechanical axis angle (MAA), posterior tibial slope, and patellar height were measured from radiographs. Changes in T2 and radiographic measures were assessed using paired t tests, and associations were assessed using Pearson correlation coefficients. ResultsThe mean (SD) MAA before and after HTO was − 6.5° (2.4) and 0.6° (3.0), respectively. There was statistically significant shortening [mean (95%CI)] of T2 in the medial femur [− 2.8 ms (− 4.2; − 1.3), p < 0.001] and medial tibia [− 2.2 ms (− 3.3; − 1.0), p < 0.001], without changes in the lateral femur [− 0.5 ms (− 1.6; 0.6), p = 0.3], lateral tibia [0.2 ms (− 0.8; 1.1), p = NS], or patella [0.5 ms (− 1.0; 2.1), p = NS). Associations between radiographic measures and T2 were low. 23% of the increase in lateral femur T2 was explained by postoperative posterior tibial slope (r = 0.48). ConclusionPerforming medial opening wedge HTO without overcorrection improves articular cartilage composition in the medial compartment of the knee without compromising the lateral compartment or the patella. Although further research is required, these results suggest HTO is a disease structure‐modifying treatment for knee OA.

ObjectivesWe systemically reviewed published studies that evaluated aerobic exercise interventions in patients with knee osteoarthritis (OA) to: (1) report the frequency, intensity, type and time (FITT) of exercise prescriptions and (2) quantify the changes in markers of cardiovascular health and systemic inflammation.Data sourcesPubMed, CINAHL, Scopus; inception to January 2019.Eligibility criteriaRandomised clinical trials (RCT), cohort studies, case series.DesignWe summarised exercise prescriptions for all studies and calculated effect sizes with 95% CIs for between-group (RCTs that compared exercise and control groups) and within-group (pre-post exercise) differences in aerobic capacity (VO2), heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP) and inflammatory markers (interleukin-6 (IL-6), tumour necrosis factor-alpha). We pooled results where possible using random effects models.ResultsInterventions from 49 studies were summarised; 8% (4/49) met all FITT guidelines; 16% (8/49) met all or most FITT guidelines. Fourteen studies (10 RCTs) reported at least one marker of cardiovascular health or systemic inflammation. Mean differences (95% CI) indicated a small to moderate increase in VO2 (0.84 mL/min/kg; 95% CI 0.37 to 1.31), decrease in HR (−3.56 beats per minute; 95% CI −5.60 to −1.52) and DBP (−4.10 mm Hg; 95% CI −4.82 to −3.38) and no change in SBP (−0.36 mm Hg; 95% CI −3.88 to 3.16) and IL-6 (0.37 pg/mL; 95% CI −0.11 to 0.85). Within-group differences were also small to moderate.ConclusionsIn studies of aerobic exercise in patients with knee OA, very few interventions met guideline-recommended dose; there were small to moderate changes in markers of cardiovascular health and no decrease in markers of systemic inflammation. These findings question whether aerobic exercise is being used to its full potential in patients with knee OA.PROSPERO registration numberCRD42018087859.

New Findings What is the central question of this study? Nitric oxide causes dilatation in peripheral vessels; however, whether nitric oxide affects basal cerebral artery dilatation has not been explored. What is the main finding and its importance? This study demonstrated that vasodilatation occurs in the right middle cerebral artery in response to exogenous nitric oxide. However, blood velocity decreased and, therefore, overall cerebral blood flow remained unchanged. This study provides new insight into the role of nitric oxide in cerebral blood flow control. AbstractRecent evidence indicates that basal cerebral conduit vessels dilate with hypercapnia, with a nitric oxide (NO) mechanism explaining one way in which parenchymal cerebral arterioles dilate. However, whether NO affects basal cerebral artery dilatation remains unknown. This study quantified the effect of an exogenous NO donor [sodium nitroglycerin (NTG); 0.4 mg sublingual spray] on the right middle cerebral artery (rMCA) cross‐sectional area (CSA), blood velocity and overall blood flow. Measures of vessel CSA (7 T magnetic resonance imaging) and MCA blood velocity (transcranial Doppler ultrasound) were made at baseline (BL) and after exogenous NTG or placebo (PLO) administration in young, healthy individuals (n = 10, two males, age range 20–23 years). The CSA increased in the rMCA [BL, 5.2 ± 1.2 mm2; PLO, 5.4 ± 1.5 mm2; NTG, 6.6 ± 1.5 mm2, P < 0.05; mean ± SD]. Concurrently, rMCA blood velocity decreased from BL during NTG compared with PLO (BL, 67 ± 10 cm s−1; PLO, 62 ± 10 cm s−1; NTG, 59 ± 9.3 cm s−1, P < 0.05; mean ± SD]. However, total MCA blood flow did not change with NTG or PLO [BL, 221 ± 37.4 ml min−1; PLO, 218 ± 35.0 ml min−1; NTG, 213 ± 46.4 ml min−1). Therefore, exogenous NO mediates a dilatory response in the rMCA, but not in its downstream vascular bed.

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