Restoration of thoracic kyphosis in adolescent idiopathic scoliosis with patient-specific rods: did the preoperative plan match postoperative sagittal alignment?

PURPOSE: To determine if the planned sagittal profile for thoracic kyphosis (TK) restoration was achieved after adolescent idiopathic scoliosis (AIS) surgery using a novel hybrid construct with apical double bands and precontoured patient-specific rods (PSR) made according to the detailed surgical plan for the desired sagittal plane. METHODS: AIS patients with a Lenke type 1-4 primary right thoracic curve who underwent corrective surgery by a single surgeon and had minimum 24-month follow-up were analyzed retrospectively from a prospective database. All patients underwent simultaneous translation on two rods with apical double bands and PSR. Clinical outcomes in terms of sagittal 2D TK (T4-T12), lumbar lordosis (LL), sagittal vertical axis (SVA), pelvic incidence (PI), pelvic tilt (PT), sacral slope (SS), PI-LL mismatch, rod angle, and rod deflection were compared between preoperative, planned, and 24-month data, while 3D apical rotation, 3D TK (T5-T12), sagittal thoracolumbar angle, degree of curvature at L1-L4 and L4-S1, proximal junctional angle, and distal junctional angle were compared at baseline and at 6 and 24 months postoperatively. SRS-22 questionnaire scores were obtained at baseline and 24 months postoperatively. RESULTS: Forty-eight patients were included. Study patients had a median coronal thoracic curve of 62.7° preoperatively and 22.4° at 24-month follow-up (p < 0.001). Median TK gain was 6.5° for the entire cohort (n = 48) and 19.1° in the Lenke type 1 and 2 hypokyphotic subgroup (n = 14). Both groups had no significant changes between planned and 24-month TK (p = 0.068 and p = 0.943, respectively), rod angle (p = 0.776 and p = 0.548, respectively), or rod deflection (p = 0.661 and p = 0.850, respectively). For the overall study cohort, median LL gain was 7.0° (p < 0.001), 3D apical derotation was 10.7° (p < 0.001), and change in 3D TK was 36° (p < 0.001). No instance of proximal junctional kyphosis was observed. SRS-22 scores for pain, self-image, and satisfaction differed significantly between the preoperative and 24-month follow-up time-points. CONCLUSIONS: With sagittal plane planning, desired TK, improved reciprocal changes in LL, and minimal changes in rod shape can be achieved in patients with AIS.

ß(1)-adrenergic receptor polymorphisms and response to ß-blockade in the African-American study of kidney disease and hypertension (AASK).

BACKGROUND: This study focuses on the relationship between ß(1)-adrenergic receptor (ADRB1) polymorphisms and blood pressure response to the ß-blocker metoprolol among African Americans with early hypertensive nephrosclerosis. METHODS: Participants from the African-American Study of Kidney Disease and Hypertension (AASK) trial were genotyped for ADRB1 polymorphisms: Ser49Gly and Arg389Gly. Cox proportional hazards models were used to determine the relationship between ADRB1 polymorphisms and time to reach a mean arterial pressure (MAP) of ≤107 mm Hg in the first year after randomization, adjusted for other predictors of blood pressure response. RESULTS: In the Ser49Gly model, Ser49/Gly49 individuals were less responsive compared to Ser49/Ser49 only among the more obese (body mass index (BMI) ≥39 kg/m(2)) participants (P < 0.05 for genotype × BMI interaction). The hazard ratio (HR) with a BMI of 39 kg/m(2) was 0.68 (95% confidence interval (CI) 0.46-0.99). In the Arg389Gly model, participants with Arg389 were less likely to respond to metoprolol: HR: 0.68 (95% CI 0.50-0.93). In addition, women were less responsive to metoprolol compared to men: HR: 0.78 (95% CI 0.60-0.995). CONCLUSIONS: Ser49/Gly49 was predictive of blood pressure response to metoprolol only among more obese African Americans with early hypertensive nephrosclerosis. In contrast to other studies suggesting increased short-term responsiveness to ß-blockers with Arg389, Arg389 individuals were less responsive in this study analyzing blood pressure over a 1-year period. This may be partly explained by decreased agonist-promoted desensitization with Arg389. However, gender, physiological adaption to stress, interactions between genes and between genes and the environment, as well as study in other patient populations need to be considered.