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Background: The cardiovascular benefits of surgical repair in pectus excavatum (PEx) continue to be debated, with limited data supporting repair in adult patients. Hepatic vein flow is used to identify right-sided diastolic dysfunction in cardiovascular disorders, including tricuspid stenosis, cardiac tamponade, and constrictive pericarditis. This study evaluates the effects of cardiac compression on diastolic function (as assessed by hepatic vein flow patterns and velocities) before and after repair of PEx., Methods: A retrospective study was performed of intraoperative transesophageal echocardiograms including hepatic vein assessments of adult patients who underwent preoperative and postoperative evaluations during repair of PEx from 2018 to 2021., Results: In total, 127 patients were included (median age, 29.0 [15.4] years; median Haller index, 4.2 [1.7]; 60.6% male). Statistically significant improvements were seen after pectus repair of right ventricular stroke volume and diastolic function as measured by increased postoperative velocities for hepatic vein waves ( P < .001 for all comparisons). Preoperatively, 5.5% of patients had constrictive-like physiology with end-diastolic retrograde flow that normalized postoperatively ( P  = .016). Approximately 10% of patients changed their pattern of hepatic vein flow after surgical procedure. Patients with more proximal cardiac compression had greater improvements in hepatic vein velocities after repair., Conclusions: Surgical relief of cardiac compression resulted in an immediate improvement in hepatic vein flow and right ventricle stroke volume in patients with PEx. These results support diastolic dysfunction in a large number of patients, with improvement in function and compliance after the surgical relief of cardiac compression., (© 2023 The Authors.)

Although infrequent, damage to cardiovascular structures can occur during or following a minimally invasive repair of pectus excavatum. We present a case of right ventricular outflow tract compression caused by a displaced intrathoracic bar. Removal of the bar resulted in an improvement in symptoms and hemodynamics. ( Level of Difficulty: Advanced. )., Competing Interests: Dr Jaroszewski has served as a consultant for Zimmer Biomet, Inc; and has received IP/royalty rights under Mayo Clinic Ventures with Zimmer Biomet, Inc. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (© 2022 The Authors.)

Immobilization causes rapid and massive bone loss. By comparing Botulinum Toxin A (BTX)-induced bone loss in mouse strains with different genetic backgrounds we investigated whether the genetic background had an influence on the severity of the osteopenia. Secondly, we investigated whether BTX had systemic effects on bone. Female mice from four inbred mouse strains (BALB/cJ, C57BL/6 J, DBA/2 J, and C3H/HeN) were injected unilaterally with BTX (n = 10/group) or unilaterally with saline (n = 10/group). Mice were euthanized after 21 days, and the bone properties evaluated using μCT, DXA, bone histomorphometry, and mechanical testing. BTX resulted in substantially lower trabecular bone volume fraction (BV/TV) and trabecular thickness in all mouse strains. The deterioration of BV/TV was significantly greater in C57BL/6 J (- 57%) and DBA/2 J (- 60%) than in BALB/cJ (- 45%) and C3H/HeN (- 34%) mice. The loss of femoral neck fracture strength was significantly greater in C57BL/6 J (- 47%) and DBA/2 J (- 45%) than in C3H (- 25%) mice and likewise the loss of mid-femoral fracture strength was greater in C57BL/6 J (- 17%), DBA/2 J (- 12%), and BALB/cJ (- 9%) than in C3H/HeN (- 1%) mice, which were unaffected. Using high resolution μCT we found no evidence of a systemic effect on any of the microstructural parameters of the contralateral limb. Likewise, there was no evidence of a systemic effect on the bone strength in any mouse strain. We did, however, find a small systemic effect on aBMD in DBA/2 J and C3H/HeN mice. The present study shows that BTX-induced immobilization causes the greatest loss of cortical and trabecular bone in C57BL/6 J and DBA/2 J mice. A smaller loss of bone microstructure and fracture strength was seen in BALB/cJ mice, while the bone microstructure and fracture strength of C3H/HeN mice were markedly less affected. This indicates that BTX-induced loss of bone is mouse strain dependent. We found only minimal systemic effects of BTX.