Gender Representation Trends in Cardiothoracic Surgery Journal Editorial Boards.

OBJECTIVE: We aimed to characterize chronologic trends of gender composition of major cardiothoracic surgery journal editorial boards in the current era. METHODS: A cross-sectional analysis was performed of gender representation in editorial board members of two North American cardiothoracic surgery journals from 2008 to 2023. Member names and roles were collected from available monthly issues. Validated software programming was used to classify gender. The annual proportion of women representation was compared to the thoracic surgery workforce. RESULTS: During the study period, 558 individuals (3,641 names) were identified, 14.3% of whom were women. The total number of editorial board women increased for both journals. The proportion of women also increased from 2.5% (3/118) in 2008 to 17.8% (71/399) in 2023 (P < .001), exceeding the percentage of women in the thoracic surgery workforce which increased from 3.8% in 2007 to 8.3% in 2021 (P < .001). The average duration of participation was longer for men than for women (53.8 vs 44.5 months, P = .01). Women in editorial board senior roles also increased from 3.3% (1/30) in 2008 to 28.6% (42/147) in 2023 (P < .001), almost triple the increase in non-designated roles from 2.3% (2/88) in 2008 to 11.5% (29/252) in 2023 (P < .001). CONCLUSIONS: In recent years, the appointment of women to high-impact cardiothoracic surgery journal editorial boards and senior roles have proportionally exceeded the overall representation of women in cardiothoracic surgery. These findings indicate progress in inclusive efforts and offer insight towards reducing academic gender disparities.

ECMO During COVID-19: A Society of Thoracic Surgeons/Extracorporeal Life Support Organization Survey.

Background: The Society of Thoracic Surgeons Workforce on Critical Care and the Extracorporeal Life Support Organization sought to identify how the coronavirus disease 2019 (COVID-19) pandemic has changed the practice of venoarterial (VA) and venovenous (VV) extracorporeal membrane oxygenation (ECMO) programs across North America. Methods: A 26-question survey covering 6 categories (ECMO initiation, cannulation, management, anticoagulation, triage/protocols, and credentialing) was emailed to 276 North American Extracorporeal Life Support Organization centers. ECMO practices before and during the COVID-19 pandemic were compared. Results: Responses were received from 93 (34%) programs. The percentage of high-volume (>20 cases per year) VV ECMO programs increased during the pandemic from 29% to 41% (P < .001), as did institutions requiring multiple clinicians for determining initiation of ECMO (VV ECMO, 25% to 43% [P = .001]; VA ECMO, 20% to 32% [P = .012]). During the pandemic, more institutions developed their own protocols for resource allocation (23% before to 51%; P < .001), and more programs created sharing arrangements to triage patients and equipment with other centers (31% to 57%; P < .001). Direct thrombin inhibitor use increased for both VA ECMO (13% to 18%; P = .025) and VV ECMO (12% to 24%; P = .005). Although cardiothoracic surgeons remained the primary cannulating proceduralists, VV ECMO cannulations performed by pulmonary and critical care physicians increased (13% to 17%; P = .046). Conclusions: The Society of Thoracic Surgeons/Extracorporeal Life Support Organization collaborative survey indicated that the pandemic has affected ECMO practice. Further research on these ECMO strategies and lessons learned during the COVID-19 pandemic may be useful in future global situations.

Cardiovascular Outcomes in Aortopathy: GenTAC Registry of Genetically Triggered Aortic Aneurysms and Related Conditions.

BACKGROUND: The GenTAC (Genetically Triggered Thoracic Aortic Aneurysm and Cardiovascular Conditions) Registry enrolled patients with genetic aortopathies between 2007 and 2016. OBJECTIVES: The purpose of this study was to compare age distribution and probability of elective surgery for proximal aortic aneurysm, any dissection surgery, and cardiovascular mortality among aortopathy etiologies. METHODS: The GenTAC study had a retrospective/prospective design. Participants with bicuspid aortic valve (BAV) with aneurysm (n = 879), Marfan syndrome (MFS) (n = 861), nonsyndromic heritable thoracic aortic disease (nsHTAD) (n = 378), Turner syndrome (TS) (n = 298), vascular Ehlers-Danlos syndrome (vEDS) (n = 149), and Loeys-Dietz syndrome (LDS) (n = 121) were analyzed. RESULTS: The 25% probability of elective proximal aortic aneurysm surgery was 30 years for LDS (95% CI: 18-37 years), followed by MFS (34 years; 95% CI: 32-36 years), nsHTAD (52 years; 95% CI: 48-56 years), and BAV (55 years; 95% CI: 53-58 years). Any dissection surgery 25% probability was highest in LDS (38 years; 95% CI: 33-53 years) followed by MFS (51 years; 95% CI: 46-57 years) and nsHTAD (54 years; 95% CI: 51-61 years). BAV experienced the largest relative frequency of elective surgery to any dissection surgery (254/33 = 7.7), compared with MFS (273/112 = 2.4), LDS (35/16 = 2.2), or nsHTAD (82/76 = 1.1). With MFS as the reference population, risk of any dissection surgery or cardiovascular mortality was lowest in BAV patients (HR: 0.13; 95% CI: 0.08-0.18; HR: 0.13; 95%: CI: 0.06-0.27, respectively). The greatest risk of mortality was seen in patients with vEDS. CONCLUSIONS: Marfan and LDS cohorts demonstrate age and event profiles congruent with the current understanding of syndromic aortopathies. BAV events weigh toward elective replacement with relatively few dissection surgeries. Nonsyndromic HTAD patients experience near equal probability of dissection vs prophylactic surgery, possibly because of failure of early diagnosis.

Venovenous Extracorporeal Membrane Oxygenation for Patients With Return of Spontaneous Circulation After Cardiac Arrest Owing to Acute Respiratory Distress Syndrome.

OBJECTIVE: The primary objective of this study was to determine the survival to hospital discharge of patients who were treated with venovenous (VV) extracorporeal membrane oxygenation (ECMO) for respiratory failure after cardiac arrest. DESIGN: Retrospective chart review. SETTING: University-affiliated tertiary care hospitals. PARTICIPANTS: The study comprised 21 patients. INTERVENTIONS: Implementation of VV ECMO in patients with return of spontaneous circulation after cardiac arrest owing to respiratory insufficiency. MEASUREMENTS AND MAIN RESULTS: The most common etiology of arrest was pneumonia-associated acute respiratory distress syndrome (8/21 [38%]). Overall, 12/21(57%) patients survived to hospital discharge. Two of 12 (17%) patients required hemodialysis upon discharge. CONCLUSION: VV ECMO may be an appropriate alternative to venoarterial ECMO in select patients with return of spontaneous circulation after cardiac arrest owing to profound respiratory failure.

Distinct enhancers at the Pax3 locus can function redundantly to regulate neural tube and neural crest expressions.

Pax3 is a transcription factor expressed in somitic mesoderm, dorsal neural tube and pre-migratory neural crest during embryonic development. We have previously identified cis-acting enhancer elements within the proximal upstream genomic region of Pax3 that are sufficient to direct functional expression of Pax3 in neural crest. These elements direct expression of a reporter gene to pre-migratory neural crest in transgenic mice, and transgenic expression of a Pax3 cDNA using these elements is sufficient to rescue neural crest development in mice otherwise lacking endogenous Pax3. We show here that deletion of these enhancer sequences by homologous recombination is insufficient to abrogate neural crest expression of Pax3 and results in viable mice. We identify a distinct enhancer in the fourth intron that is also capable of mediating neural crest expression in transgenic mice and zebrafish. Our analysis suggests the existence of functionally redundant neural crest enhancer modules for Pax3.

Identification of minimal enhancer elements sufficient for Pax3 expression in neural crest and implication of Tead2 as a regulator of Pax3.

Pax3 is a transcription factor that is required by pre-migratory neural crest cells, which give rise to the peripheral nervous system, melanocytes, some vascular smooth muscle, and numerous other derivatives [corrected]. Both mice and humans with Pax3 deficiency exhibit neural crest-related developmental defects [corrected]. Pax3 is also expressed in the dorsal neural tube, and by myogenic progenitors in the presomitic mesoderm and the hypaxial somites. Molecular pathways that regulate Pax3 expression in the roof plate probably represent early upstream signals in neural crest induction. We have identified an enhancer region in the Pax3 genomic locus that is sufficient to recapitulate expression in neural crest precursors in transgenic mice. We show that Tead2, a member of the Tead box family of transcription factors, binds to a neural crest enhancer and activates Pax3 expression. Tead2, and its co-activator YAP65, are co-expressed with Pax3 in the dorsal neural tube, and mutation of the Tead2 binding site in the context of Pax3 transgenic constructs abolishes neural expression. In addition, a Tead2-Engrailed fusion protein is able to repress retinoic acid-induced Pax3 expression in P19 cells and in vivo. These results suggest that Tead2 is an endogenous activator of Pax3 in neural crest.