Where are they now? An analysis of integrated cardiothoracic surgery residency applicants.

Changes in cardiothoracic surgery (CTS) workforce trends have affected training paradigms to include the establishment of integrated six-year CTS residency (I6) programs. This study aimed to determine commitment of selected I6 program applicants to the specialty. Internal archives at a single institution were accessed to identify applicants interviewed for an I6 position from 2014 to 2016. A systematic internet search of publicly available information was performed to identify the trainee's current specialty. Descriptive analysis was performed. Forty-seven applicants were identified. Successful search results were achieved for 97.9 % of the applicants. One applicant was excluded, resulting in a cohort of 45. 48.9 % of the applicants successfully matched into I6 programs. Of the 23 who did not match into an I6 program, 91.3 % began a General Surgery (GS) residency. When looking solely at the GS trainees, 71.4 % sought and matched into a traditional or 4/3 CTS residency. In total, 77.8 % of the cohort are currently pursuing careers in cardiothoracic surgery. The study identified a strong continued interest in the field of CT Surgery among those interviewed for integrated residency. The methodology used in this study provided an effective way to follow career choice of applicants interviewed and could be applied by additional programs to further elucidate career choice and levels of commitment.

Two Decades of Declining Medicare Reimbursement in Cardiac Surgery.

BACKGROUND: Given the uncertainty of US health care finances, an understanding of reimbursement trends has become increasingly important in the field of cardiac surgery. We aimed to assess Medicare reimbursement trends for common cardiac surgical procedures from 2000 to 2022. METHODS: Reimbursement data were extracted from the Centers for Medicare and Medicaid Services Physician Fee Schedule Look-Up Tool during the study period for 6 common cardiac operations: aortic valve replacement, mitral valve repair and replacement, tricuspid valve replacement, Bentall procedure, and coronary artery bypass grafting. Reimbursement rates were adjusted for inflation to 2022 US dollars using the Consumer Price Index. Total percentage change and compound annual growth rate were calculated. A split-time analysis was performed to assess trends before and after 2015. Least squares and linear regressions were performed. The R2 value was calculated for each procedure, and slope was used to determine change in reimbursements over time. RESULTS: Inflation-adjusted reimbursement decreased by 34.1% during the study period. The overall compound annual growth rate was -1.8%. Reimbursement trends differed by procedure (P < .001), with all reimbursements trending down (R2 > 0.62), except for mitral valve replacement (P = .21) and tricuspid valve replacement (P = .43). Coronary artery bypass grafting decreased the most (-44.4%), followed by aortic valve replacement (-40.1%), mitral valve repair (-38.5%), mitral valve replacement (-29.8%), Bentall procedure (-28.5%), and tricuspid valve replacement (-25.3%). In split-time analysis, reimbursement rates did not significantly change from 2000 to 2015 (P = .24) but decreased significantly from 2016 to 2022 (P = .001). CONCLUSIONS: Medicare reimbursement significantly decreased for most cardiac surgical procedures. These trends justify further advocacy by The Society of Thoracic Surgeons to maintain access to quality cardiac surgical care.

Lung lobectomy surgical approach and resource utilization differ by anatomic lobe in a statewide discharge registry.

Background: Anatomic lobe-specific differences with respect to pulmonary lobectomy have been suggested in the thoracic surgery literature but hard data has been lacking in larger population studies in part due to coding systems that do not distinguish pulmonary lobectomy by anatomic lobe. International Classification of Diseases, Tenth Revision (ICD-10) procedure codes, adopted in the United States in 2015, may provide novel methodologic accessibility for pulmonary lobectomy studies as they classify lobectomy operations by specific anatomic lobe. We queried the Texas Inpatient Public Use Data File (TPUDF) ICD-10 codes for both open and endoscopic approach lobectomy with a specific view to differences based on anatomic lobes. Methods: Between fourth fiscal quarter (Q4) 2015 and Q4 2017, all pulmonary lobectomy operations performed in Texas state-licensed hospitals were identified by querying the TPUDF for ICD-10 procedure codes for pulmonary lobectomy as classified by anatomic lobe. Surgical approach, additional procedures and diagnosis codes, length of hospital stay (LOS), and discharge status were recorded with aggregate values undergoing statistical analysis. Results: Right and left upper versus lower lobe resections were more prevalent however minimally invasive surgery was less commonly performed for upper than right lower lobectomy. LOS, irrespective of surgical approach, was longer for upper versus lower lobe resection as was need for transfer to additional inpatient facilities. LOS was longer and need for additional surgical or procedural interventions days after the primary procedure of lobectomy was greater for right versus left upper lobe resection, suggesting some differential properties of the right versus left pleural space. Conclusions: The marked clinical differences between anatomic lobes in the setting of pulmonary lobectomy observed in this study have the potential to translate to differences in expected hospital and health system costs and surgeon time-expenditure and experience premium that currently have no mechanism for their accounting. These findings highlight the value of ICD-10 coding for analysis of pulmonary lobectomy in administrative databases and suggest a possible path to more informed patient counseling and equitable hospital and surgeon reimbursement based on payment adjustment by anatomic lobe in pulmonary lobectomy operations.

Toward a Next-Generation Digital Chest Tube.

Chest tubes in patients who have undergone pulmonary resection with pleural air leak are painful, impair ventilatory mechanics, and increase hospital length of stay and costs. Despite these well-documented concerns, current protocols for chest tube management in this setting are not well supported by evidence. Excessive suction applied to chest tubes has been associated with prolonged air leak due to alveolar over-distension, and most practitioners intuit that suction should be minimized to the lowest level needed to maintain desired pleural apposition. Unfortunately, there is no evidence-based protocol for the establishment of minimal adequate suction. Digital suction devices in current clinical use can identify air leak resolution preventing the delay of chest tube removal but cannot guide suction minimization while an air leak persists. We recently described a monitor of lung expansion in a porcine model of pleural air leak that could detect loss of pleural apposition continuously in real-time based on electrical impedance readings obtained directly from the surface of the lung via chest tube-embedded electrodes. The value of the impedance signal was "in-range" when pleural apposition was present but became abruptly "out-of-range" when pneumothorax due to inadequate suction developed. These findings suggested that a digitally controlled suction pump system could be programmed to recognize the development of pneumothorax and automatically identify and set the minimum level of suction required to maintain pleural apposition. We present here preliminary proof of concept for this system.

Using a quality improvement initiative to reduce acute kidney injury during on-pump coronary artery bypass grafting.

INTRODUCTION: In response to a perceived high incidence of acute kidney injury following cardiopulmonary bypass at our institution, a quality improvement initiative consisting of a systematic change to a delivered oxygen (DO2) goal-directed perfusion practice was implemented. We sought to maintain DO2 > 270 mL/min/m2 to reduce the incidence of acute kidney injury. METHODS: 'The study population included all patients receiving isolated, non-emergent, on-pump coronary artery bypass grafting from January 2015 through December 2018, excluding patients requiring preoperative hemodialysis. DO2 goal-directed perfusion was instituted in February 2017. Acute kidney injury was defined using Acute Kidney Injury Network criteria. RESULTS: The pre-goal-directed perfusion cohort included 257 patients, and the post-goal-directed perfusion cohort included 226 patients. The DO2 was significantly higher in the post-goal-directed perfusion group (p < 0.001). Postoperative change in serum creatinine and incidence of acute kidney injury were significantly lower in the post-goal-directed perfusion group (p < 0.001, p = 0.001, respectively). Estimation with probit and ordered probit models support these findings. CONCLUSION: This initiative confirms previous assertions that DO2 is a critical intraoperative parameter and should direct perfusion intervention accordingly.

Agitation Techniques to Enhance Drainage of Retained Hemothorax.

Background. Retained hemothorax (RH) is a common problem in cardiothoracic and trauma surgery. We aimed to determine the optimum agitation technique to enhance thrombus dissolution and drainage and to apply the technique to a porcine-retained hemothorax. Methods. Three agitation techniques were tested: flush irrigation, ultrasound, and vibration. We used the techniques in a benchtop model with tissue plasminogen activator (tPA) and pig hemothorax with tPA. We used the most promising technique vibration in a pig hemothorax without tPA. Statistics. We used 2-sample t tests for each comparison and Cohen d tests to calculate effect size (ES). Results. In the benchtop model, mean drainages in the agitation group and control group and the ES were flush irrigation, 42%, 28%, and 2.91 (P = .10); ultrasound, 35%, 27%, and .76 (P = .30); and vibration, 28%, 19%, and 1.14 (P = .04). In the pig hemothorax with tPA, mean drainages and the ES of each agitation technique compared with control (58%) were flush irrigation, 80% and 1.14 (P = .37); ultrasound, 80% and 2.11 (P = .17); and vibration, 95% and 3.98 (P = .06). In the pig hemothorax model without tPA, mean drainages of the vibration technique and control group were 50% and 43% (ES = .29; P = .65). Discussion. In vitro studies suggested flush irrigation had the greatest effect, whereas only vibration was significantly different vs the respective controls. In vivo with tPA, vibration showed promising but not statistically significant results. Results of in vivo experiments without tPA were negative. Conclusion. Agitation techniques, in combination with tPA, may enhance drainage of hemothorax.

Minocycline reverses IL-17A/TRAF3IP2-mediated p38 MAPK/NF-κB/iNOS/NO-dependent cardiomyocyte contractile depression and death.

Minocycline, an FDA-approved second-generation semisynthetic tetracycline, exerts antioxidant, anti-apoptotic and anti-inflammatory effects, independent of its antimicrobial properties. Interleukin (IL)-17A is an immune and inflammatory mediator, and its sustained induction is associated with various cardiovascular diseases. Here we investigated (i) whether IL-17A induces cardiomyocyte contractile depression and death, (ii) whether minocycline reverses IL-17A's negative inotropic effects and (iii) investigated the underlying molecular mechanisms. Indeed, treatment with recombinant mouse IL-17A impaired adult cardiomyocyte contractility as evidenced by a 34% inhibition in maximal velocity of shortening and relengthening after 4 h (P < .01). Contractile depression followed iNOS induction at 2 h (2.13-fold, P < .01) and NO generation at 3 h (3.71-fold, P <.01). Further mechanistic investigations revealed that IL-17A-dependent induction of iNOS occurred via TRAF3IP2, TRAF6, TAK1, NF-κB, and p38MAPK signaling. 1400 W, a highly specific iNOS inhibitor, suppressed IL-17A-induced NO generation and contractile depression, where as the NO donors SNAP and PAPA-NONOate both suppressed cardiomyocyte contractility. IL-17A also stimulated cardiomyocyte IL-1ß and TNF-α secretion, however, their neutralization failed to modulate IL-17A-mediated contractile depression or viability. Further increases of IL-17A concentration and the duration of exposure enhanced IL-1ß and TNF-α secreted levels, buthad no impact on adult cardiomyocyte viability. However, when combined with pathophysiological concentrations of IL-1ß or TNF-α, IL-17A promoted adult cardiomyocyte death. Importantly, minocycline blunted IL-17A-mediated deleterious effects, indicating its therapeutic potential in inflammatory cardiac diseases.

Intrapleural Impedance Sensor Real-Time Tracking of Pneumothorax in a Porcine Model of Air Leak.

In patients with alveolar-to-pleural air leak due to recent surgery or trauma, clinicians tend to manage chest tubes with suction therapy. Nonsuction therapy is associated with shorter chest tube duration but also a higher risk of pneumothorax. We sought to develop an intrapleural electrical impedance sensor for continuous, real-time monitoring of pneumothorax development in a porcine model of air leak as a means of promoting nonsuction therapy. Using thoracoscopy, 2 chest tubes and the pleural impedance sensor were introduced into the pleural space of 3 pigs. Continuous air leak was introduced through 1 chest tube by carbon dioxide insufflation. The second chest tube was placed to suction then transitioned to no suction at increasingly higher air leaks until pneumothorax developed. Simultaneously, real-time impedance measurements were obtained from the pleural sensor. Fluoroscopy spot images were captured to verify the presence or absence of pneumothorax. Statistical Analysis Software was used throughout. With the chest tube on suction, a fully expanded lung was identified by a distinct pleural electrical impedance respiratory waveform. With transition of the chest tube to water seal, loss of contact of the sensor with the lung resulted in an immediate measurement of infinite electrical impedance. Pneumothorax resolution by restoring suction therapy was detected in real time by a return of the normal respiratory impedance waveform. Pleural electrical impedance monitoring detected pneumothorax development and resolution in real time. This simple technology has the potential to improve the safety and quality of chest tube management.

Empagliflozin reduces high glucose-induced oxidative stress and miR-21-dependent TRAF3IP2 induction and RECK suppression, and inhibits human renal proximal tubular epithelial cell migration and epithelial-to-mesenchymal transition.

Proximal tubular epithelial cells (PTEC) in the S1 segment of the kidney abundantly express sodium-glucose co-transporters (SGLT) that play a critical role in whole body glucose homeostasis. We recently reported suppression of RECK (Reversion Inducing Cysteine Rich Protein with Kazal Motifs), a membrane anchored endogenous MMP inhibitor and anti-fibrotic mediator, in the kidneys of db/db mice, a model of diabetic kidney disease (DKD), as well as in high glucose (HG) treated human kidney proximal tubule cells (HK-2). We further demonstrated that empagliflozin (EMPA), an SGLT2 inhibitor, reversed these effects. Little is known regarding the mechanisms underlying RECK suppression under hyperglycemic conditions, and its rescue by EMPA. Consistent with our previous studies, HG (25 mM) suppressed RECK expression in HK-2 cells. Further mechanistic investigations revealed that HG induced superoxide and hydrogen peroxide generation, oxidative stress-dependent TRAF3IP2 upregulation, NF-κB and p38 MAPK activation, inflammatory cytokine expression (IL-1ß, IL-6, TNF-α, and MCP-1), miR-21 induction, MMP2 activation, and RECK suppression. Moreover, RECK gain-of-function inhibited HG-induced MMP2 activation and HK-2 cell migration. Similar to HG, advanced glycation end products (AGE) induced TRAF3IP2 and suppressed RECK, effects that were inhibited by EMPA. Importantly, EMPA treatment ameliorated all of these deleterious effects, and inhibited epithelial-to-mesenchymal transition (EMT) and HK-2 cell migration. Collectively, these findings indicate that hyperglycemia and associated AGE suppress RECK expression via oxidative stress/TRAF3IP2/NF-κB and p38 MAPK/miR-21 induction. Furthermore, these results suggest that interventions aimed at restoring RECK or inhibiting SGLT2 have the potential to treat kidney inflammatory response/fibrosis and nephropathy under chronic hyperglycemic conditions, such as DKD.