Bilateral video-assisted thoracoscopic pulmonary vein isolation with excision of the left atrial appendage is feasible and safe and offers a promising, new, minimally invasive, beating-heart approach for curative surgical treatment of atrial fibrillation.

Objective We evaluated focused training in coronary artery anastomosis with a porcine heart model and portable task station. Methods At “Boot Camp,” 33 first-year cardiothoracic surgical residents participated in 4-hour coronary anastomosis sessions (6–7 attending surgeons per group of 8–9 residents). At beginning, midpoint, and session end, anastomosis components were assessed on a 3-point rating scale (1 good, 2 average, 3 below average). Performances were video recorded and reviewed by 3 surgeons in a blinded fashion. Participants completed questionnaires at session end, with follow-up surveys at 6 months. Results Ten to 18 end-to-side anastomoses with porcine model and task station were performed. Initial assessments ranged from 2.11 ± 0.58 (forceps use) to 2.44 ± 0.48 (needle angles). Midpoint scores ranged from 1.76 ± 0.63 (forceps use) to 1.91 ± 0.49 (needle angles). Session end scores ranged from 1.29 ± 0.45 (needle holder use) to 1.58 ± 0.50 (needle transfer and suture management and tension; P < .001). Video recordings confirmed improved performance (interrater reliability > 0.5). All respondents agreed that task station and porcine model were good methods of training. At 6 months, respondents noted that the anastomosis session provided a basis for training; however, only slightly more than half continued to practice outside the operating room. Conclusions Four-hour focused training with porcine model and task station resulted in improved ability to perform anastomoses. Boot Camp may be useful in preparing residents for coronary anastomosis in the clinical setting, but emphasis on simulation development and deliberate practice is necessary.

Aortic valve calcification is the most common form of valvular heart disease, but the mechanisms of calcific aortic valve disease (CAVD) are unknown. NOTCH1 mutations are associated with aortic valve malformations and adult-onset calcification in families with inherited disease. The Notch signaling pathway is critical for multiple cell differentiation processes, but its role in the development of CAVD is not well understood. The aim of this study was to investigate the molecular changes that occur with inhibition of Notch signaling in the aortic valve. Notch signaling pathway members are expressed in adult aortic valve cusps, and examination of diseased human aortic valves revealed decreased expression of NOTCH1 in areas of calcium deposition. To identify downstream mediators of Notch1, we examined gene expression changes that occur with chemical inhibition of Notch signaling in rat aortic valve interstitial cells (AVICs). We found significant downregulation of Sox9 along with several cartilage-specific genes that were direct targets of the transcription factor, Sox9. Loss of Sox9 expression has been published to be associated with aortic valve calcification. Utilizing an in vitro porcine aortic valve calcification model system, inhibition of Notch activity resulted in accelerated calcification while stimulation of Notch signaling attenuated the calcific process. Finally, the addition of Sox9 was able to prevent the calcification of porcine AVICs that occurs with Notch inhibition. In conclusion, loss of Notch signaling contributes to aortic valve calcification via a Sox9-dependent mechanism.

During embryogenesis the heart valves develop from undifferentiated mesenchymal endocardial cushions (EC), and activated interstitial cells of adult diseased valves share characteristics of embryonic valve progenitors. Twist1, a class II basic-helix-loop-helix (bHLH) transcription factor, is expressed during early EC development and is downregulated later during valve remodeling. The requirements for Twist1 down-regulation in the remodeling valves and the consequences of prolonged Twist1 activity were examined in transgenic mice with persistent expression of Twist1 in developing and mature valves. Persistent Twist1 expression in the remodeling valves leads to increased valve cell proliferation, increased expression of Tbx20, and increased extracellular matrix (ECM) gene expression, characteristic of early valve progenitors. Among the ECM genes predominant in the EC, Col2a1 was identified as a direct transcriptional target of Twist1. Increased Twist1 expression also leads to dysregulation of fibrillar collagen and periostin expression, as well as enlarged hypercellular valve leaflets prior to birth. In human diseased aortic valves, increased Twist1 expression and cell proliferation are observed adjacent to nodules of calcification. Overall, these data implicate Twist1 as a critical regulator of valve development and suggest that Twist1 influences ECM production and cell proliferation during disease.

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