The use of transesophageal echocardiography to predict surgical complexity scoring system for degenerative mitral valve repair.

BACKGROUND: For severe mitral valve (MV) degenerative disease, repair is recommended. Prediction of repair complexity and referral to high volume centers can increase rates of successful repair. This study sought to demonstrate that TEE is a feasible imaging modality to predict the complexity of surgical MV repair. METHODS: Two hundred TEE examinations of patients who underwent MV repair (2009-2011) were retrospectively reviewed and scored by two cardiac anesthesiologists. TEE scores were compared to surgical complexity scores, which were previously assigned based on published methods. Kappa values were reported for the agreement of TEE and surgical scores. McNemar's tests were used to test the homogeneity of the marginal probabilities of different scoring categories. RESULTS: TEE scores were slightly lower (2[1,3]) than surgical scores (3[1,4]). The agreement was 66% between the scoring methods, with a moderate kappa (.46). Using surgical scores as the gold standard, 70%, 71%, and 46% of simple, intermediate and complex surgical scores, respectively, were correctly scored by TEE. P1, P2, P3, and A2 prolapse were easiest to identify with TEE and had the highest agreement with surgical scoring (P1 agreement 79% with kappa .55, P2 96% [kappa .8], P3 77% [kappa .51], A2 88% [kappa .6]). The lowest agreement between the two scores occurred with A1 prolapse (kappa .05) and posteromedial commissure prolapse (kappa .14). In the presence of significant disagreement, TEE scores were more likely to be of higher complexity than surgical. McNemar's test was significant for prolapse of P1 (p = .005), A1 (p = .025), A2 (p = .041), and the posteromedial commissure (p < .0001). CONCLUSION: TEE-based scoring is feasible for prediction of the complexity of MV surgical repair, thus allowing for preoperative stratification.

Critical Care Simulation Education Program During the COVID-19 Pandemic.

BACKGROUND: Coronaviruses are important emerging human and animal pathogens. SARS-CoV-2, the virus that causes COVID-19, is responsible for the current global pandemic. Early in the course of the pandemic, New York City became one of the world's "hot spots" with more than 250,000 cases and more than 15,000 deaths. Although medical providers in New York were fortunate to have the knowledge gained in China and Italy before it came under siege, the magnitude and severity of the disease were unprecedented and arguably under appreciated. The surge of patients with significant COVID-19 threatened to overwhelm health care systems, as New York City health systems realized that the number of specialized critical care providers would be inadequate. A large academic medical system recognized that rapid redeployment of noncritical providers into such roles would be needed. An educational gap was therefore identified: numerous providers with minimal critical care knowledge or experience would now be required to provide critical-level patient care under supervision of intensivists. Safe provision of such high level of patient care mandated the development of "educational crash courses." METHODS: The purpose of this special article is to summarize the approach adopted by the Institute for Critical Care Medicine and Department of Anesthesiology, Perioperative and Pain Medicine's Human Emulation, Education, and Evaluation Lab for Patient Safety and Professional Study Simulation Center in developing a training program for noncritical care providers in this novel disease. RESULTS: Using this joint approach, we were able to swiftly educate a wide range of nonintensive care unit providers (such as surgical, internal medicine, nursing, and advanced practice providers) by focusing on refreshing critical care knowledge and developing essential skillsets to assist in the care of these patients. CONCLUSIONS: We believe that the practical methods reviewed here could be adopted by any health care system that is preparing for an unprecedented surge of critically ill patients.

Does chronic atrial fibrillation induce cardiac remodeling?

AIM: The aim of this study was to compare cardiac structure and function in patients with chronic atrial fibrillation (CAF), as opposed to patients with paroxysmal atrial fibrillation (PAF), and normal control subjects. METHODS AND RESULTS: This study included 83 patients, divided into 3 groups: group A, 32 patients with CAF for ≥6 months; group B, 29 patients in sinus rhythm with a documented history of PAF; and group C, 22 patients without history of atrial fibrillation. Patients with CAF were older (71 years vs. 64 in group B, and 64 in group C). Apart from age, groups were clinically similar. After careful clinical evaluation, comprehensive echocardiography studies were performed including cardiac chambers' size, systolic and diastolic left ventricular function. Left atrium (LA) volume index was significantly larger in CAF than PAF and control patients: 39 ± 13 versus 34 ± 9 versus 25 ± 8 (P < 0.003). Left ventricular ejection fraction was lower in CAF: 53.8 ± 7 versus 61.6 ± 6.7 versus 58.4 ± 5.2% (P < 0.001). Isovolumic relaxation time was shorter in CAF, 65 ± 16 versus 82 ± 21 versus 81 ± 13 msec (P < 0.001). E/Vp was significantly greater in CAF 2.6 ± 0.8 versus 1.7 ± 0.4 versus 1.7 ± 0.5 (P < 0.001). Additional diastolic parameters were also significantly different. CONCLUSION: These findings demonstrate that in patients with CAF structural and functional cardiac changes occur. Patients with CAF as opposed to both normal subjects and patients with PAF have larger left atria and reduced systolic and diastolic left ventricular function.

Connexin40 imparts conduction heterogeneity to atrial tissue.

Impulse propagation in cardiac tissue is a complex process in which intercellular coupling through gap junction channels is a critical component. Connexin40 (Cx40) is an abundant gap junction protein that is expressed in atrial myocytes. Alterations in the expression of Cx40 have been implicated in atrial arrhythmogenesis. The purpose of the current study was to assess the role of Cx40 in atrial impulse propagation. High-resolution optical mapping was used to study conduction in the right and left atrial appendages of isolated Langendorff-perfused murine hearts. Wild-type (Cx40(+/+)), heterozygous (Cx40(+/-)), and knockout (Cx40(-/-)) mice, both adult and embryonic, were studied to assess the effects of reduced Cx40 expression on sinus node function and conduction velocity at different pacing cycle lengths (100 and 60 ms). In both adult and late-stage embryonic Cx40(+/+) mice, heterogeneity in CV was found between the right and left atrial appendages. Either partial (Cx40(+/-)) or complete (Cx40(-/-)) deletion of Cx40 was associated with the loss of conduction heterogeneity in both adult and embryonic mice. Additionally, sinus node impulse initiation was found to be ectopic in Cx40(-/-) mice at 15.5 days postcoitus, whereas Cx40(+/+) mice showed normal activation occurring near the crista terminalis. Our findings suggest that Cx40 plays an essential role in establishing interatrial conduction velocity heterogeneity in the murine model. Additionally, we describe for the first time a developmental requirement for Cx40 in normal sinus node impulse initiation at 15.5 days postcoitus.