39 research outputs found
Digital communication platforms in cardiothoracic surgery during COVID-19 pandemic: keeping us connected or isolated?
During the COVID-19 pandemic, performing a surgeonâs duties has become challenging while adhering to social distancing mandates. To aid in the continuity of healthcare services, rapid implementation of digital communication tools became a necessity. This is an account of experiences using digital communication platforms, namely Microsoft Teams and Zoom, for clinical and educative purposes in the field of Cardiothoracic Surgery in the UK. While enabling ongoing virtual clinical meetings, conferences and learning opportunities for residents with little face-to-face contact, are these digital communication platforms keeping us connected or isolated
Direct evidence for microdomain-specific localization and remodeling of functional L-type calcium channels in rat and human atrial myocytes
BackgroundâDistinct subpopulations of L-type calcium channels (LTCCs) with different functional properties exist in cardiomyocytes. Disruption of cellular structure may affect LTCC in a microdomain-specific manner and contribute to the pathophysiology of cardiac diseases, especially in cells lacking organized transverse tubules (T-tubules) such as atrial myocytes (AMs). Methods and ResultsâIsolated rat and human AMs were characterized by scanning ion conductance, confocal, and electron microscopy. Half of AMs possessed T-tubules and structured topography, proportional to cell width. A bigger proportion of myocytes in the left atrium had organized T-tubules and topography than in the right atrium. Super-resolution scanning patch clamp showed that LTCCs distribute equally in T-tubules and crest areas of the sarcolemma, whereas, in ventricular myocytes, LTCCs primarily cluster in T-tubules. Rat, but not human, T-tubule LTCCs had open probability similar to crest LTCCs, but exhibited â40% greater current. Optical mapping of Ca2+ transients revealed that rat AMs presented â3-fold as many spontaneous Ca2+ release events as ventricular myocytes. Occurrence of crest LTCCs and spontaneous Ca2+ transients were eliminated by either a caveolae-targeted LTCC antagonist or disrupting caveolae with methyl-β-cyclodextrin, with an associated â30% whole-cell ICa,L reduction. Heart failure (16 weeks postâmyocardial infarction) in rats resulted in a T-tubule degradation (by â40%) and significant elevation of spontaneous Ca2+ release events. Although heart failure did not affect LTCC occurrence, it led to â25% decrease in T-tubule LTCC amplitude. ConclusionsâWe provide the first direct evidence for the existence of 2 distinct subpopulations of functional LTCCs in rat and human AMs, with their biophysical properties modulated in heart failure in a microdomain-specific manner
Aged-senescent cells contribute to impaired heart regeneration
Aging leads to increased cellular senescence and is associated with decreased potency of tissueâspecific stem/progenitor cells. Here, we have done an extensive analysis of cardiac progenitor cells (CPCs) isolated from human subjects with cardiovascular disease, aged 32â86 years. In aged subjects (>70 years old), over half of CPCs are senescent (p16INK4A, SAâβâgal, DNA damage ÎłH2AX, telomere length, senescenceâassociated secretory phenotype [SASP]), unable to replicate, differentiate, regenerate or restore cardiac function following transplantation into the infarcted heart. SASP factors secreted by senescent CPCs renders otherwise healthy CPCs to senescence. Elimination of senescent CPCs using senolytics abrogates the SASP and its debilitative effect in vitro. Global elimination of senescent cells in aged mice (INKâATTAC or wildâtype mice treated with D + Q senolytics) in vivo activates resident CPCs and increased the number of small Ki67â, EdUâpositive cardiomyocytes. Therapeutic approaches that eliminate senescent cells may alleviate cardiac deterioration with aging and restore the regenerative capacity of the heart.This work was supported by British Heart Foundation project grant PG/14/11/30657 (GMEâH and J.E.C.), NIH grant AG13925 (JLK), the Connor Group (JLK), Robert J. and Theresa W. Ryan (JLK), Robert and Arlene Kogod (JLK), the Noaber Foundation (JLK), Glenn/American Federation for Aging Research (AFAR) BIG Award (J.L.K.) and Italian Ministry of Health grant GRâ2010â2318945
Prognostic model to predict postoperative acute kidney injury in patients undergoing major gastrointestinal surgery based on a national prospective observational cohort study.
Background: Acute illness, existing co-morbidities and surgical stress response can all contribute to postoperative acute kidney injury (AKI) in patients undergoing major gastrointestinal surgery. The aim of this study was prospectively to develop a pragmatic prognostic model to stratify patients according to risk of developing AKI after major gastrointestinal surgery. Methods: This prospective multicentre cohort study included consecutive adults undergoing elective or emergency gastrointestinal resection, liver resection or stoma reversal in 2-week blocks over a continuous 3-month period. The primary outcome was the rate of AKI within 7 days of surgery. Bootstrap stability was used to select clinically plausible risk factors into the model. Internal model validation was carried out by bootstrap validation. Results: A total of 4544 patients were included across 173 centres in the UK and Ireland. The overall rate of AKI was 14¡2 per cent (646 of 4544) and the 30-day mortality rate was 1¡8 per cent (84 of 4544). Stage 1 AKI was significantly associated with 30-day mortality (unadjusted odds ratio 7¡61, 95 per cent c.i. 4¡49 to 12¡90; P < 0¡001), with increasing odds of death with each AKI stage. Six variables were selected for inclusion in the prognostic model: age, sex, ASA grade, preoperative estimated glomerular filtration rate, planned open surgery and preoperative use of either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. Internal validation demonstrated good model discrimination (c-statistic 0¡65). Discussion: Following major gastrointestinal surgery, AKI occurred in one in seven patients. This preoperative prognostic model identified patients at high risk of postoperative AKI. Validation in an independent data set is required to ensure generalizability