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

Nurses' perceptions of aids and obstacles to the provision of optimal end of life care in ICU

Contains fulltext : 172380.pdf (publisher's version ) (Open Access

Disparities in insurance coverage among hospitalized adult congenital heart disease patients before and after the Affordable Care Act

BackgroundData are lacking regarding the insurance status of adults with congenital heart disease (ACHD). We investigated whether the Affordable Care Act (ACA) impacted insurance status among hospitalized ACHD, identified associated sociodemographic factors, and compared coverage to adults with other chronic childhood conditions.MethodsSerial cross‐sectional analysis of National Inpatient Sample hospitalizations from 2007 to 2016 was performed for patients 18–64 years old. ACHD were identified using ICD‐9/10‐CM codes and compared to patients with sickle cell disease (SCD), cystic fibrosis (CF), and the general population. Age was dichotomized as 18–25 years (transition aged) or 26–64 years. Groups were compared by era (pre‐ACA [January 2007–June 2010]; early‐ACA [July 2010–December 2013], which eliminated pre‐existing condition exclusions; and full‐ACA [January 2014–December 2016]) using interrupted time series and multivariable Poisson regression analyses.ResultsOverall, uninsured hospitalizations decreased from pre‐ACA (12.0%) to full‐ACA (8.5%). After full ACA implementation, ACHD had lower uninsured rates than the general hospitalized population (6.0 vs. 8.6%, p < .01), but higher rates than those with other chronic childhood diseases (SCD [4.5%]; CF [1.6%]). Across ACA eras, transition aged ACHD had higher uninsured rates than older patients (8.9 vs. 7.6%, p < .01), and Hispanic patients remained less insured than other groups.ConclusionsHospitalized ACHD were better insured than the general population but less insured than those with SCD or CF. Full ACA implementation was associated with improved insurance coverage for all groups, but disparities persisted for transition aged and Hispanic patients. Ongoing evaluation of the effects of insurance and health policy on ACHD remains critical to diminish health disparities.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/167545/1/bdr21878_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/167545/2/bdr21878.pd

Cardiac Lineage Protein-1 (CLP-1) Regulates Cardiac Remodeling via Transcriptional Modulation of Diverse Hypertrophic and Fibrotic Responses and Angiotensin II-transforming Growth Factor β (TGF-β1) Signaling Axis.

It is well known that the renin-angiotensin system contributes to left ventricular hypertrophy and fibrosis, a major determinant of myocardial stiffness. TGF-β1 and renin-angiotensin system signaling alters the fibroblast phenotype by promoting its differentiation into morphologically distinct pathological myofibroblasts, which potentiates collagen synthesis and fibrosis and causes enhanced extracellular matrix deposition. However, the atrial natriuretic peptide, which is induced during left ventricular hypertrophy, plays an anti-fibrogenic and anti-hypertrophic role by blocking, among others, the TGF-β-induced nuclear localization of Smads. It is not clear how the hypertrophic and fibrotic responses are transcriptionally regulated. CLP-1, the mouse homolog of human hexamethylene bis-acetamide inducible-1 (HEXIM-1), regulates the pTEFb activity via direct association with pTEFb causing inhibition of the Cdk9-mediated serine 2 phosphorylation in the carboxyl-terminal domain of RNA polymerase II. It was recently reported that the serine kinase activity of Cdk9 not only targets RNA polymerase II but also the conserved serine residues of the polylinker region in Smad3, suggesting that CLP-1-mediated changes in pTEFb activity may trigger Cdk9-dependent Smad3 signaling that can modulate collagen expression and fibrosis. In this study, we evaluated the role of CLP-1 in vivo in induction of left ventricular hypertrophy in angiotensinogen-overexpressing transgenic mice harboring CLP-1 heterozygosity. We observed that introduction of CLP-1 haplodeficiency in the transgenic α-myosin heavy chain-angiotensinogen mice causes prominent changes in hypertrophic and fibrotic responses accompanied by augmentation of Smad3/Stat3 signaling. Together, our findings underscore the critical role of CLP-1 in remodeling of the genetic response during hypertrophy and fibrosis

Trends in mortality from aortic dissection analyzed from the World Health Organization Mortality Database from 2000 to 2017

Background: We assessed trends in aortic dissection (AD) death rates in 23 countries from 2000 to 2017. Methods: We extracted AD mortality data for countries with high usability data from the World Health Organization (WHO) Mortality Database and from the Center for Disease Control (CDC) WONDER Database for the United States of America (USA). Age Standardized Death Rates (ASDRs) per 100,000 population were computed. Trends were assessed by locally weighted scatter plot smoother (LOWESS) regression. Results: Between 2000 and 2017, ASDRs from AD decreased in Australia, Belgium, Croatia, Denmark, France, Italy, New Zealand, Norway, Sweden, the United Kingdom, and the USA for both sexes. Increasing AD mortality was observed in Austria, Czech Republic, Germany, Hungary, Israel, and Japan for both sexes. The largest absolute increases in ASDR were in Japan for men (+1.59) and women (+1.11). The largest percentage decreases were in Norway for men (−0.91) and in New Zealand (−0.6) for women. In 2017, the highest mortality rates were in Japan for both sexes (3.22 and 2.09, respectively). The lowest ASDR was in Kyrgyzstan for both sexes (0.16 and 0.10, respectively). ASDRs for AD in 2017 were higher for men than women in all countries included. Spain had the greatest difference between the gender's mortality rates with a 2.71-fold higher mortality average rate in men. Conclusion: We identified an overall decrease in AD mortality in most included countries, while an increase was noted in other countries including Israel and Japan

Demographic and state-level trends in mortality due to ischemic heart disease in the United States frmo 1999-2019

Although there have been advances in ischemic heart disease (IHD) care, variation in IHD-related mortality trends across the United States has not been well described. We used the CDC-WONDER database to evaluate variation in IHD-related mortality for demographic groups in the U.S. between 1999 and 2019. Age-adjusted mortality rates (AAMR) were stratified by sex, race, Hispanic ethnicity, and U.S. state. Crude mortality rates were evaluated using 10-year age groups. IHD-related AAMR decreased from 195 to 88 per 100,000 nationally, with slower decline from 2010-2019 (average annual percent change [AAPC] -2.6% [95% CI -2.9% to -2.2%) compared to 2002-2010 (AAPC -5.3% [95% CI -5.6% to -4.9%]). All groups had decreases in AAMR, though black populations persistently had the highest AAMR, and women had greater relative decreases than men. AAPC was -3.7% for white men; -4.7% for white women; -3.9% for black men; -4.9% for black women; -4.1% for Hispanic men, and -5.1% for Hispanic women. Populations ≥65 years old had greater relative mortality declines compared to populations <65 years. The median AAMR (2019) and AAPC (1999-2019) across states was 86.3 (range 58 – 134) and -3.8% (range -1.7% to -4.8%), respectively. In conclusion, mortality declines due to IHD have slowed in the U.S., with significant geographic variation. Black populations persistently had the highest AAMR, and declines were relatively greater for women and populations ≥65 years. The impact of demographics and geography on IHD should be further explored and addressed as part of public health measures

Supplementary Material for: Sleep Apnea as a Risk Factor for Diastolic Dysfunction: A Systematic Review and Meta-Analysis

Background: This meta-analysis assessed the relationship between obstructive sleep apnea (OSA) and echocardiographic parameters of diastolic dysfunction (DD), which are used in the assessment of heart failure with preserved ejection fraction. Methods: We searched the databases including Ovid MEDLINE, Ovid Embase, Scopus, Web of Science, Google Scholar, and EBSCO CINAHL from inception up to December 26, 2020. The search was not restricted to time, publication status, or language. Two independent investigators screened the identified studies and extracted the data in duplicate. We conducted a meta-analysis using RevMan v.5. The risk of bias was assessed using Cochrane collaboration tools. Comparisons were made between patients with OSA, diagnosed in-laboratory polysomnography or home sleep apnea testing, and patients without OSA in relation to established markers of DD. Results: Primary search identified 2,512 studies. A total of 18 studies including 2,509 participants were included. The two groups were free of conventional cardiovascular risk factors. Significant structural changes were observed between the two groups. Patients with OSA exhibited greater left atrial volume index (LAVI) (3.94 95% CI [0.8, 7.07]; p = 0.000) and left ventricular mass index (11.10 95% CI [2.56, 19.65]; p = 0.000) as compared to control group. The presence of OSA was also associated with more prolonged deceleration time (10.44 ms 95% CI [0.71, 20.16]; p = 0.04), isovolumic relaxation time (IVRT) (7.85 ms 95% CI [4.48, 11.22]; p = 0.000), and a lower ratio of early to late mitral inflow velocities (E/A) ratio (−0.62 95% CI [−1, −0.24]; p = 0.001) suggestive of early DD. The early mitral inflow velocity to mitral annular early diastolic velocity (E/e′) ratio (0.94 95% CI [0.44, 1.45]; p = 0.000) was increased. Linear correlation between severity of OSA and LAVI and IVRT parameters was observed but this association did not sustain for the E/A and E/e′. The ejection fraction was not significantly different between patients with OSA and healthy controls (−0.48 95% CI [−1.18, 0.23]; p = 0.18). Conclusion: An association between OSA and echocardiographic parameters of DD was detected that was independent of conventional cardiovascular risk factors. OSA may be independently associated with DD perhaps due to higher LV mass. Investigating the role of continuous positive airway pressure therapy in reversing or ameliorating DD is recommended