Circulating biomarkers of the CS4P and CLIP scores are not altered in a pig model of acute cardiogenic shock and additional short-term circulatory support.

Background: Cardiogenic shock (CS) is the leading cause of death in patients with myocardial infarction with a mortality rate greater than 50%. Recently, the CS 4 Proteins (CS4P) and CLIP scores have been developed to predict survival in CS patients. However, their impact in acute CS and additional short-term left ventricular (LV) circulatory support as prognostic markers is currently not known.

Dashboard of Short-Term Postoperative Patient Outcomes for Anesthesiologists: Development and Preliminary Evaluation.

Background: Anesthesiologists require an understanding of their patients' outcomes to evaluate their performance and improve their practice. Traditionally, anesthesiologists had limited information about their surgical outpatients' outcomes due to minimal contact post discharge. Leveraging digital health innovations for analyzing personal and population outcomes may improve perioperative care.

C1q and Tumor Necrosis Factor Related Protein 9 Protects from Diabetic Cardiomyopathy by Alleviating Cardiac Insulin Resistance and Inflammation.

(1) Background: Diabetic cardiomyopathy is a major health problem worldwide. CTRP9, a secreted glycoprotein, is mainly expressed in cardiac endothelial cells and becomes downregulated in mouse models of diabetes mellitus; (2) Methods: In this study, we investigated the impact of CTRP9 on early stages of diabetic cardiomyopathy induced by 12 weeks of high-fat diet; (3) Results: While the lack of CTRP9 in knock-out mice aggravated insulin resistance and triggered diastolic left ventricular dysfunction, AAV9-mediated cardiac CTRP9 overexpression ameliorated cardiomyopathy under these conditions. At this early disease state upon high-fat diet, no fibrosis, no oxidative damage and no lipid deposition were identified in the myocardium of any of the experimental groups.

miRNA-200b-A Potential Biomarker Identified in a Porcine Model of Cardiogenic Shock and Mechanical Unloading.

Background: Cardiogenic shock (CS) alters whole body metabolism and circulating biomarkers serve as prognostic markers in CS patients. Percutaneous ventricular assist devices (pVADs) unload the left ventricle by actively ejecting blood into the aorta. The goal of the present study was to identify alterations in circulating metabolites and transcripts in a large animal model that might serve as potential prognostic biomarkers in acute CS and additional left ventricular unloading by Impella pVAD support.

Analysis of myocardial cellular gene expression during pressure overload reveals matrix based functional intercellular communication.

To identify cellular mechanisms responsible for pressure overload triggered heart failure, we isolated cardiomyocytes, endothelial cells, and fibroblasts as most abundant cell types from mouse hearts in the subacute and chronic stages after transverse aortic constriction (TAC) and performed RNA-sequencing. We detected highly cell-type specific transcriptional responses with characteristic time courses and active intercellular communication. Cardiomyocytes after TAC exerted an early and sustained upregulation of inflammatory and matrix genes and a concomitant suppression of metabolic and ion channel genes.

Skeletal muscle derived Musclin protects the heart during pathological overload.

Cachexia is associated with poor prognosis in chronic heart failure patients, but the underlying mechanisms of cachexia triggered disease progression remain poorly understood. Here, we investigate whether the dysregulation of myokine expression from wasting skeletal muscle exaggerates heart failure. RNA sequencing from wasting skeletal muscles of mice with heart failure reveals a reduced expression of Ostn, which encodes the secreted myokine Musclin, previously implicated in the enhancement of natriuretic peptide signaling.

Fibroblast GATA-4 and GATA-6 promote myocardial adaptation to pressure overload by enhancing cardiac angiogenesis.

Heart failure due to high blood pressure or ischemic injury remains a major problem for millions of patients worldwide. Despite enormous advances in deciphering the molecular mechanisms underlying heart failure progression, the cell-type specific adaptations and especially intercellular signaling remain poorly understood. Cardiac fibroblasts express high levels of cardiogenic transcription factors such as GATA-4 and GATA-6, but their role in fibroblasts during stress is not known.

Intraoperative Extubation Post Arterial Switch Operation for Transposition of the Great Arteries With Intact Ventricular Septum: A One-Year, Single Center Experience.

We sought to examine the clinical impact of intraoperative extubation (IE) in neonates undergoing the arterial switch operation (ASO) for D-transposition of the great arteries with intact ventricular septum (dTGA/IVS). This was a single center retrospective study of patients who underwent ASO for dTGA/IVS in the 12 months after an institutional change in practice favoring IE when clinically feasible. A control group was obtained by identifying the same number of consecutive patients with dTGA/IVS who underwent ASO immediately prior to this institutional change in practice, none of whom were extubated intraoperatively.

Inactivation of Sox9 in fibroblasts reduces cardiac fibrosis and inflammation.

Fibrotic scarring drives the progression of heart failure after myocardial infarction (MI). Therefore, the development of specific treatment regimens to counteract fibrosis is of high clinical relevance. The transcription factor SOX9 functions as an important regulator during embryogenesis, but recent data point towards an additional causal role in organ fibrosis.

The transcription factor GATA4 promotes myocardial regeneration in neonatal mice.

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Anti-androgenic therapy with finasteride improves cardiac function, attenuates remodeling and reverts pathologic gene-expression after myocardial infarction in mice.

Maladaptive cardiac remodeling after myocardial infarction (MI) is increasingly contributing to the prevalence of chronic heart failure. Women show less severe remodeling, a reduced mortality and a better systolic function after MI compared to men. Although sex hormones are being made responsible for these differences, it remains currently unknown how this could be translated into therapeutic strategies.

The transcription factor GATA4 promotes myocardial regeneration in neonatal mice.

Heart failure is often the consequence of insufficient cardiac regeneration. Neonatal mice retain a certain capability of myocardial regeneration until postnatal day (P)7, although the underlying transcriptional mechanisms remain largely unknown. We demonstrate here that cardiac abundance of the transcription factor GATA4 was high at P1, but became strongly reduced at P7 in parallel with loss of regenerative capacity.

C1q-TNF-Related Protein-9 Promotes Cardiac Hypertrophy and Failure.

Rationale: Myocardial endothelial cells promote cardiomyocyte hypertrophy, possibly through the release of growth factors. The identity of these factors, however, remains largely unknown, and we hypothesized here that the secreted CTRP9 (C1q-tumor necrosis factor-related protein-9) might act as endothelial-derived protein to modulate heart remodeling in response to pressure overload.

Objective: To examine the source of cardiac CTRP9 and its function during pressure overload.

MicroRNA-Based Therapy of GATA2-Deficient Vascular Disease.

Background: The transcription factor GATA2 orchestrates the expression of many endothelial-specific genes, illustrating its crucial importance for endothelial cell function. The capacity of this transcription factor in orchestrating endothelial-important microRNAs (miRNAs/miR) is unknown.

Methods: Endothelial GATA2 was functionally analyzed in human endothelial cells in vitro.

Antiandrogenic therapy with finasteride attenuates cardiac hypertrophy and left ventricular dysfunction.

Background: In comparison with men, women have a better prognosis when experiencing aortic valve stenosis, hypertrophic cardiomyopathy, or heart failure. Recent data suggest that androgens like testosterone or the more potent dihydrotestosterone contribute to the development of cardiac hypertrophy and failure. Therefore, we analyzed whether antiandrogenic therapy with finasteride, which inhibits the generation of dihydrotestosterone by the enzyme 5-α-reductase, improves pathological ventricular remodeling and heart failure.

Should early extubation be the goal for children after congenital cardiac surgery?

Objective: We sought to determine the feasibility and assess the clinical outcomes associated with an early extubation strategy for all children undergoing congenital heart surgery, including neonates (age, <30 days).

Methods: We performed a linked database analysis of all patients undergoing congenital heart surgery from July 1, 2010 to December 31, 2012. We collected data on the cardiac diagnoses, preoperative status, procedure, and postoperative course, including the duration of invasive and noninvasive ventilation, failure of extubation, hemodynamic data, length of stay, complications, and mortality.

Infant repair of massive aortic aneurysm with prosthetic valved conduit.

A 4-month-old child with severe infantile Marfan syndrome underwent successful repair of an extremely dilated aortic root and severe aortic valve insufficiency using a prosthetic valved conduit.

Transfusion-related acute lung injury in the Canadian paediatric population.

Background: The incidence of transfusion-related acute lung injury (TRALI) in adults is approximately one per 5000 transfusions. The Canadian Paediatric Surveillance Program undertook the present study to determine the incidence of TRALI in the paediatric population and to describe the characteristics and outcomes of children with TRALI.

Methods: The present surveillance study was conducted over a three-year period.

Pulse oximeter plethysmograph variation and its relationship to the arterial waveform in mechanically ventilated children.

The variations induced by mechanical ventilation in the arterial pulse pressure and pulse oximeter plethysmograph waveforms have been shown to correlate closely and be effective in adults as markers of volume responsiveness. The aims of our study were to investigate: (1) the feasibility of recording plethysmograph indices; and (2) the relationship between pulse pressure variation (ΔPP), plethysmograph variation (ΔPOP) and plethysmograph variability index (PVI) in a diverse group of mechanically ventilated children. A prospective, observational study was performed.