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Objective: To associate surgeon–anesthesiologist team familiarity (TF) with cardiac surgery outcomes. Background: TF, a measure of repeated team member collaborations, has been associated with improved operative efficiency; however, examination of its relationship to clinical outcomes has been limited. Methods: This retrospective cohort study included Medicare beneficiaries undergoing coronary artery bypass grafting (CABG), surgical aortic valve replacement (SAVR), or both (CABG+SAVR) between January 1, 2017, and September 30, 2018. TF was defined as the number of shared procedures between the cardiac surgeon and anesthesiologist within 6 months of each operation. Primary outcomes were 30- and 90-day mortality, composite morbidity, and 30-day mortality or composite morbidity, assessed before and after risk adjustment using multivariable logistic regression. Results: The cohort included 113,020 patients (84,397 CABG; 15,939 SAVR; 12,684 CABG+SAVR). Surgeon–anesthesiologist dyads in the highest [31631 patients, TF median (interquartile range)=8 (6, 11)] and lowest [44,307 patients, TF=0 (0, 1)] TF terciles were termed familiar and unfamiliar, respectively. The rates of observed outcomes were lower among familiar versus unfamiliar teams: 30-day mortality (2.8% vs 3.1%, P= 0.001), 90-day mortality (4.2% vs 4.5%, P=0.023), composite morbidity (57.4% vs 60.6%, P<0.001), and 30-day mortality or composite morbidity (57.9% vs 61.1%, P<0.001). Familiar teams had lower overall risk-adjusted odds of 30-day mortality or composite morbidity [adjusted odds ratio (aOR) 0.894 (0.868, 0.922), P< 0.001], and for SAVR significantly lower 30-day mortality [aOR 0.724 (0.547, 0.959), P= 0.024], 90-day mortality [aOR 0.779 (0.620, 0.978), P=0.031], and 30-day mortality or composite morbidity [aOR 0.856 (0.791, 0.927), P< 0.001]. Conclusions: Given its relationship with improved 30-day cardiac surgical outcomes, increasing TF should be considered among strategies to advance patient outcomes. [ABSTRACT FROM AUTHOR]

Background: Cardiac surgery prediction models and outcomes from the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) have not been reported. The authors sought to develop preoperative prediction models and estimates of postoperative outcomes for cardiac surgery using the ACS-NSQIP and compare these to the Society of Thoracic Surgeons Adult Cardiac Surgery Database (STS-ACSD). Methods: In a retrospective analysis of the ACS-NSQIP data (2007-2018), cardiac operations were identified using cardiac surgeon primary specialty and sorted into cohorts of coronary artery bypass grafting (CABG) only, valve surgery only, and valve+CABG operations using CPT codes. Prediction models were created using backward selection of the 28 non-laboratory preoperative variables in ACS-NSQIP. Rates of nine postoperative outcomes and performance statistics of these models were compared to published STS 2018 data. Results: Of 28 912 cardiac surgery patients, 18 139 (62.8%) were CABG only, 7872 (27.2%) were valve only, and 2901 (10.0%) were valve +CABG. Most outcome rates were similar between the ACS-NSQIP and STS-ACSD, except for lower rates of prolonged ventilation and composite morbidity and higher reoperation rates in ACS-NSQIP (all P<0.0001). For all 27 comparisons (9 outcomes x 3 operation groups), the c-indices for the ACS-NSQIP models were lower by an average of ~0.05 than the reported STS models. Conclusions: The ACS-NSQIP preoperative risk models for cardiac surgery were almost as accurate as the STS-ACSD models. Slight differences in c-indexes could be due to more predictor variables in STS-ACSD models or the use of more disease- and operation-specific risk variables in the STS-ACSD models. [ABSTRACT FROM AUTHOR]

Cardiac surgery continues to evolve. The last year has been notable for many reasons. The guidelines for coronary revascularization introduced significant discord. The pandemic continues to affect the care on a global scale. Advances in organ procurement and dissection care move forward with better understanding and better technology. [ABSTRACT FROM AUTHOR]

COVID-19 has affected every aspect of life over the last year. This article reviews some of the effects that the pandemic had on cardiac surgery including volumes, ethical concerns with resource-intense procedures like dissection and transplant, and ECMO for COVID-19-derived refractory respiratory failure. [ABSTRACT FROM AUTHOR]

The year of 2019 continues to have notable literature advancing the practice of cardiac surgery. In this article, topics of discussion will include the evolution of cerebral protection, the advancement of arch surgical techniques, the heart transplant allocation system, and mitral repair approach and durability. [ABSTRACT FROM AUTHOR]

Calcific aortic valve disease (CAVD) is a leading cardiovascular disorder in the elderly. Diseased aortic valves are characterized by sclerosis (fibrosis) and nodular calcification. Sclerosis, an early pathological change, is caused by aortic valve interstitial cell (AVIC) proliferation and overproduction of extracellular matrix (ECM) proteins. However, the mechanism of aortic valve sclerosis remains unclear. Recently, we observed that diseased human aortic valves overexpress growth factor neurotrophin 3 (NT3). In the present study, we tested the hypothesis that NT3 is a profibrogenic factor to human AVICs. AVICs isolated from normal human aortic valves were cultured in M199 growth medium and treated with recombinant human NT3 (0.10 μg/ml). An exposure to NT3 induced AVIC proliferation, upregulated the production of collagen and matrix metalloproteinase (MMP), and augmented collagen deposition. These changes were abolished by inhibition of the Trk receptors. NT3 induced Akt phosphorylation and increased cyclin D1 protein levels in a Trk receptor-dependent fashion. Inhibition of Akt abrogated the effect of NT3 on cyclin D1 production. Furthermore, inhibition of either Akt or cyclin D1 suppressed NT3-induced cellular proliferation and MMP-9 and collagen production, as well as collagen deposition. Thus, NT3 upregulates cellular proliferation, ECM protein production, and collagen deposition in human AVICs. It exerts these effects through the Trk-Aktcyclin D1 cascade. NT3 is a profibrogenic mediator in human aortic valve, and overproduction of NT3 by aortic valve tissue may contribute to the mechanism of valvular sclerosis. [ABSTRACT FROM AUTHOR]

Calcific aortic valve disease is a chronic inflammatory process, and aortic valve interstitial cells (AVICs) from diseased aortic valves express greater levels of osteogenic factors in response to proinflammatory stimulation. Here, we report that lower cellular levels of IL-37 in AVICs of diseased human aortic valves likely account for augmented expression of bonemorphogenetic protein-2 (BMP-2) and alkaline phosphatase (ALP) following stimulation of Toll-like receptor (TLR) 2 or 4. Treatment of diseased AVICs with recombinant human IL-37 suppresses the levels of BMP-2 and ALP as well as calcium deposit formation. In mice, aortic valve thickening is observed when exposed to a TLR4 agonist or a high fat diet for a prolonged period; however, mice expressing human IL-37 exhibit significantly lower BMP-2 levels and less aortic valve thickening when subjected to the same regimens. A high fat diet in mice results in oxidized low-density lipoprotein (oxLDL) deposition in aortic valve leaflets. Moreover, the osteogenic responses in human AVICs induced by oxLDL are suppressed by recombinant IL-37. Mechanistically, reduced osteogenic responses to oxLDL in human AVICs are associated with the ability of IL-37 to inhibit NF-κB and ERK1/2. These findings suggest that augmented expression of osteogenic factors in AVICs of diseased aortic valves from humans is at least partly due to a relative IL-37 deficiency. Because recombinant IL-37 suppresses the osteogenic responses in human AVICs and alleviates aortic valve lesions in mice exposed to high fat diet or a proinflammatory stimulus, IL-37 has therapeutic potential for progressive calcific aortic valve disease. [ABSTRACT FROM AUTHOR]

Background: Shared decision making is important to ensure that patients receive therapies aligned with their goals and values. Based upon a detailed needs assessment with diverse stakeholders, pamphlet and video decision aids for destination therapy left ventricular assist devices (DT LVAD) were developed to help patients and their caregivers think through, forecast, and deliberate their options. These decision aids are the foundation of the Multicenter Trial of a Shared Decision Support Intervention for Patients and their Caregivers Offered Destination Therapy for End-Stage Heart Failure (DECIDE-LVAD) study, a multicenter, randomized trial aimed at understanding the effectiveness and implementation of a shared decision support intervention for patients considering DT LVAD. Methods/Design: A stepped-wedge randomized controlled trial was designed, guided by the RE-AIM framework and modeled after an effectiveness-implementation hybrid type II design. Six DT LVAD programs from across the United States will participate. Primary outcomes include knowledge and values-treatment concordance. Patients with advanced heart failure who are being considered for DT LVAD and their caregivers are eligible with a target enrollment of 168 dyads. From August 2014 to January 201 5, an acceptability and feasibility pilot study was performed, which clarified opportunities and challenges around decision support for DT LVAD and resulted in significant modifications to the DECIDE-LVAD study. Discussion: Study findings will provide a foundation for implementing decision support interventions, including decision aids, with patients who have chronic progressive illness facing end-of-life decisions involving invasive, preference-sensitive therapy options. [ABSTRACT FROM AUTHOR]

Background. Mechanisms of inflammation have been implicated in the pathogenesis of aortic stenosis. When stimulated, human aortic valve interstitial cells (AVICs) have been shown to become inflammatory cells. Increased levels of interleukin (IL)-1β have been found in the leaflets of stenotic aortic valves. The purpose of this study was to determine the effects of IL-1β on isolated human AVICs and to determine the intracellular signaling pathway by which the effects are mediated. The results of this study demonstrated that IL-1β induces an inflammatory phenotype in human AVICs. Methods. Human AVICs were isolated from normal aortic valves from explanted hearts of patients undergoing cardiac transplantation (n = 4) and grown in culture. When grown to confluence, the cells were treated with IL-1β (10 ng/mL). Cell culture media was analyzed for IL-6, IL-8, and monocyte chemoattractant protein-1 (enzyme-linked immunosorbent assay). Cell lysates were analyzed for intercellular adhesion molecule-1 (immunoblot). Inhibition of nuclear factor-κβ was by Bay 11-7085 (5 µM). Inhibition of extracellular signal regulated kinase-1/2 was by PD098059 (20 nM). Statistics were by analysis of variance, with p less than 0.05 significant. Results. Interluekin-1β induced an inflammatory phenotype in human AVICs. The IL-1β stimulation resulted in significantly increased production of the inflammatory cytokines, IL-6 and IL-8, the chemokine monocyte chemoattractant protein-1, and intercellular adhesion molecule-1. Inhibition of nuclear factor-κβ prevented these changes, whereas inhibition of extracellular signal regulated kinase-1/2 had no effect. Conclusions. Interleukin-1β induced an inflammatory phenotype in human AVICs, which was prevented by inhibition of nuclear factor-κβ. These data implicate IL-1β in the pathogenesis of aortic stenosis. [ABSTRACT FROM AUTHOR]

The article presents information study which examined the recovery of myocyte contractile function in relation to the use of a left ventricular assist device (LVAD). It was observed that the use of an LVAD can provide significant improvement in the size of the left ventricle and myocyte. Results further showed that there is only partial recovery of ejection fraction and myocyte contractility.

Background: Endothelial inflammatory responses mediated by Toll-like receptors (TLRs), particularly TLR2 and TLR4, play an important role in atherogenesis. While Type 1 diabetes (T1D) promotes the development and progression of atherosclerosis, the effect of T1D on TLR2/4-mediated inflammatory responses in coronary artery endothelial cells (CAECs) remains unclear. Methods: We tested the hypothesis that diabetic CAECs have enhanced inflammatory responses to TLR2/4 stimulation. Non-diabetic and diabetic CAECs were treated with TLR2 agonist peptidoglycan and TLR4 agonist lipopolysaccharide. The expression of ICAM-1, IL-6 and IL-8 were analyzed by real-time PCR, immunoblotting and ELISA, and NF-αB activation by immunoblotting and immunostaining. In additional experiments, insulin was added before TLR stimulation to determine whether insulin deficiency alone is responsible for the alteration of TLR2/4- mediated inflammatory responses. Results: Stimulation of TLR2 or TLR4 induced NF-αB activation, and the expression of ICAM-1, IL-6 and IL-8. Interestingly, the expression of inflammatory mediators was significantly enhanced in diabetic cells. The enhanced inflammatory responses correlated with augmented NF-αB activation in the absence of a change in TLR2 or TLR4 protein levels. Further, pretreatment of diabetic cells with insulin failed to suppress the enhanced inflammatory responses. Conclusions: Diabetic CAECs have enhanced inflammatory responses to stimulation of TLR2 or TLR4, and insulin alone is insufficient to correct the hyper-inflammatory responses. The mechanism underlying the enhanced inflammatory responses appears to be augmentation of pro-inflammatory signaling, rather than up-regulation of levels of TLR2 and TLR4. These findings suggest that diabetic CAECs adopt a hyper-inflammatory phenotype and that this endothelial phenotypic change may predispose coronary artery to atherogenesis. [ABSTRACT FROM AUTHOR]

Previous studies showed that Toll-like receptor 4 (TLR4) modulates the myocardial inflammatory response to ischemia-reperfusion injury, and we recently found that cytokines link TLR4 to postischemic cardiac dysfunction. Although TLR4 can be activated in cultured cells by endogenous agents including heat shock protein 70, how it is activated during myocardial ischemia-reperfusion is unknown. In the present study, we examined 1) whether heat shock cognate protein 70 (HSC70), which is constitutively expressed in the myocardium, is released during ischemia-reperfusion; 2) whether extracellular HSC70 induces the myocardial inflammatory response and modulates cardiac function; and 3) whether HSC70 exerts these effects via TLR4. We subjected isolated mouse hearts to global ischemia-reperfusion via the Langendorff technique. Immunoblotting and immunostaining detected the release of HSC70 from the myocardium during reperfusion. Treatment with an antibody specific to HSC70 suppressed myocardial cytokine expression and improved cardiac functional recovery after ischemia-reperfusion. Recombinant HSC70 induced NF-κB activation and cytokine expression and depressed myocardial contractility in a TLR4-dependent manner. These effects required the substrate-binding domain of HSC70. Fluorescence resonance energy transfer analysis of isolated macrophages demonstrated that extracellular HSC70 interacts with TLR4. Therefore, this study demonstrates for the first time that 1) the myocardium releases HSC70 during ischemia- reperfusion, 2) extracellular HSC70 contributes to the postischemic myocardial inflammatory response and to cardiac dysfunction, 3) HSC70 exerts these effects through a TLR4-dependent mechanism, and 4) the substrate-binding domain of HSC70 is required to induce these effects. Thus extracellular HSC70 plays a critical role in regulating the myocardial innate immune response and cardiac function after ischemia-reperfusion. [ABSTRACT FROM AUTHOR]

Calcific aortic valve stenosis is the most common indication for surgical valve replacement. Inflammation appears to be one of the mechanisms involved in aortic valve calcification, and valve interstitial cells seem to contribute to that process. Although Toll-like receptors (TLRs) play an important role in the cellular inflammatory response, it is unknown whether human aortic valve interstitial cells (HAVICs) express functional TLRs. We examined the expression of TLR2 and TLR4 in human aortic valve leaflets and in isolated HAVICs and analyzed the response of cultured HAVICs to the TLR2 and TLR4 agonists peptidoglycan (PGN) and LPS. Abundant TLR2 and TLR4 proteins were found in human aortic valve leaflets and in isolated HAVICs, and both receptors were detected in the membrane and cytoplasm of cultured HAVICs. Stimulation by either PGN or LPS resulted in the activation of the NF-KB signaling pathway and the production of multiple proinflammatory mediators, including IL-6, IL-8, and ICAM-1. In addition, stimulation by either PGN or LPS upregulated the expression of bone morphogenetic protein-2 (BMP-2) and Runx2, factors associated with osteogenesis. This study demonstrates for the first time that HAVICs express TLR2 and TLR4 and that stimulation of HAVICs by PGN or LPS induces the expression of proinflammatory mediators and the upregulation of osteogenesis-associated factors. These results suggest that TLR2 and TLR4 may play a role in aortic valve inflammation and stenosis. [ABSTRACT FROM AUTHOR]

: BackgroundRisk factors for 30-day operative (short-term) mortality following coronary artery bypass graft (CABG only) procedures are well established. However, little is known about how the risk factors for short-term mortality following valve replacement procedures (with or without a CABG procedure performed) compare with CABG only risk factors.: MethodsDepartment of Veterans Affairs (VA) records (65,585 records) were collected from October 1991 through March 2001 and analyzed. Risk factors for short-term mortality were compared across three subgroups of patients: CABG only surgery (n = 56,318), aortic valve replacement (AVR) with or without CABG (n = 7450), and mitral valve replacement (MVR) with or without CABG (n = 1817). Multivariable logistic regression analyses were used to compare the relative magnitude of risk for 19 candidate predictor variables across subgroups.: ResultsOnly three patient baseline characteristics differed significantly in magnitude of risk between the procedure groups. Partially or totally dependent functional status significantly increased the risk of short-term mortality for AVR patients (odds ratio [OR] 1.64, 95% confidence interval [CI] 1.29–2.09) and MVR patients (OR 2.21, 95% CI 1.48–3.30), but not for CABG only patients (OR 1.04, 95% CI 0.93–1.16). Conversely, previous heart surgery and New York Heart Association functional class III or IV symptoms conferred greater magnitude of risk for CABG only patients compared with the valve subgroups.: ConclusionsOverall, the risk factors for short-term mortality following valve replacement and CABG surgery appear to be relatively consistent. However, clinicians should be aware of the importance of preoperative functional status as a unique predictor of mortality following valve surgery. [Copyright &y& Elsevier]

Quality improvement in cardiac care has made considerable progress over the past 30 years. During that period, there has been the development of multi-institutional databases to monitor outcomes following cardiothoracic surgery. These databases initially began using only volume and unadjusted operative (30-day) mortality as outcome criteria. There has been a progressive increase in their sophistication, with the building of risk models based on preoperative variables, which accurately predict the risk of adverse outcomes. Other outcomes have been added including risk-adjusted mortality and morbidity; efficiency outcomes such as length of stay, quality of life, functional health status, neuropsychological outcomes; and long-term outcomes. [ABSTRACT FROM AUTHOR]

The initial discovery of cardiac preconditioning has evolved into an exciting series of practical surgical applications. An enormous amount of evidence demonstrating both the safety and efficacy of ischemic preconditioning is available from animal studies. The challenging premise of intentionally subjecting patients and their organs to transient ischemia has acted as a formidable psychological and ethical impediment to the widespread clinical application of organ preconditioning. A more palatable alternative to ischemic preconditioning now involves approved medications designed to manipulate the cellular machinery mediating ischemic preconditioning. Pharmacologically induced preconditioning seems to confer equal organ protection. The relatively brief (but surgically relevant) window of protection provided by strategies such as ischemic preconditioning or adenosine agonists and potassium–adenosine triphosphate channel openers may, in the future, be extended. We have developed and reported the feasibility of liposomal delivery of heat shock protein to cardiac myocytes with subsequent protection against sepsis-induced dysfunction. Targeted strategies will ultimately broaden the therapeutic potential of organ preconditioning. [ABSTRACT FROM AUTHOR]

Presents a study testing the hypothesis that hemorrhage and resuscitation (H-R) results in myocardial adaptation by a mechanism mediated by alpha1-adrenoreceptors and requiring de novo protein synthesis. Effect of acute cardioadaptation to H-R stress; Mediation of H-R-induced endogenous adaptation by alpha1-adrenoreceptors.

Determines whether ischemic preconditioning (IPC) in human atrial trabeculae is mediated by alpha1-adrenoceptors and protein kinase C and whether the protection of IPC is replicated with alpha1-adrenoceptor stimulation. Effects of IPC against reperfusion injury; Effects of pharmacological preconditioning with phenylephrine.

Examines ischemic preconditioning in reducing or preventing ischemia-reperfusion injury. Possible mechanisms behind this protective effect; Role of alpha-adrenergic and adenosine receptor signaling in this protective effect.