, there are 1 935, 646 confirmed cases of coronavirus disease 2019 (COVID-19) worldwide with 120 914 total deaths, defining COVID-19 as a pandemic. 1 The limited literature on COVID-19 in heart transplant (HT) patients thus far suggests that HT might not have a disproportionate effect on infection and severity of disease. 2,3 However, we know this immunosuppressed population is at higher risk than the general population in contracting both viral and bacterial infections. We report 2 cases of COVID-19 in HT patients.

Our results implicate Foxo3 in regulating NK cell function and suggest Foxo3 playing an important role in the antiviral innate immunity. Thus, enhanced FOXO3 activity such as in the polymorphism rs12212067 may be protective in chronic inflammation such as cancer and cardiovascular disease but disadvantageous to control acute viral infection.

Aim: Hemocompatibility-related adverse events (HRAE) are a major cause of readmissions in patients with left ventricular assist devices (LVAD). The impact of aortic insufficiency (AI) on HRAE remains uncertain. We aimed to investigate the impact of AI on HRAE. Methods and Results: Patients who underwent LVAD implantation between August 2014 and July 2017 and had echocardiograms 3 months post-LVAD implantation were enrolled. AI severity was assessed by measuring the systolic/diastolic ratio of flow and the rate of diastolic flow acceleration using Doppler echocardiography of the outflow cannula. Regurgitation fraction was derived from these parameters. Significant AI was defined as regurgitation fraction > 30%. Among 105 patients (median age, 56 years; 76% male), 36 patients (34%) had significant AI. Baseline characteristics were statistically not significantly different between those with and without significant AI except for higher rates of ischemic etiology and atrial fibrillation in the significant AI group (P < 0.05 for both). One-year survival free from HRAE was 44% in patients with AI compared to 67% in patients without significant AI (P = 0.018). The average hemocompatibility score, which defines the net burden of HRAE, was higher in the AI group (1.72 vs 0.64; P = 0.009), due mostly to higher tier I (mild HRAE; P = 0.034) and tier IIIB scores (severe HRAE; P = 0.011). Conclusion: Significant AI, as assessed by Doppler echocardiographic parameters, was associated with HRAE during LVAD support.

BACKGROUND-Historically, invasive hemodynamic guidance was not superior compared to clinical assessment in patients admitted with acute decompensated heart failure (ADHF). This study assessed the accuracy of clinical assessment versus. invasive hemodynamics in patients with ADHF.METHODS AND RESULTS-We conducted a prospective cohort study of patients admitted with ADHF. Prior to RHC, physicians categorically predicted right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP), cardiac index (CI) and hemodynamic profile (Wet/ Dry, Warm/Cold) based on physical exam and clinical data evaluation. "Warm"= CI > 2.2 L/min/m 2 ; "Wet" = PCWP >18 mmHg. 218 surveys (83 cardiology fellows, 55 attending cardiologists, 45 residents, 35 interns) evaluating 97 patients were collected. 46% were receiving inotropes prior to RHC. Positive and negative predictive values of clinical assessment compared to RHC for the "Cold and Wet" subgroup were 74.7% and 50.4%. Accuracy of categorical prediction was 43.6% for RAP, 34.4% for PCWP, 49.1% for CI, and did not differ by clinician (P >0.05 for all). Interprovider agreement was 44.4%. Therapeutic changes following RHC occurred in 71.1% overall (P <0.001).

Adiponectin (APN) is a multifunctional adipocytokine that inhibits myocardial fibrosis, dilatation, and left ventricular (LV) dysfunction after myocardial infarction (MI). Coxsackievirus B3 (CVB3) myocarditis is associated with intense extracellular matrix (ECM) remodeling which might progress to dilated cardiomyopathy. Here, we investigated in experimental CVB3 myocarditis whether APN inhibits adverse ECM remodeling following cardiac injury by affecting matrix metalloproteinase (MMP) expression. Cardiac injury was induced by CVB3 infection in APN knockout (APN‐KO) and wild‐type (WT) mice. Expression and activity of MMPs was quantified by qRT‐PCR and zymography, respectively. Activation of protein kinases was assessed by immunoblot. In cardiac myocytes and fibroblasts APN up‐regulates MMP‐9 expression via activation of 5′ adenosine monophosphate‐activated protein kinase (AMPK) and extracellular signal‐regulated kinase (ERK)1/2 which function as master regulators of inflammation‐induced MMP‐9 expression. Correspondingly, APN further increased up‐regulation of MMP‐9 expression triggered by tumor necrosis factor (TNF)α, lipopolysaccharide (LPS) and R‐848 in cardiac fibroblasts. In vivo, compared to WT mice cardiac MMP‐9 activity and serum levels of carboxy‐terminal telopeptide of type I collagen (ICTP) were attenuated in APN‐KO mice in subacute (day 7 p.i.) CVB3 myocarditis. Moreover, on day 3 and day 7 post CVB3 infection splenic MMP‐9 expression was diminished in APN‐KO mice correlating with attenuated myocardial immune cell infiltration in subacute CVB3 myocarditis. These results indicate that APN attenuates adverse cardiac remodeling following cardiac injury by up‐regulating MMP‐9 expression in cardiac and immune cells. Thus, APN mediates intensified collagen cleavage that might explain inhibition of LV fibrosis and dysfunction.

Adiponectin (APN) is an immunomodulatory adipocytokine that improves outcome in patients with virus-negative inflammatory cardiomyopathy and mice with autoimmune myocarditis. Here, we investigated whether APN modulates cardiac inflammation and injury in coxsackievirus B3 (CVB3) myocarditis. Myocarditis was induced by CVB3 infection of APN-KO and WT mice. APN reconstitution was performed by adenoviral gene transfer. Expression analyses were performed by qRT-PCR and immunoblot. Cardiac histology was analyzed by H&E-stain and immunohistochemistry. APN-KO mice exhibited diminished subacute myocarditis with reduced viral load, attenuated inflammatory infiltrates determined by NKp46, F4/80 and CD3/CD4/CD8 expression and reduced IFNβ, IFNγ, TNFα, IL-1β and IL-12 levels. Moreover, myocardial injury assessed by necrotic lesions and troponin I release was attenuated resulting in preserved left ventricular function. Those changes were reversed by APN reconstitution. APN had no influence on adhesion, uptake or replication of CVB3 in cardiac myocytes. In acute CVB3 myocarditis, cardiac viral load did not differ between APN-KO and WT mice. However, APN-KO mice displayed an enhanced acute immune response, i.e. increased expression of myocardial CD14, IFNβ, IFNγ, IL-12, and TNFα resulting in increased cardiac infiltration with pro-inflammatory M1 macrophages and activated NK cells. Up-regulation of cardiac CD14 expression, type I and II IFNs and inflammatory cell accumulation in APN-KO mice was inhibited by APN reconstitution. Our observations indicate that APN promotes CVB3 myocarditis by suppression of toll-like receptor-dependent innate immune responses, polarization of anti-inflammatory M2 macrophages and reduction of number and activation of NK cells resulting in attenuated acute anti-viral immune responses.

Background Video laryngoscopy is an effective tool in the management of difficult pediatric airway. However, evidence to guide the choice of the most appropriate video laryngoscope (VL) for airway management in pediatric patients with Pierre Robin syndrome (PRS) is insufficient. Therefore, the aim of this study was to compare the efficacy of the Glidescope® Core™ with a hyperangulated blade, the C-MAC® with a nonangulated Miller blade (C-MAC® Miller) and a conventional Miller laryngoscope when used by anesthetists with limited and extensive experience in simulated Pierre Robin sequence. Methods Forty-three anesthetists with limited experience and forty-three anesthetists with extensive experience participated in our randomized crossover manikin trial. Each performed endotracheal intubation with the Glidescope® Core™ with a hyperangulated blade, the C-MAC® with a Miller blade and the conventional Miller laryngoscope. “Time to intubate” was the primary endpoint. Secondary endpoints were “time to vocal cords”, “time to ventilate”, overall success rate, number of intubation attempts and optimization maneuvers, Cormack-Lehane score, severity of dental trauma and subjective impressions. Results Both hyperangulated and nonangulated VLs provided superior intubation conditions. The Glidescope® Core™ enabled the best glottic view, caused the least dental trauma and significantly decreased the “time to vocal cords”. However, the failure rate of intubation was 14% with the Glidescope® Core™, 4.7% with the Miller laryngoscope and only 2.3% with the C-MAC® Miller when used by anesthetists with extensive previous experience. In addition, the “time to intubate”, the “time to ventilate” and the number of optimization maneuvers were significantly increased using the Glidescope® Core™. In the hands of anesthetists with limited previous experience, the failure rate was 11.6% with the Glidescope® Core™ and 7% with the Miller laryngoscope. Using the C-MAC® Miller, the overall success rate increased to 100%. No differences in the “time to intubate” or “time to ventilate” were observed. Conclusions The nonangulated C-MAC® Miller facilitated correct placement of the endotracheal tube and showed the highest overall success rate. Our results therefore suggest that the C-MAC® Miller could be beneficial and may contribute to increased safety in the airway management of infants with PRS when used by anesthetists with limited and extensive experience.

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