Alien Registration- Maning, Aldoph J. (Rumford, Oxford County)

https://digitalmaine.com/alien_docs/12450/thumbnail.jp

Alien Registration- Maning, Aldoph J. (Rumford, Oxford County)

https://digitalmaine.com/alien_docs/12450/thumbnail.jp

Early trends in leadless pacemaker implantation: Evaluating nationwide in-hospital outcomes

Single-chamber leadless intracardiac pacemaker (LICP) implantation was approved in 2016 in the United States. However, little is known regarding trends in real-world utilization and complication rates. The purpose of this study was to assess nationwide demographics, trends, and outcomes among hospitalizations with LICP implantation in the United States. Using the National Inpatient Sample, we identified all hospitalizations with LICP or transvenous pacemaker implantation as a comparator between 2017 and 2019. We evaluated baseline patient characteristics, admitting diagnoses, procedural complications, lengths of stay, discharge dispositions, and all-cause mortality. The majority of LICP recipients were elderly (75.4 ± 12.8 years), male (55.2%), and White (76.8%) compared to Black (9.8%), or Hispanic (7.3%). Between 2017 and 2019, the average age increased along with the prevalence of heart failure, atrial fibrillation, and malignancy among recipients. Most hospitalizations were emergent (84.5%). Between 2017 and 2019, pooled procedural complications decreased significantly (10.8% vs 7.9%; P <.001), primarily due to declining infection and device retrieval rates. In-hospital mortality also decreased significantly (8.2% vs 4.2%; P <.001). History of cardiogenic shock or cardiac device infection was associated with the greatest mortality or complication risk. Compared to transvenous pacemaker, LICP implantation was associated with lower complication rates (8.6% vs 11.2%) but greater mortality (5.2% vs 1.3%; P <.001). Nationwide LICP implantations were performed in patients of increasing age, comorbidities, and acuity of illness. In-hospital mortality and procedure-related complications declined in the first 3 years after approval of LICP implantation and may reflect improving operator experience. Increased mortality compared with transvenous pacemaker implant remains a concern

Predictors of 90-Days Readmissions for New Onset Heart Failure after Acute Coronary Syndrome

Background: Coronary heart disease is one of the leading risk factors for the development of heart failure (HF). Despite major improvements in the management of acute coronary syndromes (ACS), HF remains the most common cause of readmission after ACS, followed by myocardial re-infarction. We sought to evaluate the risks and predictors for HF admission after ACS. Methods: Using the national readmission database (NRD), we examined discharge data from 2010 until 2015 and identified all patients age 18 years and older with ACS recorded as the primary discharge diagnosis; we then excluded all patients with a prior diagnosis of HF. Chi-square test and Wilcoxon rank-sum test were used to compare proportions and continuous variables, respectively. We used logistic regression modeling to estimate the unadjusted odds of readmission for the covariates of interest. Results: We identified 1,322,335 patients discharged after an ACS (36.2% STEMI). Of these, 56,345 (4.2%) were readmitted within 90-days with a new primary diagnosis of HF. The most common individual risk factors associated with HF admission were the presence of atrial fibrillation (OR 1.71), diabetes (OR 1.62) and lung disease (OR 1.49). The most common predictors for HF admission were STEMI (OR 1.28), development of acute kidney injury (AKI) (OR 1.49), length of stay \u3e 5 days (OR 1.77) and discharge against medical advice (OR 1.88). Revascularization during index admission for ACS was a strong predictor against HF admission (OR of 0.61 and 0.49 for PCI and CABG respectively). Self-pay or private insurance were also associated with lower rates of HF admissions (OR 0.68 and 0.57, respectively). Conclusions: Readmission for new-onset HF occurs in close to 5% of patients after ACS. The presence of atrial fibrillation, diabetes, development of AKI or prolonged hospitalization identifies a higher risk cohort at the time of discharge

β-Arrestin2 Improves Post-Myocardial Infarction Heart Failure via Sarco(endo)plasmic Reticulum Ca2+-ATPase-Dependent Positive Inotropy in Cardiomyocytes

Heart failure is the leading cause of death in the Western world, and new and innovative treatments are needed. The GPCR (G protein-coupled receptor) adapter proteins βarr (β-arrestin)-1 and βarr-2 are functionally distinct in the heart. βarr1 is cardiotoxic, decreasing contractility by opposing β1AR (adrenergic receptor) signaling and promoting apoptosis/inflammation post-myocardial infarction (MI). Conversely, βarr2 inhibits apoptosis/inflammation post-MI but its effects on cardiac function are not well understood. Herein, we sought to investigate whether βarr2 actually increases cardiac contractility. Via proteomic investigations in transgenic mouse hearts and in H9c2 rat cardiomyocytes, we have uncovered that βarr2 directly interacts with SERCA2a (sarco[endo]plasmic reticulum Ca2+-ATPase) in vivo and in vitro in a β1AR-dependent manner. This interaction causes acute SERCA2a SUMO (small ubiquitin-like modifier)-ylation, increasing SERCA2a activity and thus, cardiac contractility. βarr1 lacks this effect. Moreover, βarr2 does not desensitize β1AR cAMP-dependent procontractile signaling in cardiomyocytes, again contrary to βarr1. In vivo, post-MI heart failure mice overexpressing cardiac βarr2 have markedly improved cardiac function, apoptosis, inflammation, and adverse remodeling markers, as well as increased SERCA2a SUMOylation, levels, and activity, compared with control animals. Notably, βarr2 is capable of ameliorating cardiac function and remodeling post-MI despite not increasing cardiac βAR number or cAMP levels in vivo. In conclusion, enhancement of cardiac βarr2 levels/signaling via cardiac-specific gene transfer augments cardiac function safely, that is, while attenuating post-MI remodeling. Thus, cardiac βarr2 gene transfer might be a novel, safe positive inotropic therapy for both acute and chronic post-MI heart failure