Association of Double-Blind Reviews With Increases in Women as First Authors: An Initial Report From the Journal of Cardiac Failure.

INTRODUCTION: Women continue to remain under-represented in academic publishing in the field of cardiology. Some evidence suggests that double-blind peer reviews may mitigate the impact of gender bias. In July 2021, the Journal of Cardiac Failure implemented a process for the conduct of double-blind reviews after previously using single-blind reviews, with the aim of improving author diversity. The purpose of the current study was to examine the association between changes in authorship characteristics and implementation of double-blind reviews. METHODS: Manuscripts were stratified into 3 Eras: March-September 2021 (Era 1: prior to double-blind reviews); March-September 2022 (Era 2); and March-September 2023 (Era 3). All article types except invited editorials were included. Data were abstracted, including names, genders, ranks, and disciplines of the first and senior authors. RESULTS: A total of 310 manuscripts were included in the analysis. The proportion of women first authors increased from 24% in Era 1 to 34% in Era 2 to 39% in Era 3, while the percentage of women authors serving in a senior authorship role remained fairly stable over time-around 21%-22%. Even after adjusting for region, article type, first-author discipline, and last-author gender, there was an increase in female first authors over time (P = 0.015). Manuscripts with a female senior author were significantly more likely to have a female first author. CONCLUSIONS: Our findings suggest that double-blind peer review may contribute to increased gender diversity of first authors and may highlight areas for future improvement by the Journal and academic publishing in general.

Cyclic adenosine monophosphate critically modulates cardiac GLP-1 receptor's anti-inflammatory effects.

BACKGROUND: Glucagon-like peptide (GLP)-1 receptor (GLP1R) agonists exert a multitude of beneficial cardiovascular effects beyond control of blood glucose levels and obesity reduction. They also have anti-inflammatory actions through both central and peripheral mechanisms. GLP1R is a G protein-coupled receptor (GPCR), coupling to adenylyl cyclase (AC)-stimulatory Gs proteins to raise cyclic 3`-5`-adenosine monophosphate (cAMP) levels in cells. cAMP exerts various anti-apoptotic and anti-inflammatory effects via its effectors protein kinase A (PKA) and Exchange protein directly activated by cAMP (Epac). However, the precise role and importance of cAMP in mediating GLP1R`s anti-inflammatory actions, at least in the heart, remains to be determined. To this end, we tested the effects of the GLP1R agonist liraglutide on lipopolysaccharide (LPS)-induced acute inflammatory injury in H9c2 cardiac cells, either in the absence of cAMP production (AC inhibition) or upon enhancement of cAMP levels via phosphodiesterase (PDE)-4 inhibition with roflumilast. METHODS & RESULTS: Liraglutide dose-dependently inhibited LPS-induced apoptosis and increased cAMP levels in H9c2 cells, with roflumilast but also PDE8 inhibition further enhancing cAMP production by liraglutide. GLP1R-stimulated cAMP markedly suppressed the LPS-dependent induction of pro-inflammatory tumor necrosis factor (TNF)-a, interleukin (IL)-1b, and IL-6 cytokine expression, of inducible nitric oxide synthase (iNOS) expression and nuclear factor (NF)-kB activity, of matrix metalloproteinases (MMP)-2 and MMP-9 levels and activities, and of myocardial injury markers in H9c2 cardiac cells. The effects of liraglutide were mediated by the GLP1R since they were abolished by the GLP1R antagonist exendin(9-39). Importantly, AC inhibition completely abrogated liraglutide`s suppression of LPS-dependent inflammatory injury, whereas roflumilast significantly enhanced the protective effects of liraglutide against LPS-induced inflammation. Finally, PKA inhibition or Epac1/2 inhibition alone only partially blocked liraglutide`s suppression of LPS-induced inflammation in H9c2 cardiac cells, but, together, PKA and Epac1/2 inhibition fully prevented liraglutide from reducing LPS-dependent inflammation. CONCLUSIONS: cAMP, via activation of both PKA and Epac, is essential for GLP1R`s anti-inflammatory signaling in cardiac cells and that cAMP levels crucially regulate the anti-inflammatory efficacy of GLP1R agonists in the heart. Strategies that elevate cardiac cAMP levels, such as PDE4 inhibition, may potentiate the cardiovascular, including anti-inflammatory, benefits of GLP1R agonist drugs.

The association of pre-transplant atrial fibrillation with in-hospital outcomes in patients undergoing orthotopic liver transplantation: A propensity score matching analysis.

INTRODUCTION: In this study, we sought to evaluate the prevalence and association of pre-transplant atrial fibrillation (AF) on 30-day postoperative outcomes in patients undergoing orthotopic liver transplant (OLT). METHOD: The National Inpatient Sample Database was queried from 2011 to 2017 for relevant ICD-9 and ICD-10 procedural and diagnostic codes. Baseline characteristics and in-hospital outcomes were compared in patients who underwent OLT with AF and those without. RESULTS: Among 45,357 patients who underwent OLT, women made up 35.8% of the overall population. The prevalence of AF before transplant was 2932 (6.5%) with a trend toward increasing prevalence, with an average annual change rate of 4.19%. Applying propensity score matching to control for potential confounding factors, there was no association between pre-transplant AF and in-hospital mortality in patients undergoing OLT, however there was a higher incidence of perioperative complications including: acute kidney injury, ventricular tachycardia, major bleeding, blood product transfusion, and septic shock. CONCLUSION: In patients undergoing OLT, pre-transplant AF is increasing in prevalence and appears to be associated with similar in-hospital mortality but worse perioperative outcomes. Greater emphasis should be placed on AF in the preoperative cardiovascular risk stratification of patients undergoing OLT.

Carvedilol Selectively Stimulates ßArrestin2-Dependent SERCA2a Activity in Cardiomyocytes to Augment Contractility.

Heart failure (HF) carries the highest mortality in the western world and ß-blockers [ß-adrenergic receptor (AR) antagonists] are part of the cornerstone pharmacotherapy for post-myocardial infarction (MI) chronic HF. Cardiac ß1AR-activated ßarrestin2, a G protein-coupled receptor (GPCR) adapter protein, promotes Sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA)2a SUMO (small ubiquitin-like modifier)-ylation and activity, thereby directly increasing cardiac contractility. Given that certain ß-blockers, such as carvedilol and metoprolol, can activate ßarrestins and/or SERCA2a in the heart, we investigated the effects of these two agents on cardiac ßarrestin2-dependent SERCA2a SUMOylation and activity. We found that carvedilol, but not metoprolol, acutely induces ßarrestin2 interaction with SERCA2a in H9c2 cardiomyocytes and in neonatal rat ventricular myocytes (NRVMs), resulting in enhanced SERCA2a SUMOylation. However, this translates into enhanced SERCA2a activity only in the presence of the ß2AR-selective inverse agonist ICI 118,551 (ICI), indicating an opposing effect of carvedilol-occupied ß2AR subtype on carvedilol-occupied ß1AR-stimulated, ßarrestin2-dependent SERCA2a activation. In addition, the amplitude of fractional shortening of NRVMs, transfected to overexpress ßarrestin2, is acutely enhanced by carvedilol, again in the presence of ICI only. In contrast, metoprolol was without effect on NRVMs' shortening amplitude irrespective of ICI co-treatment. Importantly, the pro-contractile effect of carvedilol was also observed in human induced pluripotent stem cell (hIPSC)-derived cardiac myocytes (CMs) overexpressing ßarrestin2, and, in fact, it was present even without concomitant ICI treatment of human CMs. Metoprolol with or without concomitant ICI did not affect contractility of human CMs, either. In conclusion, carvedilol, but not metoprolol, stimulates ßarrestin2-mediated SERCA2a SUMOylation and activity through the ß1AR in cardiac myocytes, translating into direct positive inotropy. However, this unique ßarrestin2-dependent pro-contractile effect of carvedilol may be opposed or masked by carvedilol-bound ß2AR subtype signaling.

Correction: Maning et al. Antagonistic Roles of GRK2 and GRK5 in Cardiac Aldosterone Signaling Reveal GRK5-Mediated Cardioprotection via Mineralocorticoid Receptor Inhibition. Int. J. Mol. Sci. 2020, 21, 2868.

The authors wish to make the following correction to this paper [...].

Bicaval vs biatrial anastomosis techniques in orthotopic heart transplantation: An updated analysis of the UNOS database.

BACKGROUND: Despite the significant increase in the number of orthotopic heart transplants (OHT) performed yearly using the bicaval anastomosis technique, the impact on long-term outcomes remains a topic of debate. We analyzed the United Network for Organ Sharing (UNOS) database in search of the latest insight. METHODS: We performed a retrospective analysis of the UNOS database from 2006 to 2016 to identify first-time OHT recipients. Patients were primarily stratified according to anastomosis technique: bicaval vs biatrial. Baseline characteristics and clinical status were recorded. The primary endpoint was all-cause mortality. Secondary outcomes included need for permanent pacemaker (PPM), and length of hospital stay (LOS). The Kaplan-Meier method was used to compare survival between the two groups. The Cox proportional hazards regression model was used to conduct multivariable analysis. Statistical significance established at P < .0001. RESULTS: A total of 26 990 patients were identified. Of those who met the inclusion criteria (21 597), 16 573 (77%) underwent bicaval anastomosis. There were no major differences in baseline characteristics between the two groups. The bicaval anastomosis technique was not associated with increased survival during the study period (hazard ratio: 0.97; P = .3557), but the bicaval group required postoperative PPM less often (2.51% vs 5.79%, P < .0001) and was associated with shorter LOS on multivariable analysis. CONCLUSIONS: The use of either bicaval or biatrial anastomosis during OHT offers comparable survival advantage. Nonetheless, bicaval anastomosis is associated with less need for postoperative PPM and slightly shorter LOS.

Evaluating the impact of chronic obstructive pulmonary disease on in-hospital outcomes following left ventricular assist device implantation.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a cause of ventricular dysfunction. However, in the setting of patients with heart failure undergoing left ventricular assist device (LVAD) implantation, there is a paucity of data on the association between COPD and in-hospital outcomes. METHODS AND RESULTS: Retrospective cohort study based on the NIS including patients ≥18 years who underwent LVAD implantation from 2011 to 2017. Multivariate regression was used to evaluate the impact of COPD on in-hospital outcomes. A total of 25,503 patients underwent LVAD implantation, of which 13.8% also had COPD. COPD group was older (median 62 vs. 58 years), and more males (82% vs. 76.4%, p < .001 for both). COPD group had more hypertension, diabetes, atrial tachyarrhythmias, dyslipidemia, prior stroke, coronary artery diseases, pulmonary hypertension, and chronic kidney disease (p < .001 for all). No differences in strokes, infections, mechanical circulatory support, and LVAD thrombosis. There was a higher incident of inpatient acute kidney injury, major bleeding, cardiac complications, thromboembolism, and cardiac arrest in patients without COPD (p < .05 for all). Compared with no-COPD group, COPD group had a lower mortality (6.2% vs. 12.4%; odds ratio, 0.59; confidence interval, 0.512-0.685; p < .05). CONCLUSION: Patients with COPD undergoing LVAD implantation have more comorbidities, without an associated increase mortality.

Antagonistic Roles of GRK2 and GRK5 in Cardiac Aldosterone Signaling Reveal GRK5-Mediated Cardioprotection via Mineralocorticoid Receptor Inhibition.

Aldosterone (Aldo), when overproduced, is a cardiotoxic hormone underlying heart failure and hypertension. Aldo exerts damaging effects via the mineralocorticoid receptor (MR) but also activates the antiapoptotic G protein-coupled estrogen receptor (GPER) in the heart. G protein-coupled receptor (GPCR)-kinase (GRK)-2 and -5 are the most abundant cardiac GRKs and phosphorylate GPCRs as well as non-GPCR substrates. Herein, we investigated whether they phosphorylate and regulate cardiac MR and GPER. To this end, we used the cardiomyocyte cell line H9c2 and adult rat ventricular myocytes (ARVMs), in which we manipulated GRK5 protein levels via clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 and GRK2 activity via pharmacological inhibition. We report that GRK5 phosphorylates and inhibits the cardiac MR whereas GRK2 phosphorylates and desensitizes GPER. In H9c2 cardiomyocytes, GRK5 interacts with and phosphorylates the MR upon ß2-adrenergic receptor (AR) activation. In contrast, GRK2 opposes agonist-activated GPER signaling. Importantly, GRK5-dependent MR phosphorylation of the MR inhibits transcriptional activity, since aldosterone-induced gene transcription is markedly suppressed in GRK5-overexpressing cardiomyocytes. Conversely, GRK5 gene deletion augments cardiac MR transcriptional activity. ß2AR-stimulated GRK5 phosphorylates and inhibits the MR also in ARVMs. Additionally, GRK5 is necessary for the protective effects of the MR antagonist drug eplerenone against Aldo-induced apoptosis and oxidative stress in ARVMs. In conclusion, GRK5 blocks the cardiotoxic MR-dependent effects of Aldo in the heart, whereas GRK2 may hinder beneficial effects of Aldo through GPER. Thus, cardiac GRK5 stimulation (e.g., via ß2AR activation) might be of therapeutic value for heart disease treatment via boosting the efficacy of MR antagonists against Aldo-mediated cardiac injury.

Chemically synthesized Secoisolariciresinol diglucoside (LGM2605) improves mitochondrial function in cardiac myocytes and alleviates septic cardiomyopathy.

Sepsis is the overwhelming systemic immune response to infection, which can result in multiple organ dysfunction and septic shock. Myocardial dysfunction during sepsis is associated with advanced disease and significantly increased in-hospital mortality. Our group has shown that energetic failure and excess reactive oxygen species (ROS) generation constitute major components of myocardial dysfunction in sepsis. Because ROS production is central to cellular metabolic health, we tested if the synthetic anti-oxidant lignan secoisolariciresinol diglucoside (SDG; LGM2605) would alleviate septic cardiac dysfunction and investigated the underlying mechanism. Using the cecal ligation and puncture (CLP) mouse model of peritonitis-induced sepsis, we observed impairment of cardiac function beginning at 4 h post-CLP surgery. Treatment of mice with LGM2605 (100 mg/kg body weight, i.p.) 6 h post-CLP surgery reduced cardiac ROS accumulation and restored cardiac function. Assessment of mitochondrial respiration (Seahorse XF) in primary cardiomyocytes obtained from adult C57BL/6 mice that had undergone CLP and treatment with LGM2605 showed restored basal and maximal respiration, as well as preserved oxygen consumption rate (OCR) associated with spare capacity. Further analyses aiming to identify the cellular mechanisms that may account for improved cardiac function showed that LGM2605 restored mitochondria abundance, increased mitochondrial calcium uptake and preserved mitochondrial membrane potential. In addition to protecting against cardiac dysfunction, daily treatment with LGM2605 and antibiotic ertapenem (70 mg/kg) protected against CLP-associated mortality and reversed hypothermia when compared against mice receiving ertapenem and saline. Therefore, treatment of septic mice with LGM2605 emerges as a novel pharmacological approach that reduces cardiac ROS accumulation, protects cardiac mitochondrial function, alleviates cardiac dysfunction, and improves survival.

Deletion of Osteopontin Enhances ß2-Adrenergic Receptor-Dependent Anti-Fibrotic Signaling in Cardiomyocytes.

Cardiac ß2-adrenergic receptors (ARs) are known to inhibit collagen production and fibrosis in cardiac fibroblasts and myocytes. The ß2AR is a Gs protein-coupled receptor (GPCR) and, upon its activation, stimulates the generation of cyclic 3',5'-adenosine monophosphate (cAMP). cAMP has two effectors: protein kinase A (PKA) and the exchange protein directly activated by cAMP (Epac). Epac1 has been shown to inhibit cardiac fibroblast activation and fibrosis. Osteopontin (OPN) is a ubiquitous pro-inflammatory cytokine, which also mediates fibrosis in several tissues, including the heart. OPN underlies several cardiovascular pathologies, including atherosclerosis and cardiac adverse remodeling. We found that the cardiotoxic hormone aldosterone transcriptionally upregulates OPN in H9c2 rat cardiac myoblasts-an effect prevented by endogenous ß2AR activation. Additionally, CRISPR-mediated OPN deletion enhanced cAMP generation in response to both ß1AR and ß2AR activation in H9c2 cardiomyocytes, leading to the upregulation of Epac1 protein levels. These effects rendered ß2AR stimulation capable of completely abrogating transforming growth factor (TGF)-ß-dependent fibrosis in OPN-lacking H9c2 cardiomyocytes. Finally, OPN interacted constitutively with Gαs subunits in H9c2 cardiac cells. Thus, we uncovered a direct inhibitory role of OPN in cardiac ß2AR anti-fibrotic signaling via cAMP/Epac1. OPN blockade could be of value in the treatment and/or prevention of cardiac fibrosis.

Novel Insights into the Crosstalk between Mineralocorticoid Receptor and G Protein-Coupled Receptors in Heart Adverse Remodeling and Disease.

The mineralocorticoid hormone aldosterone regulates sodium and potassium homeostasis but also adversely modulates the maladaptive process of cardiac adverse remodeling post-myocardial infarction. Through activation of its mineralocorticoid receptor (MR), a classic steroid hormone receptor/transcription factor, aldosterone promotes inflammation and fibrosis of the heart, the vasculature, and the kidneys. This is why MR antagonists reduce morbidity and mortality of heart disease patients and are part of the mainstay pharmacotherapy of advanced human heart failure. A plethora of animal studies using cell type⁻specific targeting of the MR gene have established the importance of MR signaling and function in cardiac myocytes, vascular endothelial and smooth muscle cells, renal cells, and macrophages. In terms of its signaling properties, the MR is distinct from nuclear receptors in that it has, in reality, two physiological hormonal agonists: not only aldosterone but also cortisol. In fact, in several tissues, including in the myocardium, cortisol is the primary hormone activating the MR. There is a considerable amount of evidence indicating that the effects of the MR in each tissue expressing it depend on tissue- and ligand-specific engagement of molecular co-regulators that either activate or suppress its transcriptional activity. Identification of these co-regulators for every ligand that interacts with the MR in the heart (and in other tissues) is of utmost importance therapeutically, since it can not only help elucidate fully the pathophysiological ramifications of the cardiac MR's actions, but also help design and develop novel better MR antagonist drugs for heart disease therapy. Among the various proteins the MR interacts with are molecules involved in cardiac G protein-coupled receptor (GPCR) signaling. This results in a significant amount of crosstalk between GPCRs and the MR, which can affect the latter's activity dramatically in the heart and in other cardiovascular tissues. This review summarizes the current experimental evidence for this GPCR-MR crosstalk in the heart and discusses its pathophysiological implications for cardiac adverse remodeling as well as for heart disease therapy. Novel findings revealing non-conventional roles of GPCR signaling molecules, specifically of GPCR-kinase (GRK)-5, in cardiac MR regulation are also highlighted.

Biased agonism/antagonism at the AngII-AT1 receptor: Implications for adrenal aldosterone production and cardiovascular therapy.

Many of the effects of angiotensin II (AngII), including adrenocortical aldosterone release, are mediated by the AngII type 1 receptor (AT1R), a receptor with essential roles in cardiovascular homeostasis. AT1R belongs to the G protein-coupled receptor (GPCR) superfamily, mainly coupling to the Gq/11 type of G proteins. However, it also signals through ßarrestins, oftentimes in parallel to eliciting G protein-dependent signaling. This has spurred infinite possibilities for cardiovascular pharmacology, since various beneficial effects are purportedly exerted by AT1R via ßarrestins, unlike AT1R-induced G protein-mediated pathways that usually result in damaging cardiovascular effects, including hypertension and aldosterone elevation. Over the past decade however, a number of studies from our group and others have suggested that AT1R-induced ßarrestin signaling can also be damaging for the heart, similarly to the G protein-dependent one, with regard to aldosterone regulation. Additionally, AT1R-induced ßarrestin signaling in astrocytes from certain areas of the brain may also play a significant role in central regulation of blood pressure and hypertension pathogenesis. These findings have provided the impetus for testing available angiotensin receptor blockers (ARBs) in their efficacy towards blocking both routes (i.e. both G protein- and ßarrestin-dependent) of AT1R signaling in vitro and in vivo and also have promoted structure-activity relationship (SAR) studies for the AngII molecule in terms of ßarrestin signaling to certain cellular effects, e.g. adrenal aldosterone production. In the present review, we will recount all of these recent studies on adrenal and astrocyte AT1R-dependent ßarrestin signaling while underlining their implications for cardiovascular pathophysiology and therapy.

Checkpoint inhibitor myocarditis with preceding immunosuppression and tolerance of sequential anthracycline therapy.

A man in his 50s with no known cardiac history and diffuse large B-cell lymphoma on nivolumab presented with acute dyspnoea and swelling. Physical examination revealed volume overload. Work-up noted new elevation of B-type natriuretic peptide and troponin, with new lateral T-wave inversions on ECG. He was admitted to cardiac intensive care for decompensated heart failure. Echocardiography showed ejection fraction 51% with diffuse hypokinesis and reduction of global longitudinal strain. Cardiac MRI demonstrated diffuse myocardial fibrosis with oedema suggesting acute injury. Endomyocardial biopsy revealed lymphocytic and macrophagic infiltrate with cardiomyocyte damage, compatible with immune checkpoint inhibitor (ICI) myocarditis. Immunotherapy was discontinued and he was treated with diuresis, steroids and initiation of goal-directed medical therapy for heart failure. He required additional treatment with anthracyclines. He was monitored with cardio-oncology follow-up after every cycle of anthracycline and tolerated a cumulative 312 mg/m2 therapy. The safety of anthracycline administration after ICI-myocarditis has not been described.

US trends of in-hospital morbidity and mortality for acute myocardial infarctions complicated by cardiogenic shock.

BACKGROUND: There is limited real-world data highlighting recent temporal in-hospital morbidity and mortality trends for cases of acute myocardial infarction complicated by cardiogenic shock. The role of mechanical circulatory support within this patient population remains unclear. METHODS: The US National Inpatient Sample database was sampled from 2011 to 2018 identifying 206,396 hospitalizations with a primary admission diagnosis of ST- or Non-ST elevation myocardial infarction complicated by cardiogenic shock. The primary outcomes included trends of all-cause in-hospital mortality, mechanical circulatory support use, and sex-specific trends for acute myocardial infarction complicated by cardiogenic shock (AMI-CS) over the study period. RESULTS: The annual number of AMI-CS hospitalizations increased from 22,851 in 2011 to 30,015 in 2018 and in-hospital mortality trends remained similar (42.9 % to 43.7 %, ptrend < 0.001). The proportion of patients receiving any temporary MCS device decreased (46.4 % to 44.4 %). The use of intra-aortic balloon pump (IABP) decreased (44.9 % to 32.9 %) and the use of any other non-IABP MCS device increased (2.5 % to 15.6 %), ptrend<0.001. Sex-specific mortality indicate female in-hospital mortality remained similar (50.3 % to 51 %, ptrend<0.001), but higher than male in-hospital mortality, which increased non-significantly (38.8 % to 40.2 %, ptrend = 0.372). CONCLUSIONS: From 2011 to 2018, hospitalizations for AMI-CS patients have increased in number. However, there has been no recent appreciable change in AMI-CS mortality despite a changing treatment landscape with decreasing use of IABPs and increasing use of non-IABP MCS devices. Further research is necessary to examine the appropriate use of MCS devices within this population.

In-hospital outcomes of septal myectomy vs. alcohol septal ablation for hypertrophic cardiomyopathy with outflow tract obstruction: An update and insights from the national inpatient sample from 2011 to 2019.

Septal Myectomy (SM) and Alcohol Septal Ablation (ASA) improve symptoms in patients with Hypertrophic Cardiomyopathy with outflow tract obstruction (oHCM). However, outcomes data in this population is predominantly from specialized centers. The National Inpatient Database was queried from 2011 to 2019 for relevant international classification of diseases (ICD)-9 and -10 diagnostic and procedural codes. We compared baseline characteristics and in-hospital outcomes of patients with oHCM who underwent SM vs ASA. A p-value < 0.001 was considered statistically significant. We identified 15,119 patients with oHCM who underwent septal reduction therapies, of whom 57.4% underwent SM, and 42.6% underwent ASA. Patients who underwent SM had higher all-cause mortality (OR: 1.8 (1.3-2.5)), post-procedure ischemic stroke (OR: 2.3 (1.7-3.2)), acute kidney injury (OR: 1.4 (1.2-1.7)), vascular complications (OR: 3.6 (2.3-5.3)), ventricular septal defect (OR: 4.4 (3.2-6.1)), cardiogenic shock (OR: 1.7 (1.3-2.3)), sepsis (OR: 3.2 (1.9-5.4)), and left bundle branch block (OR: 3.5 (3-4)), compared to ASA. Patients who underwent ASA had higher post-procedure complete heart block (OR: 1.3 (1.1-1.4)), right bundle branch block (OR: 6.3 (5-7.7)), ventricular tachycardia (OR: 2.2 (1.9-2.6)), supraventricular tachycardia (OR: 1.6 (1.4-2)), and more commonly required pacemaker insertion (OR: 1.4 (1.3-1.7)) (p < 0.001 for all) compared to SM. This nationwide analysis evidenced that patients undergoing SM had higher in-hospital mortality and periprocedural complications than ASA; however, those undergoing ASA had more post-procedure conduction abnormalities and pacemaker implantation. The implications of these findings warrant further investigation regarding patient selection strategies for these therapies.

Trends and In-Hospital Outcomes of Patients With Baseline Right Bundle Branch Block Who Underwent Transcatheter Aortic Valve Implantation.

This study aimed to explore contemporary in-hospital outcomes and trends of transcatheter aortic valve implantation (TAVI) outcomes in patients with baseline right bundle branch block (RBBB) using data collected from a nationwide sample. Using the National Inpatient Sample, we identified patients hospitalized for an index TAVI procedure from 2016 to 2019. Primary outcomes included in-hospital all-cause mortality, complete heart block, and permanent pacemaker (PPM) implantation. A total of 199,895 hospitalizations for TAVI were identified. RBBB was present in 10,495 cases (5.3%). Patients with RBBB were older (median age 81 vs 80 years, p <0.001) and less likely to be female (35% vs 47.4%, p <0.001). After adjusting for differences in baseline characteristics and elective versus nonelective admission, patients with RBBB had a higher incidence of complete heart block (adjusted odds ratio [aOR] 4.77, confidence interval [CI] 4.55 to 5.01, p <0.001) and PPM implantation (aOR 4.15, CI 3.95 to 4.35, p <0.001) and no difference in-hospital mortality rate (aOR 0.85, CI 0.69 to 1.05, p = 0.137). Between 2016 and 2019, there was a 3.5% and 2.9% decrease in in-hospital PPM implantation in patients with and without RBBB, respectively. In conclusion, from 2016 to 2019, the rate of in-hospital PPM implantation decreased during index TAVI hospitalization in both patients with and without RBBB. However, in those with baseline RBBB, complete heart block complication rates requiring PPM implantation remain relatively high. Further research and advances are needed to continue to reduce complication rates and the need for PPM implantation.

Impact of Chronic Heart Failure on Acute Pulmonary Embolism in-Hospital Outcomes (From a Contemporary Study).

There is a paucity of evidence on the impact of chronic heart failure (HF) on acute pulmonary embolism (PE) hospitalization outcomes. The aim of this study was to evaluate the in-hospital outcomes of patients with chronic HF and acute PE. A total of 1,391,145 hospitalizations with acute PE from the National Inpatient Sample Database from 2011 to 2019 were included. The database was queried for relevant International Classification of Diseases, Ninth and Tenth Revisions procedural and diagnostic codes. Baseline characteristics and in-hospital outcomes for patients with acute PE were compared in patients with and without a history of chronic HF. Multivariate logistic regression analyses were performed, adjusting for age, race, gender, and statistically significant co-morbidities between cohorts. A p value <0.001 was considered significant. Overall, the mean age was 65.2±16 years; 50.9% of patients were women, and 230,875 patients (16.6%) had chronic HF. The patients in the chronic HF cohort were predominantly older (mean age 69.0 vs 61.4 years) and male (49.9% vs 48.3%). In the multivariate model, chronic HF was associated with increased all-cause mortality (odds ratio [OR] 1.6, 95% confidence interval [CI], 1.57 to 1.63, 10.4% vs 5.7%), acute respiratory distress (OR 1.7, 95% CI 1.70 to 1.74, 39.5% vs 22.1%), cardiac arrest (OR 1.4, 95% CI 1.40 to 1.49, 3.9% vs 2.2%), and cardiogenic shock (OR 3.0, 95% CI 2.85 to 3.06, 4.2% vs 1.2%). All p values were <0.001. In conclusion, patients with PE and chronicHF are associated with increased in-hospital complications compared with patients with PE and without chronic HF. Prospective studies are needed to evaluate optimal management strategies in this population at high risk.