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Tolvaptan, a selective vasopressin type-2 antagonist, has been shown to increase serum sodium (Na) and urine output in hyponatremic left ventricular assist device (LVAD) patients in retrospective studies. In this prospective randomized pilot study, we aimed to assess the efficacy of tolvaptan in this population.We conducted a prospective, randomized, non-blinded pilot study of LVAD recipients with post-operative hyponatremia (Na 135 mEq/L) (NCT05408104). Eligible participants were randomized to receive tolvaptan 15 mg daily in addition to usual care versus usual care alone. The primary outcome was a change in Na level and estimated glomerular filtration rate (eGFR), from the first post-operative day of hyponatremia (the day of randomization) to discharge.A total of 33 participants were enrolled, and 28 underwent randomization (median age 55 [IQR 50-62]), 21% women, 54% Black, 32% ischemic cardiomyopathy, median baseline Na 135 (IQR 134-138). Fifteen participants were randomized to tolvaptan (TLV) and 13 were randomized to usual care alone (No-TLV). Mean change in Na from randomization to discharge in the TLV group was 2.7 mEq/L (95%CI 0.7-4.7, p = 0.013) and 1.8 (95%CI 0.5-4.0, p = 0.11) in the No-TLV group, though baseline and final Na levels were similar between groups. The mean change in eGFR was 2.6 ml/min/1.73 mTLV significantly increases urine output, with nominal improvement in Na level, in hyponatremic post-operative LVAD patients without adversely impacting renal function.

As left ventricular assist device (LVAD) survival rates continue to improve, evaluating site-specific variability in outcomes can facilitate identifying targets for quality-improvement initiative opportunities in the field.Deidentified center-specific outcomes were analyzed for HeartMate 3 (HM3) patients enrolled in the MOMENTUM 3 pivotal and continued access protocol trials. Centers25th percentile for HM3 volumes were excluded. Variability in risk-adjusted center mortality was assessed at 90 days and 2 years (conditional upon 90-day survival). Adverse event (AE) rates were compared across centers.In the 48 included centers (1958 patients), study-implant volumes ranged between 17 and 106 HM3s. Despite similar trial-inclusion criteria, patient demographics varied across sites, including age quartile ((Q)1-Q3:57-62 years), sex (73%-85% male), destination therapy intent (60%-84%), and INTERMACS profile 1-2 (16%-48%). Center mortality was highly variable, nadiring at ≤ 3.6% (≤ 25th percentile) and peaking at ≥ 10.4% (≥ 75th percentile) at 90 days and ≤ 10.2% and ≥ 18.7%, respectively, at 2 years. Centers with low mortality rates tended to have lower 2-year AE rates, but no center was a top performer for all AEs studied.Mortality and AEs were highly variable across MOMENTUM 3 centers. Studies are needed to improve our understanding of the drivers of outcome variability and to ascertain best practices associated with high-performing centers across the continuum of intraoperative to chronic stages of LVAD support.

As the prevalence of advanced heart failure continues to rise, treatment strategies for select patients include heart transplantation or durable left ventricular assist device (LVAD) support, both of which improve quality of life and extend survival. Recently, the HeartMate 3 has been incorporated into clinical practice, the United Network for Organ Sharing donor heart allocation system was revised, and the management of LVAD-related complications has evolved. Contemporary LVAD recipients have greater preoperative illness severity, but survival is higher and adverse event rates are lower compared with prior eras. This is driven by advances in device design, patient selection, surgical techniques, and long-term management. However, bleeding, infection, neurologic events, and right ventricular failure continue to limit broader implementation of LVAD support. Ongoing efforts to optimize management of patients implanted with current devices and parallel development of next-generation devices are likely to further improve outcomes for patients with advanced heart failure.

We examined the impact and time course of de novo human leukocyte antigen (HLA) allosensitization following left ventricular assist device (LVAD) implantation.Forty patients had a calculated panel reactive antibody (cPRA) prior to LVAD surgery between January 2014 and December 2018. Of these patients, we retrospectively studied 33 patients who had pre-LVAD cPRA10%. De novo allosensitization was defined as cPRA ≥10% within 3 months following LVAD surgery, and "persistent allosensitization" was defined as cPRA ≥10% at time of heart transplant or death. One-third (11/33) of our cohort developed de novo allosensitization within 3-months post-LVAD. Median duration of follow-up during LVAD support was 588 days (IQR 337-1071 days), or approximately 19 months. In an adjusted, multivariable analysis, female sex remained associated with de novo allosensitization (adjusted odds ratio [95%CI]: 11 (1.4-85), P = 0.026). De novo allosensitization was subsequently associated with persistent allosensitization (P = 0.024). Both axial-flow and centrifugal-flow LVADs had similar rates of allosensitization. Compared to those with no allosensitization, patients with de novo allosensitization did not appear to have inferior post-transplant outcomes of death or treated rejection.In our single-center experience, one-third of patients developed de novo allosensitization which did not appear to associate with inferior post-transplant outcomes. Female sex was associated with de novo allosensitization.

BACKGROUND: Prognostic awareness (PA) – the understanding of limited life expectancy – is critical for effective goals of care discussions (GOCD) in which patients discuss their goals and values in the context of their illness. Yet little is known about PA and GOCD in patients with advanced heart failure (HF). This study aims to determine the prevalence of PA among advanced HF patients and patient characteristics associated with PA and GOCD. METHODS: We assessed the prevalence of self-reported PA and GOCD using data from a multisite communication intervention trial among advanced HF patients with an implantable cardiac defibrillator at high risk of death. RESULTS: Of 377 patients, (mean age 62 years, 30% female, 42% non-white), 78% had PA. Increasing age was a negative predictor of PA (OR=0.95, 95% CI 0.92, 0.97, p < 0.01). No other patient characteristics were associated with PA. Of those with PA, 26% had a GOCD. Higher comorbidities and prior advance directives were associated with GOCD, but were of only borderline statistical significance in a fully adjusted model. Symptom severity (OR=1.77, 95% CI 1.19, 2.64, p 0.005) remained a robust and statistically significant positive predictor of having a GOCD in the fully adjusted model. CONCLUSIONS: In a sample of advanced HF patients, the frequency of PA was high, but fewer patients with PA discussed their end-of-life care preferences with their physician. Improved efforts are needed to ensure all advanced HF patients have an opportunity to have GOCD with their doctors. Clinicians may need to target older HF patients, and continue to focus on those with signs of worsening illness (higher symptoms). REGISTRATION: Clinicaltrials.gov - NCT01459744

STRUCTURED ABSTRACTBackgroundThe degree of myocardial injury, reflected by troponin elevation, and associated outcomes among hospitalized patients with Coronavirus Disease (COVID-19) in the US are unknown.ObjectivesTo describe the degree of myocardial injury and associated outcomes in a large hospitalized cohort with laboratory-confirmed COVID-19.MethodsPatients with COVID-19 admitted to one of five Mount Sinai Health System hospitals in New York City between February 27th and April 12th, 2020 with troponin-I (normal value ResultsThe median age was 66.4 years, with 59.6% men. Cardiovascular disease (CVD) including coronary artery disease, atrial fibrillation, and heart failure, was more prevalent in patients with higher troponin concentrations, as were hypertension and diabetes. A total of 506 (18.5%) patients died during hospitalization. Even small amounts of myocardial injury (e.g. troponin I 0.03-0.09ng/mL, n=455, 16.6%) were associated with death (adjusted HR: 1.77, 95% CI 1.39-2.26; P0.09 ng/dL, n=530, 19.4%) were associated with more pronounced risk (adjusted HR 3.23, 95% CI 2.59-4.02).ConclusionsMyocardial injury is prevalent among patients hospitalized with COVID-19, and is associated with higher risk of mortality. Patients with CVD are more likely to have myocardial injury than patients without CVD. Troponin elevation likely reflects non-ischemic or secondary myocardial injury.Unstructured AbstractMyocardial injury reflected as elevated troponin in Coronavirus Disease (COVID-19) is not well characterized among patients in the United States. We describe the prevalence and impact of myocardial injury among hospitalized patients with confirmed COVID-19 and troponin-I measurements within 24 hours of admission (N=2,736). Elevated troponin concentrations (normal

In the contemporary era, nearly 85% of children with congenital heart disease will reach adulthood. Despite optimal medical and surgical treatment, many will experience a progressive decline in cardiopulmonary function leading to advanced heart failure. These patients present unique anatomic and physiological challenges to the care team, and unlike adults with acquired heart disease who progress to severe heart failure, advanced treatment options such as mechanical circulatory support and cardiac transplant may be limited. Severe ventricular dysfunction and/or pulmonary hypertension may not be amenable to corrective repair. Heart transplantation with or without mechanical circulatory support may be the only option for highly selected patients. The aim of this review is to describe advanced heart failure therapies for adults with congenital heart disease, including the general approach to evaluation and management, pre- and post-operative care, anticipated short- and long-term outcomes, and future directions for clinical care and research.

Venoarterial extracorporeal membrane oxygenation (ECMO) is a rescue therapy that can stabilize patients with hemodynamic compromise, with or without respiratory failure, for days or weeks. In cardiology, the main indications for ECMO include cardiac arrest, cardiogenic shock, post-cardiotomy shock, refractory ventricular tachycardia, and acute management of complications of invasive procedures. The fundamental premise underlying ECMO is that it is a bridge-to recovery, to a more durable bridge, to definitive treatment, or to decision. As a very resource- and effort-intensive intervention, ECMO should not be used on unsalvageable patients. As the use of this technology continues to evolve rapidly, it is important to understand the indications and contraindications; the logistics of ECMO initiation, management, and weaning; the general infrastructure of the program (including the challenges associated with transferring patients supported by ECMO); and ethical considerations, areas of uncertainty, and future directions.

A 51-year-old male with untreated hepatitis C infection, cirrhosis, and dilated cardiomyopathy with a HeartMate II LVAD presented with right heart failure and cardiogenic shock, INR of 7, hemolysis, and renal failure. Acute LVAD thrombosis was suspected. Alteplase was injected into the inflow cannula of the LVAD with little effect. Intravenous alteplase was given but failed to restore an adequate pump output, resulting in the need for emergency pump exchange. The patient had an uncomplicated postoperative recovery and was discharged uneventfully. Inspection of the pump identified a thrombus wedged between the spines of the impeller. Our case highlights the challenges in managing pump thrombosis which is often resistant to thrombolysis and may instead rely upon prompt surgical intervention to be resolved.

Medical advances in the care of cardiac patients have resulted in more patients surviving an acute myocardial infarction (MI) than ever before. Each year hundreds of thousands of these survivors undergo remodeling of their left ventricle and often progress to clinical congestive heart failure. The extent of remodeling has been linked to the size of the infarct, whether or not the myocardium has been revascularized, and the control of loading conditions. The extent of infarction can be measured several ways, including the amount of enzyme released as well as infarct imaging with nuclear perfusion or magnetic resonance imaging. Methods to prevent adverse remodeling of the ventricle have included pharmacotherapy with beta-blockers, nitrates, and modulators of the renin-angiotensin-aldosterone system. Surgical intervention has proven useful for select patients with aneurysmal areas of remodeling. Researchers are now investigating several approaches to preventing and reversing cardiac remodeling. These include the use of stem cells to regenerate myocardium and post-infarct pacing to prevent remodeling. Improved therapies are needed to help reduce the number of patients progressing from myocardial infarction to end-stage heart failure.

Although there has been substantial progress in the treatment of congestive heart failure over the last several decades, it is clear that heart failure continues to burden our aging population. As the epidemic of heart failure grows, there remains an unmistakable need for novel diagnostic and therapeutic options in its management. In this article, we review recent innovations in the management of congestive heart failure, highlighting several recent clinical trials.