Orthotropic heart transplantation remains the most effective therapy for patients with end-stage heart failure, with a median survival of ≈13 years. Yet, a number of complications are observed after orthotropic heart transplantation, including atrial and ventricular arrhythmias. Several factors contribute to arrhythmias, such as autonomic denervation, effect of the surgical technique, acute and chronic rejection, and transplant vasculopathy among others. To minimize risk of future arrhythmias, the bicaval technique and minimizing ischemic time are current surgical standards. Sinus node dysfunction is the most common indication for early (within 30 days) pacemaker implantation, whereas atrioventricular block incidence increases as time from transplant increases. Atrial fibrillation can occur in the first few weeks following transplantation but is uncommon in the long term unless secondary to a precipitant such as acute rejection. The most common atrial arrhythmias are atrial flutters, which are mainly typical, but atypical circuits can be observed such as those that involve the remnant donor atrium in regions immediately adjacent to the atrioatrial anastomosis suture line. Choosing the appropriate pharmacological therapy requires careful consideration due to the potential interaction with immunosuppressive agents. Despite historical concerns, adenosine is effective and safe at reduced doses if administered under cardiac monitoring. Catheter ablation has emerged as an effective treatment strategy for symptomatic supraventricular tachycardias, including ablation of atypical flutter circuits. Cardiac allograft vasculopathy is an important risk factor for sudden cardiac death, yet the role of prophylactic implantable cardioverter-defibrillator implant for sudden death prevention is unclear. Current indications for implantable cardioverter-defibrillator implantation are as in the nontransplant population. A number of questions for future research are posed.

Durable implantable left ventricular assist devices (LVADs) have been shown to improve survival and quality of life for patients with stage D heart failure. Even though LVADs remain underused overall, the number of patients with heart failure supported with LVADs is steadily increasing. Therefore, general cardiologists will increasingly encounter these patients. In this review, we provide an overview of the field of durable LVADs. We discuss which patients should be referred for consideration of advanced heart failure therapies. We summarize the basic principles of LVAD care, including medical and surgical considerations. We also discuss the common complications associated with LVAD therapy, including bleeding, infections, thrombotic issues, and neurologic events. Our goal is to provide a primer for the general cardiologist in the recognition of patients who could benefit from LVADs and in the principles of managing patients with LVAD. Our hope is to “demystify” LVADs for the general cardiologist.

Heart failure (HF), a prevalent global health issue characterized by the heart’s impaired ability to pump or fill blood, affects millions worldwide and continues to pose significant challenges despite advancements in treatment. This review delves into the critical and increasingly recognized role of inflammation in the development and progression of this complex syndrome. While the incidence of HF has seen a decline in some regions due to improved cardiac care, its overall prevalence is rising, particularly among younger adults and those with heart failure with a preserved ejection fraction (HFpEF). Given the persistently high rates of hospitalization and mortality associated with HF, understanding the underlying mechanisms, including the contribution of inflammation, is crucial for identifying novel therapeutic strategies. Inflammation in heart failure is a multifaceted process involving the activation of the immune system, both innate and adaptive, and encompasses various mechanisms such as the release of pro-inflammatory mediators, endothelial dysfunction, and neurohormonal activation. Myocardial damage triggers the innate immune response, while humoral immunity and chronic systemic inflammation, often linked to cardiovascular risk factors and autoimmune diseases, also play significant roles. Notably, heart failure and inflammation have a reciprocal relationship, with HF itself contributing to inflammatory processes within the cardiac tissue and systemically. Understanding these intricate pathways, including the involvement of specific immune cells and molecular mediators, is essential for comprehending the pathogenesis of heart failure and exploring potential therapeutic interventions. The review further examines various inflammatory biomarkers that have been implicated in heart failure, such as cytokines (including TNF-α and IL-1) and C-reactive protein (CRP). While these markers often correlate with the severity and prognosis of HF, clinical trials targeting specific inflammatory mediators have largely yielded disappointing results, highlighting the complexity of the inflammatory response in this context. The exploration of these biomarkers and the challenges encountered in translating anti-inflammatory strategies into effective treatments underscore the need for continued research to unravel the precise role of inflammation across different HF subtypes and to develop more targeted and effective anti-inflammatory therapies.

Background: The coronavirus disease 2019 (COVID-19) pandemic continues to afflict millions of people worldwide. Patients with end-stage heart failure and left ventricular assist devices (LVADs) may be at risk for severe COVID-19 given a high prevalence of complex comorbidities and functional impaired immunity. The objective of this study is to describe the clinical characteristics and outcomes of COVID-19 in patients with end-stage heart failure and durable LVADs. Methods: The Trans-CoV-VAD registry is a multi-center registry of LVAD and cardiac transplant patients in the United States with confirmed COVID-19. Patient characteristics, exposure history, presentation, laboratory data, course, and clinical outcomes were collected by participating institutions and reviewed by a central data repository. This report represents the participation of the first 9 centers to report LVAD data into the registry. Results: A total of 40 patients were included in this cohort. The median age was 56 years (interquartile range, 46–68), 14 (35%) were women, and 21 (52%) were Black. Among the most common presenting symptoms were cough (41%), fever, and fatigue (both 38%). A total of 18% were asymptomatic at diagnosis. Only 43% of the patients reported either subjective or measured fever during the entire course of illness. Over half (60%) required hospitalization, and 8 patients (20%) died, often after lengthy hospitalizations. Conclusions: We present the largest case series of LVAD patients with COVID-19 to date. Understanding these characteristics is essential in an effort to improve the outcome of this complex patient population.

Background: Current guidelines recommend use of sacubitril‐valsartan in patients with heart failure with reduced ejection fraction (HFrEF). Early data suggested low uptake of sacubitril‐valsartan, but contemporary data on real‐world use and their associated cost are limited. Methods and Results: This was a retrospective study of individuals enrolled in Optum Clinformatics, a national insurance claims data set from 2016 to 2018. We included all adult patients with HFrEF with 2 outpatient encounters or 1 inpatient encounter with an International Classification of Diseases, Tenth Revision ( ICD‐10 ), diagnosis of HFrEF and 6 months of continuous enrollment, also receiving β‐blockers and angiotensin‐converting enzyme inhibitors/angiotensin receptor blockers within 6 months of HFrEF diagnosis. We included 70 245 patients with HFrEF, and 5217 patients (7.4%) received sacubitril‐valsartan prescriptions. Patients receiving care through a cardiologist compared with a primary care physician alone were more likely to receive sacubitril‐valsartan (odds ratio, 1.61 [95% CI, 1.52–1.71]). Monthly out‐of‐pocket (OOP) cost for sacubitril‐valsartan, compared with angiotensin‐converting enzyme inhibitors/angiotensin receptor blockers, was higher for both commercially insured patients (mean, $69 versus $6.74) and Medicare Advantage (mean, $62 versus $2.52). For patients with commercial insurance, OOP cost was lower in 2016 than in 2018. For patients with Medicare Advantage, there was a significant geographic variation in the OOP costs across the country, ranging from $31 to $68 per month across different regions, holding all other patient‐related factors constant. Conclusions: Sacubitril‐valsartan use was infrequent among patients with HFrEF. Patients receiving care with a cardiologist were more likely to receive sacubitril‐valsartan. OOP costs remain high, potentially limiting use. Significant geographic variation in OOP costs, unexplained by patient factors, was noted.

Background: Congestive heart failure is a leading cause of morbidity and mortality worldwide. One of the signs of congestive heart failure is fluid overload including pulmonary edema, peripheral edema, and ascites. The cause of fluid overload remains incompletely understood, and management of these patients continues to be a challenge. The role of lymphatic circulation abnormalities in the cause and pathophysiology of fluid overload also remains unclear. Here we report on a study in a large animal model of right heart failure caused by severe tricuspid regurgitation comparing cardiovascular and lymphatic findings in a group of animals that did not develop ascites with a group of animals that developed ascites. Methods and Results: Thirteen Yorkshire pigs were included in this study divided into 2 groups. Group 1 included 6 animals that did not develop ascites, and Group 2 included 7 animals that had developed ascites. The groups were compared on hemodynamic parameters as well as comparison of the animal's lymphatic anatomy and function. There was no difference between the groups in degree of tricuspid regurgitation and central venous pressure, with inferior vena cava pressure measuring 11.6±1.6 versus 13.2±3.7 ( P =0.534) and superior vena cava pressure measuring 12.0±2.3 versus 13.7±3.2 ( P =0.366). There was also no difference between the groups in all measured hemodynamic parameters, including right ventricular pressure, pulmonary artery pressure, and left ventricular function. The weighted liver size in the ascites group was significantly larger than in the nonascites group (30.3±12.4 versus 63.3±14.0 mL/kg, respectively; P =0.001). The 2 groups also differed in the number of animals with regurgitant thoracic duct flow (Group 1: 1/6,17% versus Group 2: 6/7, 86%; P =0.029) and the minimal thoracic duct diameter (Group 1: 2.3±0.3 versus Group 2: 4.2±2.2; P =0.035). Conclusions: In animals with right heart failure caused by severe tricuspid regurgitation, fluid overload did not correlate with hemodynamic parameters but rather with changes in the lymphatic system, including regurgitant lymphatic flow, minimal thoracic duct diameter, and liver size. This study is consistent with lymphatic dysfunction and not cardiovascular function playing a significant role in the cause of fluid overload. Further studies are needed to confirm these findings.