Body mass index and natriuretic peptides trends before and after left ventricular assist device

Over the last 2 decades, numerous advancements in medical therapies have improved patient outcomes in heart failure (HF). However, a significant number of patients still progress to end-stage HF, in which treatment options are largely limited to cardiac transplantation. As patient demands for transplant continue to exceed the supply of available organs, mechanical assist devices—specifically, the left ventricular assist device (LVAD)—were initially introduced as a bridge to cardiac transplantation. LVADs have 2 important beneficial effects. First, LVADs are placed in parallel to the native left ventricle (LV), causing pressure and volume unloading of the LV. Second, LVADs restore cardiac output and subsequent perfusion to the organs. As a result of these 2 effects, it became evident that some patients had actual improvement in LV function after LVAD placement. The term reverse remodeling was used to describe the improvement in myocardial function that was observed in patients with a seemingly end-stage disease. With reverse remodeling, a new hope for the treatment of HF was born—using LVADs as a bridge to recovery; however, to date, this promise has largely been unrealized. This probably is reflective of the fact that the sequela of mechanical ventricular unloading are quite complex and appear to involve the engagement of competing biological pathways including regression of cardiomyocyte hypertrophy as well as progressive cell atrophy. Although the promise of ventricular recovery still persists, its actualization will await a more comprehensive dissection of these competing biological processes. This review will discuss the beneficial clinical effects of LVAD support as well as review what is known about the cellular and molecular response to mechanical unloading and mechanisms of reverse remodeling. Key research findings have been summarized in the Table. View this table: Table. Summary of Research of LVAD Support on Clinical Effects and the Cellular and Molecular Changes That May Contribute to Reverse …

The field of cardiac mechanical assist devices has achieved a number of striking technical breakthroughs over the past 40 years.1 Emblematic of the type of important technical accomplishments that have been achieved in this field has been the development of the portable, battery-driven left ventricular assist device (LVAD) for patients with intractable cardiac failure. Although LVADs have been used primarily as a “bridge to transplantation,” a number of centers have now begun to implant LVADs as an alternative to transplantation.2 Indeed, as the technology in this field improves, it is entirely conceivable that LVADs will evolve into small, unobtrusive devices that will run on small, portable, long-lasting battery supplies that will not require external connection to the outside. This, in turn, will allow LVADs to serve as a very reliable alternative to transplantation for many patients with advanced heart failure who cannot receive transplants or who cannot be weaned from LVAD support. Thus far, the clinical experience with LVADs as a bridge to transplantation has consistently shown dramatic improvements in cardiac output3 4 and New York Heart Association functional class.4 5 Importantly, these clinical changes have been attended by concomitant decreases in levels of neurohormones6 7 and cytokines,8 suggesting that LVAD support may alter the heart failure “milieu.” In an effort to explain these salutary changes in clinical status, investigators have turned to more basic studies and begun to examine myocardial ultrastructure before and after LVAD implantation. These latter studies have shown decreased myocyte necrosis9 10 and apoptosis,11 decreased myocytolysis,3 and improved myocyte contractility.12 The beneficial changes in the biology of the failing myocardium after LVAD support have also been …

In this issue of Circulation, Birks et al 1 report their recent experience using the combination of continuous-flow (CF) circulatory support and pharmacological therapy to treat advanced heart failure in patients requiring left ventricular assist device (LVAD) support. Thirty-three patients underwent HeartMate II (HMII) LVAD implantation at Harefield hospital during the 3-year study period. Twenty-three patients (70%) with nonischemic cardiomyopathy were considered appropriate for the recovery protocol at the time of HMII LVAD implantation, and 20 patients (61%) who survived LVAD implantation formed the study cohort. With their strategy of aggressive neurohormonal blockade (phase I) followed by high-dose clenbuterol (phase II), 12 (60%) of the study cohort met criteria for LVAD explantation, and all 10 (50%) who survived the perioperative period demonstrated sustained recovery over 56 to 1112 days of follow-up. Therefore, 30% of all patients and 43% of all nonischemic patients undergoing HMII implantation could be managed to long-lasting recovery. In an era in which transplant waiting times have blurred the distinction between bridge-totransplant and destination therapy for some patients, this single-center experience is intriguing and offers hope for a new strategy for select patients supported with CF LVADs. Article see p 381 Reports in the literature regarding rates of cardiac recovery during pulsatile LVAD support are quite varied (Table 1). The Columbia University group reported a 1% rate of sustained cardiac recovery in 111 patients with both ischemic and nonischemic etiology of heart failure. 2 In contrast, the German Heart Institute reported that 13% of patients with nonischemic heart failure demonstrated sustained recovery (minimum follow-up of 36 months) after LVAD explantation. 3 The LVAD Working Group was the first multicenter, prospective initiative to study recovery.4 Sixty-seven LVAD patients (only 1 CF LVAD) with both ischemic and nonischemic causes underwent serial echocardiograms at reduced flow to seek recovery. Six percent of the whole cohort and 7% of all nonischemic patients could undergo LVAD explantation. None of these reports described the consistent use of pharmacological therapy during LVAD support, and it was not until the first Harefield recovery study 5 that data regarding combined pharmacological and mechanical support were available. In the first Harefield study, 15 LVAD patients (1 CF LVAD) received maximal doses of heart failure medications, followed by high-dose clenbuterol. All patients had a nonischemic etiology, and most (80%) had heart failure for 6 months. The authors reported that 75% of patients receiving clenbuterol could undergo LVAD explantation and 46% of all patients with nonischemic heart failure presenting for LVAD could be managed successfully to recovery in this way. These data from Harefield represented the most successful reported recovery strategy to date, and prompted a multicenter study in the United States (to replicate the Harefield recovery protocol) called the Harefield Recovery Protocol Study (HARPS). HARPS has now completed enrollment of 17 patients with the HMI pulsatile LVAD, 13 of whom received both maximal neurohormonal blockade and high-dose clenbuterol. Results from the US HARPS study will be presented in the near future. With the approval of the HMII LVAD for both bridge-to

Left Ventricular Assist Devices and Renal Ramifications.

Leadless pacemaker interrogation interference after conversion of a left ventricular assist device

424 Minimally invasive left ventricular assist device implantation improves clinical outcomes

Introduction Owing to increasing numbers of heart failure patients a search for new biomarkers predicting prognosis is desirable. Background The purpose of this study was to analyze levels of cancer biomarkers in patients with severe heart failure before or after left ventricular assist device (LVAD) implantation and estimate its impact on survival during LVAD support. Methods We retrospectively analyzed data of all consecutive 168 LVAD recipients (92.8%- male, mean age 53.3 years ( median - 56.6, SD 12.0 ), median INTERMACS profile- 3.0, ischemic etiology of heart failure- 52.4%, 41.0% post CRT-D and 54.8% post ICD implantation, 36.9 post IABP, 5.4% post ECMO%, 11.9% post CABG and 8.9% post other cardiac surgery before LVAD implantation) implanted with continuous-flow LVAD (59.5%-HeartMate3, 35.1%- HeartWare, 5.4%-Heart Mate II) in our institution within years 2009-2023. Among comorbidities 63% of patients had atrial fibrillation or flutter, 41.6%- diabetes, 37.5%- arterial hypertension, 48.8%-renal failure, 7.1% pulmonary obstructive disease, 56.5% had pulmonary hypertension with mean pulmonary artery pressure above 25 mm Hg in right heart catheterization and 47% of patients had a history of cardiac arrest or sustained ventricular arrythmia before LVAD implantation. The overall mortality was 44.0 %. 31% patients were transplanted during LVAD support and in 4 patients (2.3%) LVAD was explanted or deactivated. Patient were followed to death, heart transplantation, LVAD explantation or the end of observation in our institution. Mean time of LVAD support was 885 days (1-2570). 23% of patients had right ventricular failure (RVF) early post LVAD implantation while 7.7% had late form of RVF. Results Serum concentrations of cancer biomarkers: carcinoembryonic antigen (CEA), carbohydrate antigen (CA)19-9, carbohydrate antigen(CA)-125 and alpha fetoprotein (AFP) taken before (56 patients -33.3%) or after (24 patients-14.3%) LVAD implantation were analyzed. Mean values, rate of abnormal results and correlation of abnormal results of CEA, CA19-9, CA-125, AFP with mortality during LVAD support were depicted in Table 1. No statistically significant correlations were found between levels of abovementioned cancer biomarkers and mortality though a trend towards increased mortality could be observed for abnormal results of CEA and Ca 19-9 taken before LVAD implantation. No malignant neoplasms were found in all analyzed patients except of one in whom a recurrence of lymphoma was found 2 months after LVAD implantation. Conclusions Patients with severe heart failure before and after LVAD implantation may present abnormal values of cancer biomarkers despite no found neoplasms. Our observation suggests that elevated cancer biomarker levels could predict mortality in heart failure patients after LVAD implantation. Further research is needed to confirm this thesis and investigate mechanisms of this phenomenon.

<i>Circulation: Cardiovascular Interventions</i> Editors’ Picks

Evolution of general surgical problems in patients with left ventricular assist devices

Axial-flow LVADs have become an integral tool in the management of end-stage heart failure. Consequently, nonsurgical bleeding has emerged as a major source of morbidity and mortality in this fragile population. The mechanisms responsible for these adverse events include acquired von Willebrand disease, GI tract angiodysplasia formation, impaired platelet aggregation, and overuse of anticoagulation therapy. Because of ongoing concerns for pump thrombosis and thromboembolic events, the thrombotic/bleeding paradigm has led to a difficult clinical dilemma for those managing patients treated with axial flow LVADs. As the field progresses, advances in the understanding of the pathological mechanisms underlying bleeding/thrombosis risk, careful risk stratification, and potential use of novel anticoagulants will all play a role in the management of the LVAD patient.

Background The spleen has been recognized as an important organ to reserve 20–30% of the total blood volume. Generally, splenomegaly has been thought to be related to congestion. However, in the setting of hypovolemic shock or hypoxemia, it has been reported that spleen contracted and splenic volume decreased. On the other hand, in advanced heart failure (HF), the hemodynamics is characterized by both low cardiac output (LO) and systemic congestion, and patients sometimes need support of left ventricular assist device (LVAD). However, it remains unclear about the association between spleen size and hemodynamic parameters in patients with LO who need LVAD support. Purpose The purpose of this study was to investigate the relationship between spleen size and hemodynamic parameters in advanced HF before and after LVAD implantation. Methods We enrolled 12 advanced HF patients with LVAD (11 males, 45±10 years). All patients underwent blood test, echocardiography, right heart catheterization, and computed tomography (CT) before and after LVAD implantation. Spleen size was measured by CT volumetry. We excluded patients with splenic infarction, or any infections, or mean right atrial pressure (RAP) &lt;5mmHg because of a possibility of hypovolemic status. LO was defined as CI less than 2.2L/min/m2. Results At pre- and post-LVAD implantation, cardiac output, cardiac index (CI), mean RAP, and mean pulmonary capillary wedge pressure were 3.1±0.6 vs. 4.9±0.9L/min, p=0.002; 1.7±0.3 vs. 2.8±0.3L/min/m2, p=0.002; 14±5 vs. 9±3mmHg, p=0.059; and 30±7 vs. 10±3mmHg, p=0.002, respectively. The serum brain natriuretic peptide level had significantly decreased (1101 [517–1446] vs 74 [35–216] pg/mL, p=0.002). In all patients, CI had increased to over 2.2L/min/m2. The splenic volume significantly increased from pre- to post-LVAD implantation (172±48 vs. 233±78mL, p=0.002) (Figure). Furthermore, all patients were divided into two groups; elevated RAP group (n=4) and non-elevated RAP group (n=8) after LVAD support. In elevated RAP group, there were no significant changes in the spleen size between pre- and post-LVAD implantation (167±45 vs. 223±111mL, p=0.068). On the other hand, in non-elevated RAP group, the spleen volume had significantly increased from pre- to post-LVAD support (172±53 vs. 231±62mL, p=0.011). In addition, there was one patient whose hemodynamic state had changed to LO again because of LVAD failure due to pump thrombosis. In this case, the splenic volume was 212mL before LVAD implantation with LO, and increased to 418mL after LVAD implantation with non-LO, although decreased to 227mL after LVAD pump failure with LO again. Splenic volume changes Conclusions The spleen may change its size in order to keep cardiac output by regulating cardiac preload depending on the systemic perfusion in advanced HF with LVAD. Acknowledgement/Funding None

Thyroid Function at Left Ventricular Assist Device (LVAD) Implantation Predicts Prognosis During LVAD Support

Impact of Social Determinants on Outcomes in Patients with Left Ventricular Assist Devices

Recurrent orthostatic syncope due to left atrial and left ventricular collapse after a continuous-flow left ventricular assist device implantation

Relation of Preoperative Serum Albumin Levels to Survival in Patients Undergoing Left Ventricular Assist Device Implantation