No Pulse, No Panic! Navigating Cardiac Arrest in LVAD-Supported Patients.

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 …

Systolic Nonclosure of the Mitral Valve: Two Left Ventricular Assist Device Patients with Pan-Cardiac Cycle Mitral Valve Opening During Shock States

SGLT2 inhibitors and cardiovascular outcomes in patients with left ventricular assist devices.

Perioperative considerations in the patient with a left ventricular assist device.

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

The success of left ventricular assist device (LVAD) therapy is hampered by complications such as thrombosis and bleeding. Understanding blood flow interactions between the heart and the LVAD might help optimize treatment and decrease complication rates. We hypothesized that LVADs modify shear stresses and blood transit in the left ventricle (LV) by changing flow patterns and that these changes can be characterized using 2D echo color Doppler velocimetry (echo-CDV). We used echo-CDV and custom postprocessing methods to map blood flow inside the LV in patients with ongoing LVAD support (Heartmate II, N = 7). We compared it to healthy controls (N = 20) and patients with dilated cardiomyopathy (DCM, N = 20). We also analyzed intraventricular flow changes during LVAD ramp tests (baseline ± 400 rpm). LVAD support reversed the increase in blood stasis associated with DCM, but it did not reduce intraventricular shear exposure. Within the narrow range studied, the ventricular flow was mostly insensitive to changes in pump speed. Patients with significant aortic insufficiency showed abnormalities in blood stasis and shear indices. Overall, this study suggests that noninvasive flow imaging could potentially be used in combination with standard clinical methods for adjusting LVAD settings to optimize flow transport and minimize stasis on an individual basis.

Background Left ventricular assist device (LVAD) is a promising new therapy in patients with advanced heart failure. Previous studies suggested that continuous blood flow impairs endothelial function. Whether the third-generation LVAD (HeartWareR, HeartWare Inc., Framingham, MA, USA) system affects endothelial regulation of microvascular flow, endothelial nitric oxide (NO) bioavailability and endothelial production of vWF is not known.Methods Fifteen LVAD-supported heart failure patients and 13 age/body mass index matched heart failure patients (HF) were included. The microvascular endothelial function of skin vessels was assessed with laser Doppler imager (LDI) using 3 different hyperaemic challenges: acetylcholine (Ach) iontophoresis, sodium nitroprusside (SNP) iontophoresis and local heating to 44°C. NO-mediated vasodilation was further evaluated by comparing heating hyperaemic response in skin area pretreated either by a saline solution (control) or a specific NO-synthase inhibitor (L-N-arginine-methyl-ester, L-NAME). vWF antigen was also measured in LVAD and HF patients.Results SNP-induced vasodilation did not differ between LVAD and HF patients, and we observed a trend towards an increased vasodilator response to Ach in LVAD patients (P =0.06). Compared to HF patients, skin thermal hyperaemia was increased in LVAD patients in both control and L-NAME pretreated skin (all P < 0.001). The hyperaemic reaction attributable to NO-mediated vasodilation correlated negatively with HF duration (r = –0.50, P < 0.01, n = 28), but did not differ between LVAD and HF patients. Both groups disclosed also similar vWF antigen serum levels.Conclusion This case-control study indicates that third-generation LVAD therapy does not alter skin microvascular endothelial function and vWF production of patients with HF

Background Left ventricular assist device (LVAD) is a promising new therapy in patients with advanced heart failure. Previous studies suggested that continuous blood flow impairs endothelial function. Whether the third-generation LVAD (HeartWare®, HeartWare Inc., Framingham, MA, USA) system affects endothelial regulation of microvascular flow, endothelial nitric oxide (NO) bioavailability and endothelial production of vWF is not known. Methods Fifteen LVAD-supported heart failure patients and 13 age/body mass index matched heart failure patients (HF) were included. The microvascular endothelial function of skin vessels was assessed with laser Doppler imager (LDI) using 3 different hyperaemic challenges: acetylcholine (Ach) iontophoresis, sodium nitroprusside (SNP) iontophoresis and local heating to 44°C. NO-mediated vasodilation was further evaluated by comparing heating hyperaemic response in skin area pretreated either by a saline solution (control) or a specific NO-synthase inhibitor (L-N-arginine-methyl-ester, L-NAME). vWF antigen was also measured in LVAD and HF patients. Results SNP-induced vasodilation did not differ between LVAD and HF patients, and we observed a trend towards an increased vasodilator response to Ach in LVAD patients (P = 0.06). Compared to HF patients, skin thermal hyperaemia was increased in LVAD patients in both control and L-NAME pretreated skin (all P

Activated partial thromboplastin time overestimates anti-coagulation in left ventricular assist device patients

Go with the flow: progress in mechanical circulatory support.

Care for patients with ventricular assist devices and suspected COVID-19 infection.

Medical Management of Left Ventricular Assist Device Patients: A Practical Guide for the Nonexpert Clinician

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.

HFSA/SAEM/ISHLT clinical expert consensus document on the emergency management of patients with ventricular assist devices.

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