Left ventricular assist devices (LVADs) offer a therapeutic strategy for patients with end-stage heart failure. Increased device utilization has also increased the incidence of device-related complications including gastrointestinal bleeding (GIB). Multiple mechanisms have been proposed in the pathophysiology of continuous-flow LVAD-associated GIB including physiologic changes associated with high shear and nonpulsatile flow such as gastrointestinal arteriovenous malformations and acquired von Willebrand syndrome. Strategies to minimize the morbidity and mortality of LVAD-associated GIB are needed. Octreotide, a somatostatin analogue, has been described as an adjunct to current therapies and interventions. Factors that contribute to LVAD-associated GIB may be targeted by the pharmacologic effects of octreotide, including improved platelet aggregation, increased vascular resistance, and decreased splanchnic circulation. Octreotide has demonstrated clinical benefit in several case series and clinical trials for the treatment of LVAD-associated GIB. The focus of this article will be to review the pathophysiology of LVAD-associated GIB, discuss pharmacologic and nonpharmacologic treatment modalities, and review available literature on the role of octreotide in the management of LVAD-associated GIB.
Background Impella devices are being increasingly used to manage cardiogenic shock. The incidence of thrombosis and hemolysis in patients on Impella support increases with longer durations of use, and the management of Impella thrombosis remains ill‐defined. Methods In this case series, we describe our institutional use of tissue plasminogen activator (tPA) alteplase in the Impella purge solution (0.04 or 0.08 mg/ml tPA in sterile water) for management of suspected Impella thrombosis in five patients, each with a different clinical course, treatment, and outcome. Given the limited evidence on the diagnosis of Impella thrombosis, suspicion was driven by the presence of decreased purge flow rates, increased purge pressures, and markers of hemolysis such as elevated lactate dehydrogenase and hematuria. Outcomes In all cases, tPA administration resulted in resolution of low purge flow rates and high purge pressures. No major bleeding complications were directly associated with tPA. Two patients were bridged successfully to heart transplantation, two patients underwent left ventricular assist device implantation, and one patient died after withdrawal of care. Conclusion Based on our experience, tPA administration appears to be a viable and safe salvage option to delay or prevent device exchange in the setting of suspected Impella thrombosis.
Adverse events of therapeutic hypothermia were numerous and frequent, necessitating monitoring. Neurological recovery is primarily driven by the type of arrest, the rapidity of ROSC, the time needed to provide and achieve therapeutic hypothermia, the development of seizures or infection, and the use of insulin or epinephrine.
HR≥95 at 3 months following HTx is associated with reduced exercise tolerance in stable HTx recipients. Medical HR reduction after HTx could improve exercise performance after HTx and merits further investigation.
The primary objective of this study was to describe the impact on bleeding rates of 2 different strategies for transitioning from a direct oral anticoagulant (DOAC) to a parenteral anticoagulant: a delayed, clinically driven strategy versus the standard per-package-insert strategy. This was a single-center descriptive cohort study conducted at a large academic medical center. Included patients were 18 years or older, admitted as an inpatient, and had received at least 1 dose of a DOAC prior to initiation of therapeutic parenteral anticoagulation. The primary end point was the incidence of major bleeds on the transition from a DOAC to a parenteral anticoagulant via a standard versus an intentionally delayed strategy. The secondary outcomes evaluated renal function, reason for delay, DOAC anti-factor Xa concentration, international normalized ratio values, blood product administration, and thrombotic complications. A total of 300 patients were included. The primary end point of bleeding was higher in the delayed group than the standard group, 25% and 12%, respectively (odds ratio, 0.39; P < .05). In both groups, patients who bled had a higher severity of illness, a greater incidence of acute kidney injury, and, when available, higher median DOAC anti-factor Xa concentrations. Despite a more conservative approach, patients in the delayed group experienced more bleeding, most likely attributable to a higher severity of illness, which highlights emerging challenges of inpatient anticoagulation management. Further prospective studies analyzing DOAC pharmacodynamics and pharmacokinetics in acutely ill patients are warranted.
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