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• In those with cardiac amyloidosis and heart failure-related cardiogenic shock, there was significant augmentation of cardiac index after intra-aortic balloon pump (IABP) and significant decreases in left ventricular and right ventricular filling pressures. • Predictors of lack of response to IABP by cardiac index were a smaller baseline left ventricular end-diastolic diameter size per centimeter and higher pre-IABP systemic vascular resistance. • Most patients with Society for Cardiovascular Angiography and Interventions stage C heart failure-related cardiogenic shock were stabilized successfully and bridged to advanced therapies with IABP alone. In those with heart failure-related cardiogenic shock (HF-CS), an intra-aortic balloon pump (IABP) may improve hemodynamics and be useful as a bridge to advanced therapies. We explore whether those with cardiac amyloidosis and HF-CS might experience hemodynamic improvement and describe the hemodynamic response after IABP. We retrospectively identified consecutive patients with a diagnosis of cardiac amyloid, either light chain or transthyretin, who were admitted to our intensive care unit with HF-CS. Patients were excluded if an IABP was placed during heart transplant or for shock related to acute myocardial infarction. Invasive hemodynamics before and after IABP placement were assessed. We identified 23 patients with cardiac amyloid who had an IABP placed for HF-CS. The 1-year survival rate was 74% and most (65%) were bridged to heart transplant, although 1 patient was bridged to destination left ventricular assist device. After IABP, the mean arterial pressure, cardiac index, and cardiac power index were significantly increased, whereas mean right atrial pressure, mean pulmonary artery pressure, and pulmonary capillary wedge pressure were all significantly decreased. A smaller left ventricular end-diastolic diameter (per cm) was associated with a higher likelihood of a cardiac index of <2.2 L/min/m2 after IABP (odds ratio 0.16, 95% confidence interval 0.01–0.93, P =.04). IABP significantly improved cardiac index while decreasing right atrial pressure, mean pulmonary artery pressure, and pulmonary capillary wedge pressure in cardiac amyloidosis patients with HF-CS. [Display omitted] [ABSTRACT FROM AUTHOR]

Decreased medial cheek fat volume during aging leads to loss of a youthful facial shape. Increasing facial volume by methods such as adipose-derived stem cell (ASC) injection can produce facial rejuvenation. High-intensity focused ultrasound (HIFU) can increase adipogenesis in subcutaneous fat by modulating cilia on ASCs, which is accompanied by increased HSP70 and decreased NF-κB expression. Thus, we evaluated the effect of HIFU on increasing facial adipogenesis in swine (n = 2) via modulation of ASC cilia. Expression of CD166, an ASC marker, differed by subcutaneous adipose tissue location. CD166 expression in the zygomatic arch (ZA) was significantly higher than that in the subcutaneous adipose tissue in the mandible or lateral temporal areas. HIFU was applied only on the right side of the face, which was compared with the left side, where HIFU was not applied, as a control. HIFU produced a significant increase in HSP70 expression, decreased expression of NF-κB and a cilia disassembly factor (AURKA), and increased expression of a cilia increasing factor (ARL13B) and PPARG and CEBPA, which are the main regulators of adipogenesis. All of these changes were most prominent at the ZA. Facial adipose tissue thickness was also increased by HIFU. Adipose tissue volume, evaluated by magnetic resonance imaging, was increased by HIFU, most prominently in the ZA. In conclusion, HIFU increased ASC marker expression, accompanied by increased HSP70 and decreased NF-κB expression. Additionally, changes in cilia disassembly and length and expression of adipogenesis were observed. These results suggest that HIFU could be used to increase facial volume by modulating adipogenesis. [ABSTRACT FROM AUTHOR]

Cardiogenic shock (CS) is a heterogeneous clinical syndrome characterized by low cardiac output leading to end-organ hypoperfusion. Organ dysoxia ranging from transient organ injury to irreversible organ failure and death occurs across all CS etiologies but differing by incidence and type. Herein, we review the recognition and management of respiratory, renal and hepatic failure complicating CS. We also discuss unmet needs in the CS care pathway and future research priorities for generating evidence-based best practices for the management of extra-cardiac sequelae. The complexity of CS admitted to the contemporary cardiac intensive care unit demands a workforce skilled to care for these extra-cardiac critical illness complications with an appreciation for how cardio-systemic interactions influence critical illness outcomes in afflicted patients. [ABSTRACT FROM AUTHOR]

Background: Patients with left ventricular assist devices (LVADs) require systemic anticoagulation. The use of enoxaparin for bridging to warfarin remains understudied in this population. Methods: This single‐center retrospective study was performed to characterize enoxaparin use and associated thrombotic and bleeding outcomes in adult outpatients with LVADs from January 2018 to July 2021. Results: Fifty‐four enoxaparin bridging events were evaluated in 49 patients. Most patients with HeartMate II (HM2) and HeartWare (HVAD) devices received enoxaparin dosed 1 mg/kg every 12 h. In patients with HeartMate 3 (HM3) devices, an equal number of patients received 0.5 mg/kg every 12 h and 1 mg/kg every 12 h, with a smaller subset receiving intermediate doses. The median duration of bridging was 6 days (4–8 [IQR]). One major bleeding event required discontinuation of enoxaparin and hospitalization in a patient with an HM3 device. Thrombotic events occurred in four patients with two incidents of pump thrombosis requiring pump exchange and two ischemic strokes. All thrombotic events occurred in patients with HVAD or HM2 devices. Conclusion: These results suggest that enoxaparin bridging in LVAD patients was well‐tolerated with low bleeding and thrombotic rates, particularly with the HM3 device. [ABSTRACT FROM AUTHOR]