Background: Left ventricular assist device (LVAD) and inotrope therapy serve as a bridge to transplant (BTT) or as destination therapy in patients who are not heart transplant candidates. End-stage heart failure patients often have impaired renal function, and renal outcomes after LVAD therapy versus inotrope therapy have not been evaluated.
Methods: In this study, 169 patients with continuous flow LVAD therapy and 20 patients with continuous intravenous inotrope therapy were analyzed. The two groups were evaluated at baseline and at 3 and 6 months after LVAD or inotrope therapy was started. The incidence of acute kidney injury (AKI), need for renal replacement therapy (RRT), BTT rate, and mortality for 6 months following LVAD or inotrope therapy were studied. Results between the groups were compared using Mann-Whitney U test and Chi-square with continuity correction or Fischer's exact at the significance level of 0.05.
Results: Mean glomerular filtration rate (GFR) was not statistically different between the two groups, with P = 0.471, 0.429, and 0.847 at baseline, 3 and 6 months, respectively. The incidence of AKI, RRT, and BTT was not statistically different. Mortality was less in the inotrope group (P < 0.001).
Conclusion: Intravenous inotrope therapy in end-stage heart failure patients is non-inferior for mortality, incidence of AKI, need for RRT, and renal function for 6-month follow-up when compared to LVAD therapy. Further studies are needed to compare the effectiveness of inotropes versus LVAD implantation on renal function and outcomes over a longer time period.
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http://dx.doi.org/10.14740/jocmr3039w | DOI Listing |
Br J Hosp Med (Lond)
December 2024
Queen Elizabeth Hospital Birmingham, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.
Cardiogenic shock (CS) is associated with significant mortality. Advances in pharmacological therapies and mechanical circulatory support (MCS) devices have markedly improved the therapeutic approach to CS, though treatment efficacy and safety vary. The recent DanGer shock trial showed a significant reduction in 6-month mortality for CS patients due to acute myocardial infarction.
View Article and Find Full Text PDFJ Crit Care Med (Targu Mures)
October 2024
Bauchi State University Gadau, Bauchi, Nigeria.
Background: Acute kidney injury (AKI) is a disease that affects millions of people globally making it a major public health concern. It is defined as an abrupt decrease in kidney function that occurs within ours affecting both the structure and functionality of the kidneys.The outcome of AKI and the determinants in Nigeria are largely unknown.
View Article and Find Full Text PDFCirc Heart Fail
January 2025
The CardioVascular Center, Tufts Medical Center, Boston, MA (S.L.H., K.D.E., G.G., N.K.K.).
The integrative physiology of the left ventricle and systemic circulation is fundamental to our understanding of advanced heart failure and cardiogenic shock. In simplest terms, any increase in aortic stiffness increases the vascular afterload presented to the failing left ventricle. The net effect is increased myocardial oxygen demand and reduced coronary perfusion pressure, thereby further deteriorating contractile function.
View Article and Find Full Text PDFESC Heart Fail
January 2025
Division of Cardiology, Department of Medicine, Hospital of the University of Pennsylvania, Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
Aims: Right ventricular (RV) failure (RVF) after left ventricular assist device (LVAD) implant is an important cause of morbidity and mortality. Modern, data-driven approaches for defining and predicting RVF have been under-utilized.
Methods: Two hundred thirty-two patients were identified with a mean age of 55 years; 40 (17%) were women, 132 were (59%) Caucasian and 74 (32%) were Black.
Br J Pharmacol
January 2025
Department of Pharmacology, University of Oxford, Oxford, UK.
Background And Purpose: TMEM16A chloride channels constitute a depolarising mechanism in arterial smooth muscle cells (SMCs) and contractile cerebral pericytes. TMEM16A pharmacology is incompletely defined. We elucidated the mode of action and selectivity of a recently identified positive allosteric modulator of TMEM16A (PAM_16A) and of a range of TMEM16A inhibitors.
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