1,720,975 research outputs found
Adaptive licensing - A way forward in the approval process of new therapeutic agents in Europe
No full textA selective angiotensin-II type 2 receptor agonist reduced cancer cachexia-induced cardiomyopathy
No full textMineralocorticoid receptor antagonists in heart failure with preserved ejection fraction (HFpEF)
No full textEfficacy of Left Ventricular Augmentation With Algisyl-LVR in the Treatment of Advanced Heart Failure Patients With Ischemic and Non-Ischemic Cardiomyopathy: Results of the AUGMENT-HF Multicenter Randomized Controlled Trial
No full textFollow-Up Results from AUGMENT-HF: A Multicenter Randomized Controlled Clinical Trial of the Efficacy of Left Ventricular Augmentation with Algisyl-LVR in the Treatment of Heart Failure
No full textFollow-Up Results from AUGMENT-HF: A Multicenter Randomized Controlled Clinical Trial of the Efficacy of Left Ventricular Augmentation with Algisyl-LVR in the Treatment of Heart Failure
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Robustness of outcomes in trials evaluating sodium–glucose co‐transporter 2 inhibitors for heart failure
Full text linkAims: Recent trials have evaluated sodium–glucose co‐transporter 2 inhibitors in patients with heart failure (HF). We sought to assess the robustness of findings from these trials using the fragility index (FI).
Methods and results: Fragility index is defined as the minimum number of patients that must be moved from the ‘non‐event’ to the ‘event’ group to turn a statistically significant result to non‐significant. In addition to FI, fragility quotient [(FQ); FI divided by the sample size] was calculated to assess the proportion of events that must be moved to change the significance. For statistically non‐significant outcomes, reverse fragility index (RFI) and reverse fragility quotient (RFQ) were calculated. Robustness of findings after pooling data from all three trials was also assessed. A robust reduction in first HF hospitalization or cardiovascular mortality was seen with dapagliflozin (FI = 62 and FQ = 0.013), empagliflozin (FI = 50 and FQ = 0.013), and sotagliflozin (FI = 60 and FQ = 0.049). Dapagliflozin nominally improved all‐cause and cardiovascular mortality, with modest FI (n = 8 and 5) and FQ (0.002 and 0.001). Empagliflozin and sotagliflozin did not demonstrate statistically significant reductions in all‐cause mortality, with modest RFI (empagliflozin: RFI = 26 and RFQ = 0.007; sotagliflozin: RFI = 6 and RFQ = 0.005). A similar trend was seen with cardiovascular mortality (empagliflozin: RFI = 24 and RFQ = 0.006; sotagliflozin: RFI = 7 and RFQ = 0.006). Upon meta‐analysis, the result for first HF hospitalization or cardiovascular mortality was robust (FI = 95 and FQ = 0.010). The reductions in all‐cause (FI = 12 and FQ = 0.001) and cardiovascular mortality (FI = 9 and FQ = 0.001), while statistically significant, were fragile.
Conclusion: Improvement in the composite outcome of first HF hospitalization or cardiovascular death was highly concordant and robust across sodium–glucose co‐transporter 2 inhibitor trials. In contrast, secondary endpoints of all‐cause and cardiovascular mortality were statistically fragile, underscoring the need to power trials for mortality to fully understand the benefit of therapies on fatal events
Functional outcomes with Carillon device over 1 year in patients with functional mitral regurgitation of Grades 2+ to 4+: results from the REDUCE‐FMR trial
No full textSarcopenia, cachexia, and muscle performance in heart failure: Review update 2016
No full textCachexia in the context of heart failure (HF) has been termed cardiac cachexia, and represents a progressive in-voluntary weight loss. Cachexia is mainly the result of an imbalance in the homeostasis of muscle protein synthesis and degradation due to a lower activity of protein synthesis pathways and an over-activation of protein degradation. In addition, muscle wasting leads to of impaired functional capacity, even after adjusting for clinical relevant variables in patients with HF. However, there is no sufficient therapeutic strategy in muscle wasting in HF patients and very few studies in animal models. Exercise training represents a promising intervention that can prevent or even reverse the process of muscle wasting, and worsening the muscle function and performance in HF with muscle wasting and cachexia. The pathological mechanisms and effective therapeutic approach of cardiac cachexia remain uncertain, because of the difficulty to establish animal cardiac cachexia models, thus novel animal models are warranted. Furthermore, the use of improved animal models will lead to a better understanding of the pathways that modulate muscle wasting and therapeutics of muscle wasting of cardiac cachexia. (C) 2017 Elsevier B.V. All rights reserved
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