RESUMO
Left ventricular assist devices are a treatment option for end-stage heart failure patients. Despite advancing technologies, bleeding and thromboembolic events strongly decrease the survival and the quality of life of these patients. Little is known about prognostic factors determining these adverse events in this group of patients. Therefore, we plan to investigate 90 consecutive left ventricular assist device (LVAD) patients and study in vitro fibrin clot properties (clot lysis time, clot permeability, fibrin ultrastructure using a scanning electron microscope) and the calibrated automated thrombogram in addition to the von Willebrand factor antigen, fibrinogen, D-dimer, prothrombin time/international normalized ratio (PT/INR), and activated partial thromboplastin time (APTT) to identify prognostic factors of adverse outcomes during the course of therapy. We plan to assess the hemostasis system at four different time points, i.e., before LVAD implantation, 3-4 months after LVAD implantation, 6-12 months after LVAD implantation, and at the end of the study (at 5 years or at the time of the adverse event). Adverse outcomes were defined as bleeding events (bleeding in general or in the following subtypes: severe bleeding, fatal bleeding, gastrointestinal bleeding, intracranial bleeding), thromboembolic events (stroke or transient ischemic attack, pump thrombosis, including thrombosis within the pump or its inflow or outflow conduits, arterial peripheral thromboembolism), and death.
RESUMO
Higher serum phosphorus has detrimental health effects. Even high-normal rage sP is associated with worse outcomes. The relationship of serum phosphorus with prognostic markers in heart failure remains unclear. We investigated the association of serum phosphorus with heart failure prognostic factors and risk of mortality related to serum phosphorus. In 1029 stable heart failure patients, we investigated the distribution of markers of more advanced heart failure stage across quintiles of serum phosphorus and estimated the relative risk of mortality in comparison to reference. Higher serum phosphorus levels sP were associated with markers of a worse outcome. The best survival was observed in low-normal serum levels. The unadjusted hazard ratio for mortality increased toward higher phosphorus quintiles but not to lower levels of sP. The correction for age, sex, BMI, percent weight loss, inflammation, kidney function, and LVEF did not modify the risk profile substantially. The adjustment for NYHA, natriuretic peptides, serum sodium, and treatment characteristics broke down the risk relationship completely. A higher serum phosphorus is associated with markers of a more risky profile of heart failure. Elevated serum levels of phosphorus sP does not provide independent prognostic information beyond the strongest markers of the severity of the syndrome. The potential involvement of higher serum phosphorus as a mediator in the pathophysiology of heart failure warrants further study.