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- W1998271799 abstract "Rev Esp Cardiol. 2005;58(3):241-3 241 In recent years there has been a huge proliferation in the number of studies examining the diagnostic and prognostic value of the numerous and varied biochemical markers of chronic heart failure. These markers are the mediators or expression of the neurohumoral activation associated with this disease—a consequence of left ventricular dysfunction and its hemodynamic and clinical manifestations (reduction in cardiac output and hypotension, an increase in filling pressure, and pulmonary congestion).1 Neurohumoral activation in heart failure is maintained over the long term and leads to hemodynamic changes (increased cardiac activity, peripheral vasoconstriction, hydrosaline retention and increased volaemia) mediated by sympathetic hyperactivity, the activation of the renin-angiotensin-aldosterone system, and increased endothelial production of vasopressin and endothelin. This translates into increased plasma concentrations of different markers such as noradrenaline, angiotensin II, aldosterone, vasopressin, and endothelin, among others. In turn, this neurohumoral activation and its effects stimulate other responses with opposing effects (e.g., those involving vasodilators, diuretics, natriuretics and antiproliferative molecules), which results in increased plasma concentrations of the different natriuretic peptides, bradykinins, adrenomedullin and nitrous oxide etc.1 The result of all these regulations and contraregulations is that patients with heart failure show a great quantity of circulating neurohormones and other mediators in high concentrations. These substances ED I TO R I A L S" @default.
- W1998271799 created "2016-06-24" @default.
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- W1998271799 date "2005-03-01" @default.
- W1998271799 modified "2023-10-03" @default.
- W1998271799 title "Biochemical Markers in Heart Failure: Are They All the Same?" @default.
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- W1998271799 doi "https://doi.org/10.1016/s1885-5857(06)60484-2" @default.
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