Natriuretic peptide-guided therapy
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ecchis1 · C. Esposito2 · S. Cantatrione1 1 Presidio Sanitario Intermedio “Elena d’ Aosta”, Cardiology Unit, Napoli, Napoli 2 Institute of Hygiene and Preventive Medicine, Second University of Napoli, Napoli
Natriuretic peptide-guided therapy Further research required for still-unresolved issues
Many studies have been undertaken to demonstrate the ability of markers of endoventricular myocardial strain, known as B-type natriuretic peptides (NPs), to serve as a guide in detecting systemic and pulmonary congestion, even when it is not clinically evident, and to modulate pharmacological therapy accordingly [1, 2, 3, 4, 5, 6, 7, 8, 9]. It is known that in the setting of volume expansion or pressure overload, the resulting wall stress promotes synthesis of pre-proB-type natriuretic peptide (preproBNP) in the ventricular myocardium [10]. Subsequently, the peptide is cleaved first to proBNP, then to the biologically active B-type natriuretic peptide (BNP) and the inactive fragment, amino-terminal (NT)-proBNP [10]. It is also known that the release of BNP induces improved myocardial relaxation and plays an important regulatory role in response to acute increases in ventricular volume by antagonizing the vasoconstriction, sodium retention, and antidiuretic effects of the activated rennin–angiotensin–aldosterone system (RAAS) [11]. Nevertheless, it was found that the favorable vasodilatory and natriuretic properties of NP are not sufficient to counteract the noxious effect of RAAS hyperactivation in a significant percentage of cases [12]. Thus, the signaling function regarding hemodynamic imbalance, as exerted by NPs when massively secreted, is more important than their possible role in the effective counterbal-
ance against the vasoconstrictive and sodium-retentive systems [13]. Therefore, the high circulating levels of these molecules after their massive release in the blood are reliable markers of a pathological increase in ventricular filling pressures, that is, of hemodynamic congestion—often, but not necessarily, associated with the presence of signs and symptoms of “clinical” congestion. Thus, high circulating levels of NPs should prompt physicians to adopt measures to unload systemic and pulmonary circulations, such as increasing the dosing of vasodilator drugs and diuretics [14, 15]. On the contrary, the evidence of decreasing NP levels within the normal range should be considered a favorable prognostic sign and/or lead to cautious weaning of the i.v. administered diuretics and the high doses of vasodilator drugs (trinitrine, nitroprusside etc.) that are initially employed to cope with an episode of acutely decompensated heart failure (ADHF) [16]. There are still major unresolved issues regarding the use of these biochemical markers as a guide for the treatment of heart failure. Indeed, there is no agreement on the cut-off beyond which we should consider the intensification of therapy as an opportune or mandatory option [6, 7, 16]. A further obstacle to using these biomarkers for drug-dosing adjustment derives from
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