Toward The Future Use Of Natriuretic Peptides For Targeting Therapy

Perhaps the best approach toward keeping a patient with heart failure out of the hospital is to avoid recurrent volume overload manifest by increases above the level of BNP at discharge. Early after discharge, a rise in the level of BNP is often associated with volume overload and may prompt an increase in the dosing of diuretics. As is the practice at several institutions (61), when a patient comes to an urgent-care center with recurrent symptoms, BNP is measured. Ifthere is no difference from baseline values, decompensation is unlikely. Because BNP is not a stand-alone test, it should be used in conjunction with other features of the examination, clinical history, and testing. In my experience, clinical features of decompensation along with an increase of 50% or more from baseline are often associated with worsening of heart failure.

Fig. 15. Survival stratified by quartile of change in BNP with therapy in Val-HeFT Trial. (From ref. 67, with permission.)

BNP may also be usefUl for guiding the selection oftherapy. The Australia-New Zealand Heart Failure Group analyzed plasma neurohormones for prediction of adverse outcomes and response to treatment in 415 patients with LV dysfunction randomly assigned to receive carvedilol or placebo (62) and found that BNP was the best predictor of a benefit from carvedilol. In a randomized trial of 69 patients allocated to NT-proBNP-guided treatment vs symptom-guided therapy (63), patients receiving NT-proBNP-guided therapy had greater use of heart failure medications; lower levels of NT-proBNP; and a reduced incidence of cardiovascular death, readmission, and new episodes of decompensated heart failure. This study has prompted a number of larger studies including the multicenter Rapid Assessment of Bedside BNP In Treatment of Heart Failure trial.

It also appears that treatment with angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blocker agents, spironolactone, and perhaps ^-blockers reduces levels of BNP. In the Valsartan Heart Failure Trial (Val-HeFT), changes in BNP over time induced by pharmacological therapy were shown to correlate with subsequent morbidity and mortality (Fig. 15) (64). Patients with the greatest percentage decrease in BNP and norepinephrine from baseline had the lowest morbidity and mortality, whereas patients with the greatest percentage increase in BNP and norepinephrine were at greatest risk.

It is my practice to aim for BNP levels <200-300 pg/mL with standard therapy of ACE inhibitors and ^-blockers and diuretics. Patients with BNP levels between 200 and 500 pg/ mL are often NYHA functional class II/III and may require increased dosing of diuretics, especially spironolactone. Patients who despite standard medical treatment have advanced symptoms along with high BNP levels (400-600 pg/mL) may be candidates for continuous and palliative outpatient infusions of inotropes or vasodilators. In addition, biventricular pacing (if QRS is >120-130 ms) cardiac transplantation or LV assist device might be considered. In the future, stem cell or gene therapy may have a role in the treatment of these patients.

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