Plasma brain natriuretic peptide levels indicate the distance from decompensated heart failure.

نویسندگان

  • Toshio Nishikimi
  • Hiroaki Matsuoka
چکیده

the Distance From Decompensated Heart Failure To the Editor: We read with great interest the recent article by Tang et al1 on plasma brain natriuretic peptide (BNP) levels in ambulatory patients with established chronic symptomatic systolic heart failure. They concluded that both symptomatic and asymptomatic patients present with a wide range of plasma BNP levels and that this heterogeneity may preclude the use of plasma BNP levels for deciding therapy and monitoring response. We agree with the analysis of their results; however, we disagree with their interpretation. BNP increases not only in response to pressure or volume loads, but also in response to neurohumoral factors and cytokines, independently of hemodynamic load. The clinical implications of increased plasma BNP levels differ depending on the underlying condition. For example, elevated BNP levels can mean increased filling pressure in dilated cardiomyopathy,2 the development of ventricular remodeling in myocardial infarction of recent onset,3 and left ventricular hypertrophy in hypertension.4 Plasma BNP levels are also influenced by many factors, including age, renal function, and arrhythmias. Because heart failure has diverse causes and patients have various clinical characteristics, we must analyze the meaning of increased BNP levels in individual patients. Nevertheless, measurement of plasma BNP remains important in heart failure, because decompensated heart failure does not occur in the absence of elevated plasma BNP levels. In patients with heart failure, symptoms are often very subjective and unrelated to cardiac status. Exercise capacity in heart failure is known not to correlate with cardiac function. In contrast, plasma BNP is secreted mainly from the ventricles and correlates with cardiac indices in heart disease; BNP markedly increases in decompensated heart failure.5 Thus, it seems reasonable to assume that the plasma BNP level in heart failure is inversely related to the distance from decompensated heart failure. For example, in patients with low BNP levels, the distance from decompensated heart failure is far; such patients are at low risk for the development of decompensated heart failure. In patients with high BNP levels, the distance is very close to decompensated heart failure, which easily develops even without symptoms. Intensive medical therapy should be considered in such patients. In patients with low BNP levels, including those with severe symptoms, intensive medical therapy would probably not be beneficial. Thus, medical therapy based solely on patients’ symptoms may be cost ineffective. Medical therapy based on the more objective indices such as plasma BNP levels is more likely to lead to a better outcome and more efficient use of valuable resources.

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عنوان ژورنال:
  • Circulation

دوره 109 25  شماره 

صفحات  -

تاریخ انتشار 2004