Why the study?
Does intensified heart failure medication reduce NT-proBNP levels in patients with advanced chronic heart failure and excessively high baseline NT-proBNP?
Observational (n=118)
Does intensified heart failure medication reduce NT-proBNP levels in patients with advanced chronic heart failure and excessively high baseline NT-proBNP?
In patients with advanced heart failure, excessively high NT-proBNP levels correlate with cardiac and renal abnormalities, but levels are halved following successful intensified medical therapy regardless of baseline.
Excessively high NT-proBNP may flag cardiac-renal dysfunction in advanced HF; leaves open its role for serial monitoring in prospective studies.
The clinical significance of excessively high serum NT-proBNP is poorly understood in chronic heart failure (HF). One-hundred eighteen patients with advanced chronic HF (NYHA functional class III or IV) were admitted; of these patients, 42.4% exhibited NT-proBNP levels > 10,000 pg/ml. The patients were divided into three groups as follows: ≥ 400 and < 10,000 pg/ml, group I (n = 68); ≥ 10,000 and < 20,000 pg/ml, group II (n = 28); and ≥ 20,000 pg/ml, group III (n = 22). The determinants of elevated NT-proBNP levels and responsiveness to HF medications were compared among these groups. A subgroup of HF patients with normal serum creatinine was analyzed separately. Overall, cardiac, renal and laboratory parameters (serum creatinine, potassium and uric acid, positively; and eGFR and hemoglobin, negatively) correlated with serum NT-proBNP levels. In patients with normal serum creatinine, left ventricular ejection fraction, serum potassium and hemoglobin correlated with serum NT-proBNP levels. In-hospital mortality was higher in patients with the highest NT-proBNP levels. After successful HF treatment, the patients in each group lost body weight and improved to NYHA class I or II, and NT-proBNP levels were halved, irrespective of their baseline levels. Excessively high NT-proBNP levels were related to cardiac, renal and laboratory abnormalities; therefore, the role and underlying mechanism of high NT-proBNP levels must be studied further. Excessively high NT-proBNP levels in HF patients correlated with cardiac, renal and laboratory parameters. After successful HF treatment, NT-proBNP levels were halved, irrespective of their baseline levels. The precise role and underlying mechanism of NT-proBNP warrant further study.
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Nakano et al. (2016) conducted an observational in advanced chronic heart failure (n=118). Excessively high serum NT-proBNP levels vs. Lower NT-proBNP levels was evaluated on Determinants of elevated NT-proBNP levels and responsiveness to HF medications.
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