RESUMO
AIMS: Renal dysfunction in patients with chronic heart failure predicts a poor prognosis. Tolvaptan has a diuretic effect in patients with chronic kidney disease and heart failure without adverse effects on renal function. We aimed to determine the effects of tolvaptan and predictors of worsening renal function in patients with heart failure. METHODS AND RESULTS: This post hoc analysis was a sub-analysis of a single-centre prospectively randomized trial on the early and short-term tolvaptan administration. We enrolled 201 participants with decompensated heart failure between January 2014 and March 2019 (early group, n = 104; age: 79.0 ± 12.8 years; late group, n = 97; age: 80.3 ± 10.8 years). Renal ultrasonography was performed before and after the administration of tolvaptan. Urine output and oral water intake significantly increased during tolvaptan administration. The difference between water intake and urine volume increased during tolvaptan administration. Changes in body weight, blood pressure, heart rate, and estimated glomerular filtration rate (eGFR) in both groups were comparable. The changes in peak-systolic velocity (PSV), acceleration time (AT) of the renal arteries, and resistance index were comparable. The changes in PSV and end-diastolic velocity (EDV) of the interlobar arteries increased following tolvaptan administration (Δmax PSV: 0.0 ± 14.8 cm/s before tolvaptan vs. 5.6 ± 15.7 cm/s after tolvaptan, P = 0.002; Δmean PSV: 0.4 ± 12.3 vs. 4.9 ± 12.7 cm/s, P = 0.002; Δmax EDV: -0.2 ± 3.5 vs. 1.4 ± 4.0 cm/s, P = 0.001; Δmean EDV: -0.0 ± 3.1 vs. 1.1 ± 3.4 cm/s, P = 0.003). The renal artery AT was negatively correlated with the eGFR (Δmax AT: beta = -0.2354, P = 0.044; Δmean AT: beta = -0.2477, P = 0.035). CONCLUSIONS: Tolvaptan increased the PSV and EDV of the interlobar artery, which may mean tolvaptan increased renal blood flow. The renal artery AT may be a surrogate for worsening renal function.
RESUMO
INTRODUCTION: Previous trials showed that tolvaptan improves acute heart failure (HF). However, the optimal timing for administering tolvaptan to achieve the best outcome remains unclear. Therefore, the current study investigated the relationship between the timing of tolvaptan treatment initiation and clinical outcomes in patients with acute decompensated HF. METHODS: We prospectively evaluated 201 patients with acute decompensated HF, randomly divided into 2 groups based on the timing of tolvaptan initiation. The early group was administered tolvaptan approximately 1 week after day 1 or 2 (n = 104), whereas the late group was administered the same drug 1 week after the early group (n = 97). RESULTS: All-cause mortality, cardiovascular death, and hospitalization during the follow-up period were comparable between both groups. The early group had shorter durations of oxygenation, carperitide infusion, and hospitalization than the late group (p = 0.013, 0.003, 0.006, respectively). The early group demonstrated a significantly faster decrease in pleural effusion than the late group (p = 0.001). The 2 groups had comparable maximum and minimum serum sodium and potassium levels and minimum estimated glomerular filtration rates during hospitalization. The early group spent significantly less money on all diuretics administered over the first 2 weeks and on tolvaptan and carperitide administered during the hospitalization period than the late group (p < 0.001). CONCLUSIONS: Early and short-term administration of tolvaptan was feasible, contributed to a more rapid improvement in patients with acute decompensated HF, and reduced health-care costs.
