P1581Early blood pressure reduction by intravenous vasodilators associates with acute kidney injury in patients with hypertensive acute decompensated heart failure

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Y Arao ◽  
A Sawamura ◽  
M Nakatochi ◽  
H Oishi ◽  
H Kato ◽  
...  

Abstract Background In patients with hypertensive acute decompensated heart failure (ADHF), intravenous vasodilators are commonly used. However, little is known about optimal use in blood pressure (BP) management to avoid acute kidney injury (AKI). Purpose To investigate the association between systolic BP (SBP) changes in first 6 h and incidence of AKI within 48 h in patients with hypertensive ADHF. Methods Post-hoc analysis was performed on a prospectively enrolled cohort. We investigated 245 patients with ADHF and SBP >140 mmHg on arrival (mean age, 76 years; 40% female). We defined “SBP-fall” as maximum percent reduction in SBP 6h after intravenous treatment. AKI was defined as serum creatinine (SCr) ≥0.3 mg/dL, or urine output <0.5 mL/kg/h at 48 h. Results Mean SBP, SBP-fall and SCr level at arrival were 180 mmHg, 29.4%, and 1.21 mg/dL, respectively. Sixty-six patients experienced AKI. There were no significant differences in age, NYHA functional class, SBP and SCr at admission between AKI and Non-AKI group. AKI group had the greater SBP-fall compared with Non-AKI (36.7%versus 27.2%, p≤0.0001). Logistic regression analyses revealed that SBP-fall had an independent predictor of AKI (Table). In addition, SBP-fall had positive association with the number of concomitant used intravenous vasodilators in first 6 h (Figure). Logistic regression analyses for AKI Univariate Multivariate AUC OR 95% CI P OR 95% CI P Ages, years, per 10 years 1.04 0.82–1.33 0.17 0.75 SBP at arrival, per 10 mmHg 1.01 0.93–1.11 0.77 SBP-fall, per 10% 1.49 1.22–1.81 <0.001 1.54 1.24–1.91 <0.001 HR, per 10 beat/min 1.12 1.00–1.25 0.049 1.07 0.95–1.21 0.28 COPD 2.95 1.06–8.21 0.04 3.06 0.99–9.43 0.054 SCr, per 1 mg/dL 1.40 0.83–2.37 0.21 Furosemide i.v. 1.12 0.42–2.95 0.82 Carperitide 3.22 1.69–6.13 0.0002 4.39 2.16–8.93 <0.001 NTG/ISDN i.v. 0.97 0.54–1.74 0.92 CCB i.v. 1.86 0.76–4.53 0.18 OR, odds ratio; CI, confidence interval; AUC, area under the curve; SBP, systolic blood pressure; COPD, chronic obstructive pulmonary disease; SCr, serum creatinine; i.v., intravenous; NTG, nitroglycerin; ISDN, isosorbide dinitrate; CCB, calcium channel blocker. SBP-fall odds ration for AKI Conclusion In the first 6h of management for hypertensive ADHF patients, aggressive SBP reduction by the combination use of vasodilator agents predicted the incidence of AKI.

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Pareek ◽  
A M D Kristensen ◽  
M Vaduganathan ◽  
T Biering-Sorensen ◽  
C Byrne ◽  
...  

Abstract Background The Systolic Blood Pressure Intervention Trial (SPRINT) found that intensive blood pressure (BP) lowering reduced the rates of cardiovascular events and mortality but increased the risk of certain adverse events, in patients with and without chronic kidney disease at baseline. However, it is unclear whether intensive BP management is well-tolerated and modifies risk uniformly across the entire spectrum of renal function. Purpose To assess the relationship between renal function, treatment response to intensive BP lowering, and cardiovascular (CV) outcomes. Methods SPRINT was a randomized, controlled trial in which 9,361 individuals ≥50 years of age, at high CV risk but without diabetes who had a systolic BP (SBP) 130–180 mmHg, were randomized to intensive (target SBP <120mmHg) or standard antihypertensive treatment (target SBP <140mmHg). The primary efficacy endpoint was the composite of acute coronary syndromes, stroke, acute decompensated heart failure, or death from CV causes. The primary safety endpoint was the composite of serious adverse events (SAE). Renal function was assessed using the estimated glomerular filtration rate (GFR), calculated with the Modification of Diet in Renal Disease equation. We first assessed whether a linear association was present between eGFR and clinical endpoints using restricted cubic splines. We then examined the prognostic implications of eGFR, unadjusted and adjusted for demographic, clinical, and laboratory variables. We further explored the effects of intensive BP lowering across the eGFR spectrum. Results Baseline eGFR was available for 9,324 (>99%) individuals. Mean eGFR was similar between the two groups (intensive group 71.8 ml/min/1.73m2 vs. standard group 71.7 ml/min/1.73m2; P=0.92). Median follow-up was 3.3 years (range 0–4.8), with 561 primary efficacy events (6%) and 3,522 SAE (38%) recorded during the study period. Baseline eGFR was non-linearly associated with the risk of the primary efficacy endpoint, death from CV causes, death from any cause, acute decompensated heart failure, SAE, electrolyte abnormality, and acute kidney injury (test for non-linearity, P<0.05; test for overall trend, P<0.001) and remained significantly associated with all tested endpoints upon multivariable adjustment (P<0.05). Baseline eGFR significantly modified the effects of intensive BP lowering on the primary efficacy endpoint (P=0.02), acute decompensated heart failure (P=0.01), SAE (P=0.01), and acute kidney injury (P=0.04). The Figure shows treatment effects (hazard ratios) across the spectrum of eGFR for these four endpoints. P-values are for the interaction between eGFR and treatment effect. Significant interactions were not detected for other endpoints. Figure 1 Conclusions In SPRINT, lower eGFR was associated with a greater risk of both CV events and SAE. Patients with higher eGFR appeared to derive more benefit from intensive BP lowering while the relationship with safety events was complex.


2013 ◽  
Vol 77 (3) ◽  
pp. 687-696 ◽  
Author(s):  
Akihiro Shirakabe ◽  
Noritake Hata ◽  
Nobuaki Kobayashi ◽  
Takuro Shinada ◽  
Kazunori Tomita ◽  
...  

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