Ter Maaten Jozine M, Damman Kevin, Hanberg Jennifer S, Givertz Michael M, Metra Marco, O'Connor Christopher M, Teerlink John R, Ponikowski Piotr, Cotter Gad, Davison Beth, Cleland John G, Bloomfield Daniel M, Hillege Hans L, van Veldhuisen Dirk J, Voors Adriaan A, Testani Jeffrey M
From the University Medical Center, University of Groningen, The Netherlands (J.M.t.M., K.D., H.L.H., D.J.v.V., A.A.V.); Program of Applied Translational Research, Yale University School of Medicine, New Haven, CT (J.M.t.M., J.S.H., J.M.T.); Brigham and Women's Hospital, Boston, MA (M.M.G.); University of Brescia, Italy (M.M.); Inova Heart and Vascular Institute, Falls Church, VA (C.M.O.); University of California at San Francisco and San Francisco Veterans Affairs Medical Center (J.R.T.); Medical University, Clinical Military Hospital, Wroclaw, Poland (P.P.); Momentum Research, Durham, NC (G.C., B.D.); University of Hull, Kingston upon Hull, United Kingdom (J.G.C.); Merck Research Laboratories, Rahway, NJ (D.M.B.); Department of Internal Medicine, Yale University School of Medicine, New Haven, CT (J.M.T.).
Circ Heart Fail. 2016 Aug;9(8). doi: 10.1161/CIRCHEARTFAILURE.116.003109.
Chloride plays a role in renal salt sensing, neurohormonal activation, and regulation of diuretic targets, and hypochloremia predicts mortality in acute heart failure (AHF). AHF therapies, such as diuretics, alter chloride homeostasis. We studied the association between (changes in) chloride levels and diuretic responsiveness, decongestion, and mortality in patients with AHF.
Patients hospitalized for AHF in the PROTECT trial (n=2033) with serum chloride levels within 24 hours of admission and 14 days later were studied (n=1960). Hypochloremia was defined as serum chloride <96 mEq/L. Mean baseline chloride was 100.8±5.0 mEq/L. Low baseline chloride was associated with high bicarbonate, poor diuretic response, less hemoconcentration, and worsening heart failure (all P<0.01). Newly developed hypochloremia at day 14 was common and associated with a decline in renal function and an increase in blood urea nitrogen (P<0.01). In multivariable analyses, chloride measured at day 14, but not baseline chloride, was strongly and independently associated with mortality through 180 days (hazard ratio per unit decrease: 1.07 [1.03-1.10]; P<0.001). In comparison, sodium was not significantly associated with mortality after multivariable adjustment at any time point. Hypochloremia at baseline that resolved was not associated with mortality (P=0.55), but new or persistent hypochloremia at day 14 was associated with increased mortality (hazard ratio: 3.11 [2.17-4.46]; P<0.001).
Low serum chloride at AHF hospital admission was strongly associated with impaired decongestion. New or persistent hypochloremia 14 days later was independently associated with reduced survival, whereas hypochloremia that resolved by day 14 was not.
URL: http://www.clinicaltrials.gov. Unique identifier: NCT00354458.
氯离子在肾脏盐类感知、神经激素激活及利尿剂靶点调节中发挥作用，低氯血症可预测急性心力衰竭（AHF）患者的死亡率。AHF的治疗方法，如利尿剂，会改变氯离子的内环境稳定。我们研究了AHF患者氯离子水平（变化）与利尿剂反应性、充血缓解及死亡率之间的关联。
对PROTECT试验中因AHF住院的患者（n = 2033）进行研究，这些患者在入院24小时内及14天后测定血清氯离子水平（n = 1960）。低氯血症定义为血清氯离子<96 mEq/L。平均基线氯离子水平为100.8±5.0 mEq/L。低基线氯离子水平与高碳酸氢盐、利尿剂反应不佳、血液浓缩程度较低及心力衰竭加重相关（均P<0.01）。第14天新出现的低氯血症很常见，且与肾功能下降及血尿素氮升高相关（P<0.01）。在多变量分析中，第14天测定的氯离子水平而非基线氯离子水平，与180天内的死亡率密切且独立相关（每单位降低的风险比：1.07 [1.03 - 1.10]；P<0.001）。相比之下，在任何时间点进行多变量调整后，钠离子与死亡率均无显著关联。基线时已缓解的低氯血症与死亡率无关（P = 0.55），但第i4天新出现或持续存在的低氯血症与死亡率增加相关（风险比：3.11 [2.17 - 4.46]；P<0.001）。
AHF住院时血清氯离子水平低与充血缓解受损密切相关。14天后新出现或持续存在的低氯血症与生存率降低独立相关，而到第14天已缓解的低氯血症则不然。
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