METHODS: Patients of DC (n = 30) with grade III ascites and serum sodium (Na) <130/systolic blood pressure (SBP) <90/type II HRS (group I) and ACLF patients (n = 30) with Na <130/SBP <90/AKI (group II) were included. HVPG was done at baseline and repeated 3 h after 10 mg midodrine. Primary outcome was HVPG response (reduction by >20% or to <12 mmHg).
RESULTS: In group I, midodrine significantly reduced HVPG (19.2 ± 4.6 to 17.8 ± 4.2, p = .02) and heart rate (HR) (86.3 ± 11.6 to 77.9 ± 13.1, p < .01) and increased mean arterial pressure (MAP) (74.1 ± 6.9 to 81.9 ± 6.6 mmHg, p < .01). In group II also, midodrine reduced HVPG (19.1 ± 4.1 to 17.0 ± 4.2) and HR (92.4 ± 13.7 to 84.6 ± 14.1) and increased MAP (85.4 ± 7.3 to 91.2 ± 7.6 mmHg), p < .01 for all. HVPG response was achieved in 3/30 (10%) in group I and 8/30 (26.7%) in group II. On logistic regression analysis, prerenal AKI (OR 11.04, 95% CI 1.83-66.18, p < .01) and increase in MAP (OR 1.22, 95% CI 1.03-1.43, p = .02) were independent predictors of response. Increase in MAP by 8.5 mmHg with midodrine had best cut-off with AUROC of .76 for response.
CONCLUSIONS: In decompensated cirrhosis and ACLF patients with contraindications to NSBB, midodrine is useful in decreasing HVPG. Dose of midodrine should be titrated to increase MAP atleast by 8.5 mmHg.
方法:纳入III级腹水和血清钠(Na)<130/收缩压(SBP)<90/II型HRS(I组)的DC患者(n=30)和Na<130/SBP<90/AKI(II组)的ACLF患者(n=30)。HVPG在基线时进行,并在10mg米多君后重复3小时。主要结果是HVPG反应(降低>20%或<12mmHg)。
结果:在第一组中,米多君显着降低HVPG(19.2±4.6至17.8±4.2,p=.02)和心率(HR)(86.3±11.6至77.9±13.1,p<.01),并升高平均动脉压(MAP)(74.1±6.9至81.9±6.6mmHg,p<.01)。在第二组中,米多君降低了HVPG(19.1±4.1至17.0±4.2)和HR(92.4±13.7至84.6±14.1),并增加了MAP(85.4±7.3至91.2±7.6mmHg),p<0.01为所有。HVPG反应在I组中达到3/30(10%),在II组中达到8/30(26.7%)。在逻辑回归分析中,肾前AKI(OR11.04,95%CI1.83-66.18,p<.01)和MAP升高(OR1.22,95%CI1.03-1.43,p=.02)是反应的独立预测因子。用米多君使MAP增加8.5mmHg具有最佳截止值,AUROC为0.76。
结论:在有NSBB禁忌症的失代偿期肝硬化和ACLF患者中,米多君可用于降低HVPG。米多君的剂量应滴定以使MAP至少增加8.5mmHg。