Department of Hepatology, Institute of Liver & Biliary Sciences, New Delhi, India.
Department of Epidemiology and Clinical Research, Institute of Liver & Biliary Sciences, New Delhi, India.
Am J Gastroenterol. 2020 Oct;115(10):1624-1633. doi: 10.14309/ajg.0000000000000653.
Hepatic venous pressure gradient (HVPG) of ≥10 mm Hg predicts clinical decompensation (CD) in compensated cirrhosis. A proportion of cirrhotic patients at presentation have high HVPG (≥20 mm Hg) and are compensated. The natural history, spectrum of CD, and mortality in this group is largely unknown.
Consecutive compensated cirrhotic patients with HVPG ≥6 mm Hg (n = 741) were followed up for 3-6 months for the development of any CD. Patients were classified based on the baseline HVPG (6 to <12 mm Hg [low HVPG, Gr.A, n = 163], 12 to <20 mm Hg [intermediate HVPG, Gr.B, n = 437] and ≥20 mm Hg [high HVPG, Gr.C, n = 141]). We analyzed the predictors of first CD, HVPG response to carvedilol, and mortality in these groups.
CD developed in 217 (29.3%) patients during a mean follow-up of 1.6 ± 0.4 years, and those who developed CD had higher baseline HVPG (17.02 ± 4.79 vs 14.28 ± 4.86; P < 0.001). First CD was seen earlier (1.3 ± 0.7 years vs 1.5 ± 0.6 years and 1.6 ± 0.5 years, P = 0.02) and more frequently (44.7% vs 11% and 31.1%, P < 0.01) in high HVPG groups compared with low and intermediate HVPG groups, with higher mortality rates. Patients in the high HVPG group compared with the low HVPG group more often had NASH-cirrhosis (35.5% vs 19.6%; P 0.001), higher liver stiffness values (45.06 ± 20.46 vs 20.09 ± 5.47 kPa, P < 0.001), and lower platelet counts (113.37 ± 72.57 vs 151.7 ± 87.30/cmm, P < 0.001). Patients with HVPG ≥12 mm Hg received carvedilol, and a repeat HVPG performed in a proportion after 9.3 ± 2.4 months showed response (≥20% reduction in HVPG or <12 mm Hg) in 31.6% patients (Gr. B, 44.9% > Gr. C, 22.2%, P < 0.05). Baseline HVPG (HVPG ≥12 to <20 mm Hg [Hazard ratio: 2.73] and HVPG ≥20 mm Hg [Hazard ratio: 4.48], P < 0.001) independently predicted CD.
HVPG ≥20 mm Hg in patients with compensated cirrhosis independently predicts early and more frequent CD and poor outcomes. These patients should be labeled as "high-risk compensated cirrhosis," and early and effective interventions to reduce portal pressure should be initiated to improve long-term outcomes.
肝静脉压力梯度（HVPG）≥10mmHg 可预测代偿性肝硬化的临床失代偿（CD）。一部分初诊时 HVPG 较高（≥20mmHg）的肝硬化患者仍处于代偿期。目前对于这部分患者的自然病史、CD 谱和死亡率尚不清楚。
连续纳入 HVPG≥6mmHg 的代偿性肝硬化患者（n=741），随访 3-6 个月以观察任何 CD 的发生。根据基线 HVPG（6-<12mmHg[低 HVPG，Gr.A，n=163]、12-<20mmHg[中 HVPG，Gr.B，n=437]和≥20mmHg[高 HVPG，Gr.C，n=141]）对患者进行分组。我们分析了这些组中首次 CD、卡维地洛对 HVPG 的反应和死亡率的预测因素。
在平均 1.6±0.4 年的随访期间，217（29.3%）例患者发生 CD，且发生 CD 的患者基线 HVPG 更高（17.02±4.79 vs 14.28±4.86；P<0.001）。高 HVPG 组较低 HVPG 组和中 HVPG 组更早（1.3±0.7 年 vs 1.5±0.6 年和 1.6±0.5 年，P=0.02）和更频繁（44.7% vs 11%和 31.1%，P<0.01）出现首次 CD，且死亡率更高。与低 HVPG 组相比，高 HVPG 组患者更常患有 NASH 肝硬化（35.5% vs 19.6%；P<0.001）、更高的肝硬度值（45.06±20.46 vs 20.09±5.47kPa，P<0.001）和更低的血小板计数（113.37±72.57 vs 151.7±87.30/cmm，P<0.001）。HVPG≥12mmHg 的患者接受卡维地洛治疗，9.3±2.4 个月后进行重复 HVPG，结果显示（HVPG 降低≥20%或<12mmHg）在 31.6%的患者中得到应答（Gr.B：44.9%>Gr.C：22.2%，P<0.05）。基线 HVPG（HVPG≥12-<20mmHg[风险比：2.73]和 HVPG≥20mmHg[风险比：4.48]，P<0.001）独立预测 CD。
代偿性肝硬化患者的 HVPG≥20mmHg 独立预测早期和更频繁的 CD 及不良结局。这些患者应被标记为“高危代偿性肝硬化”，应尽早采取有效干预措施降低门静脉压力，以改善长期预后。
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