Centro di Alcologia at the Dipartimento di Medicina Interna e Scienze Biomediche, University of Parma Medical School, Parma, Italy.
Alcohol Clin Exp Res. 2012 Feb;36(2):242-50. doi: 10.1111/j.1530-0277.2011.01636.x. Epub 2011 Oct 20.
Little is known about brachial artery flow-mediated vasodilatation (FMD) in active and medium-term withdrawing heavy alcoholics (HA).
FMD and some parameters of cardiovascular (CV) risk were measured in 29 HA (average alcohol intake 135, range 86 to 215 g per day) at baseline and after a 9 ± 7 months withdrawal and in 35 teetotalers.
HA showed baseline impaired maximal % FMD (8.5 ± 5.4 SD vs. 14.9 ± 7.4, <0.001 vs. teetotalers), higher systolic (SBP) and diastolic (DBP) blood pressure (+24 mm Hg, <0.001; +15 mm Hg, <0.01), uric acid (5.3 ± 1.1 vs. 4.4 ± 0.8 mg/dl, <0.05), high-sensitivity C-reactive protein (hs-CRP; 2.7 ± 2.0 vs. 1.0 ± 0.9 mg/l, <0.02), endothelin-1 (ET-1, 0.88 ± 0.36 vs. 0.37 ± 0.10 pg/ml,<0.001), asymmetric dimethylarginine (ADMA, 0.50 ± 0.21 vs. 0.41 ± 0.12 μmol/l, p < 0.001), homeostasis model assessment of insulin resistance (HOMA-IR) (2.3 ± 1.1 vs. 1.2 ± 0.4, <0.001), and urinary 8-isoprostane (U8-iso-PGF2α) (237.2 ± 172.4 vs. 168.5 ± 96.6 pg/mg creatinine, <0.05). After withdrawal, SBP fell by 15 mm Hg, DBP by 11 mm Hg (p < 0.001), and hs-CRP by 0.94 mg/l (p < 0.02), all remaining still higher than teetotalers (<0.05, 0.01, 0.05 respectively). ET-1, HOMA-IR, and U8-iso-PGF2α were unchanged (p = NS vs. baseline, <0.05 to 0.001 vs. teetotalers). Maximal % FMD rose (to 10.6 ± 6.2, p < 0.04), but it still remained impaired (<0.04 vs. teetotalers). ADMA increased further to 0.64 ± 0.15 μmol/l (<0.05 vs. baseline, <0.02 vs. teetotalers).
HA show marked endothelial dysfunction (ED) and high BP, impaired insulin sensitivity, inflammation, increased oxidative stress, and elevated ET-1 and ADMA, which are unaffected or only partially reversed by a medium-term alcohol withdrawal. ED and related abnormalities persist in detoxified alcoholics, thus contributing to a greater CV morbidity and mortality.
关于活跃和中期戒酒的重度酗酒者（HA）的肱动脉血流介导的舒张功能（FMD）知之甚少。
在基线和 9±7 个月戒酒后，测量了 29 名 HA（平均饮酒量为 135，范围为 86 至 215 克/天）和 35 名滴酒不沾者的 FMD 和一些心血管（CV）风险参数。
HA 显示基线时最大 %FMD 受损（8.5±5.4 SD 与 14.9±7.4，<0.001 与滴酒不沾者），收缩压（SBP）和舒张压（DBP）更高（+24 mmHg，<0.001；+15 mmHg，<0.01），尿酸（5.3±1.1 与 4.4±0.8 mg/dl，<0.05），高敏 C 反应蛋白（hs-CRP；2.7±2.0 与 1.0±0.9 mg/l，<0.02），内皮素-1（ET-1，0.88±0.36 与 0.37±0.10 pg/ml，<0.001），不对称二甲基精氨酸（ADMA，0.50±0.21 与 0.41±0.12 μmol/l，p<0.001），胰岛素抵抗的稳态模型评估（HOMA-IR）（2.3±1.1 与 1.2±0.4，<0.001）和尿 8-异前列腺素 F2α（U8-iso-PGF2α）（237.2±172.4 与 168.5±96.6 pg/mg 肌酐，<0.05）。戒酒后，SBP 下降 15 mmHg，DBP 下降 11 mmHg（p<0.001），hs-CRP 下降 0.94 mg/l（p<0.02），所有这些仍高于滴酒不沾者（<0.05、0.01、0.05）。ET-1、HOMA-IR 和 U8-iso-PGF2α 无变化（p=NS 与基线，<0.05 至 0.001 与滴酒不沾者）。最大 %FMD 升高（至 10.6±6.2，p<0.04），但仍受损（<0.04 与滴酒不沾者）。ADMA 进一步增加至 0.64±0.15 μmol/l（<0.05 与基线，<0.02 与滴酒不沾者）。
HA 表现出明显的内皮功能障碍（ED）和高血压、胰岛素敏感性受损、炎症、氧化应激增加以及 ET-1 和 ADMA 升高，这些在中期戒酒期间不受影响或仅部分逆转。在戒酒后的酗酒者中，ED 和相关异常仍然存在，从而导致更大的心血管发病率和死亡率。
