MONITORING OF HEART RATE VARIABILITY DURING ALCOHOL WITHDRAWAL SYNDROME

该项目的目的是检查男性和女性戒酒者的心率变异性（HRV）的措施。我们的问题是，4至6周的戒酒是否会导致心脏信号复杂性测量正常化回到基线，如健康对照受试者所定义的那样，或者降低的信号复杂性是否在4至6周内保持稳定。我们感兴趣的结果变量是从EKG获得的心搏间期时间序列的赫斯特指数，这是一个很好的测量HRV的指标。赫斯特指数是时间序列自相关的非线性度量，在我们以前的工作中发现，在停止饮酒后48小时获得酒精戒断综合征的症状时，酒精中毒受试者的赫斯特指数增加。我们已经确定，在酗酒受试者中，信号复杂性的测量值在5周结束时不会恢复到基线，而是达到比对照组更高的渐近线。 我们还发现，在这一措施中存在性别和年龄差异。我们随着时间的推移对这种响应进行了建模，并找到了一个很好的适合S形响应结构的模型。其他研究者的工作发现，在本研究中发现的酒精受试者中，自相关测量值降低的受试者有更大的猝死风险，因此我们假设酒精中毒者心率的自主控制改变也可能是这一人群猝死的危险因素，正如几项大型流行病学研究所确定的那样。我们正在终止这个项目，因为我们正在转向非人类灵长类动物和啮齿动物模型，以回答这项工作产生的几个机械问题。

The purpose of the project was to examine measures of heart rate variability (HRV) in male and female alcoholics admitted for drinking cessation. Our question was whether abstention from alcohol use for a period of 4 to 6 weeks would result in normalization of the cardiac signal complexity measure back to baseline, as defined by healthy comparison subjects or if the decreased signal complexity remained stable for a period of 4 to 6 weeks. Our outcome variable of interest was the Hurst exponent of the interbeat interval time series obtained from the EKG, which is a good measure of HRV. The Hurst exponent is a non-linear measure of the autocorrelation of the time series, and in our previous work was found to be increased in alcoholic subjects when obtained 48 hours after cessation of alcohol use with no symptoms of alcohol withdrawal syndrome present. We have determined that in alcoholic subjects, measures of signal complexity do not return to baseline at the end of 5 weeks, but reach an asymptote which is higher than controls. We also found that there were gender and age differences in this measure. We modeled this response over time and found a good fit to a sigmoid response construct. Work by other investigators has found that subjects with decreased measures of autocorrelation as found in this study in alcoholic subjects have a greater risk of sudden death, therefore we hypothesize that altered autonomic contol of heart rate in alcoholics may also be a risk factor for sudden death in this population, as has been determined from several large epidemiologic studies. We are terminating this project as we are moving to non-human primates and rodent models to answer several mechanistic questions resulting from this work.