PDF(Pubmed)
Abstract：
Variability and prolongation of ventricular repolarization - measured by changes in QT interval and QT variability are independently associated with ventricular arrhythmias, sudden death, and mortality but such studies did not examine the role of sleep-disordered breathing. We aimed to determine whether sleep-disordered breathing moderated the association between measures of ventricular repolarization and overall mortality.
Eight hundred participants were randomly selected from each of the following four groups in the Sleep Heart Health Study: mild, moderate, severe or no sleep disordered breathing (n = 200 each). Overnight electrocardiograms were analyzed for QTc duration and QT variability (standard deviation of QT intervals, normalized QT interval variance and the short-term interval beat-to-beat QT variability). Cox proportional hazards penalized regression modeling was used to identify predictors of mortality.
Eight hundred of 5600 participants were randomly selected. The participants (68 ± 10 years; 56.8% male) were followed for an average of 8.2 years during which time 222 (28.4%) died. QTc, SDQT, and QTVN were associated with the presence of SDB (p = 0.002, p = 0.014, and p = 0.024, respectively). After adjusting for covariates, the presence of sleep-disordered breathing did not moderate the association between QTc length, QT variability and mortality (p > 0.05).
Sleep-disordered breathing was associated with some measures of ventricular repolarization. However, sleep-disordered breathing was not an effect modifier for the relationship between QTc and QT variability and mortality.
Eight hundred participants were randomly selected from each of the following four groups in the Sleep Heart Health Study: mild, moderate, severe or no sleep disordered breathing (n = 200 each). Overnight electrocardiograms were analyzed for QTc duration and QT variability (standard deviation of QT intervals, normalized QT interval variance and the short-term interval beat-to-beat QT variability). Cox proportional hazards penalized regression modeling was used to identify predictors of mortality.
Eight hundred of 5600 participants were randomly selected. The participants (68 ± 10 years; 56.8% male) were followed for an average of 8.2 years during which time 222 (28.4%) died. QTc, SDQT, and QTVN were associated with the presence of SDB (p = 0.002, p = 0.014, and p = 0.024, respectively). After adjusting for covariates, the presence of sleep-disordered breathing did not moderate the association between QTc length, QT variability and mortality (p > 0.05).
Sleep-disordered breathing was associated with some measures of ventricular repolarization. However, sleep-disordered breathing was not an effect modifier for the relationship between QTc and QT variability and mortality.
摘要：
通过QT间期和QT变异性的变化测量心室复极的变异性和延长与室性心律失常独立相关。猝死,和死亡率，但此类研究没有检查睡眠呼吸紊乱的作用。我们的目的是确定睡眠呼吸紊乱是否减轻了心室复极测量值与总死亡率之间的关联。
在睡眠心脏健康研究中，从以下四组中随机选择了八百名参与者：轻度，中度,严重或没有睡眠呼吸紊乱（每个n=200）。分析隔夜心电图的QTc持续时间和QT变异性（QT间期的标准偏差，归一化QT间期方差和短期间期搏动QT变异性)。Cox比例风险惩罚回归模型用于确定死亡率的预测因子。
随机选择了8600名参与者。参与者（68±10年；56.8％的男性）平均随访8.2年，在此期间222人（28.4％）死亡。QTc,SDQT,和QTVN与SDB的存在相关（分别为p=0.002，p=0.014和p=0.024）。在调整协变量后，睡眠呼吸紊乱的存在并没有缓和QTc长度之间的关联，QT变异性和死亡率(p>0.05)。
睡眠呼吸紊乱与心室复极的一些测量结果相关。然而,睡眠呼吸紊乱不是QTc和QT变异性与死亡率之间关系的效应调节剂.
在睡眠心脏健康研究中，从以下四组中随机选择了八百名参与者：轻度，中度,严重或没有睡眠呼吸紊乱（每个n=200）。分析隔夜心电图的QTc持续时间和QT变异性（QT间期的标准偏差，归一化QT间期方差和短期间期搏动QT变异性)。Cox比例风险惩罚回归模型用于确定死亡率的预测因子。
随机选择了8600名参与者。参与者（68±10年；56.8％的男性）平均随访8.2年，在此期间222人（28.4％）死亡。QTc,SDQT,和QTVN与SDB的存在相关（分别为p=0.002，p=0.014和p=0.024）。在调整协变量后，睡眠呼吸紊乱的存在并没有缓和QTc长度之间的关联，QT变异性和死亡率(p>0.05)。
睡眠呼吸紊乱与心室复极的一些测量结果相关。然而,睡眠呼吸紊乱不是QTc和QT变异性与死亡率之间关系的效应调节剂.
