From the Division of Internal Medicine, Department of Medicine (T.K., S.A., P.K., S.B., D.C.), Cardiovascular Research Institute Basel (T.K., M.B., S.A., S.B., P.K., S.B., D.C.), and Cardiology Division, Department of Medicine (M.B.), University Hospital Basel, Switzerland; Population Health Research Institute, David Braley Cardiac, Vascular and Stroke Research Institute (S.T., M.B., G.P., D.C.) and Department of Pathology and Molecular Medicine, Michael G. DeGroote School of Medicine (S.T., G.P.), McMaster University, Hamilton, Ontario, Canada; Division of Cardiology, Hamilton General Hospital, Hamilton Health Sciences, Canada (M.B.); Labormedizinisches Zentrum Dr. Risch, Schaan, Principality of Liechtenstein (M.R., L.R.); Division of Laboratory Medicine, Kantonspital Graubünden, Chur, Switzerland (M.R.); Division of Clinical Biochemistry, Medical University, Innsbruck, Austria (L.R.); Private University, Triesen, FL (L.R.); and Center for Arrhythmia Prevention, Division of Preventive Medicine and Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (C.M.A.).
Circ Arrhythm Electrophysiol. 2017 Jan;10(1). doi: 10.1161/CIRCEP.116.004735.
Increasing height is an independent risk factor for atrial fibrillation, but the underlying mechanisms are unknown. We hypothesized that height-related differences in electric conduction could be potential mediators of this relationship.
We enrolled 2149 adults aged 25 to 41 years from the general population. Height was directly measured, and a resting 12-lead ECG obtained under standardized conditions. Multivariable linear regression models were used to evaluate the association between measured height and ECG parameters. Mendelian randomization analyses were then performed using 655 independent height-associated genetic variants previously identified in the GIANT consortium. Median age was 37 years, and median height was 1.71 m. Median PR interval, QRS duration, and QTc interval were 156, 88, and 402 ms, respectively. After multivariable adjustment, β-coefficients (95% confidence intervals) per 10 cm increase in measured height were 4.17 (2.65-5.69; P<0.0001) for PR interval and 2.06 (1.54-2.58; P<0.0001) for QRS duration. Height was not associated with QTc interval or the Sokolow-Lyon index. An increase of 10 cm in genetically determined height was associated with increases of 4.33 ms (0.76-7.96; P=0.02) in PR interval and 2.57 ms (1.33-3.83; P<0.0001) in QRS duration but was not related to QTc interval or Sokolow-Lyon index.
In this large population-based study, we found significant associations of measured and genetically determined height with PR interval and QRS duration. Our findings suggest that adult height is a marker of altered cardiac conduction and that these relationships may be causal.
身高增加是心房颤动的一个独立危险因素，但潜在机制尚不清楚。我们假设与身高相关的电传导差异可能是这种关系的潜在介导因素。
我们从一般人群中招募了 2149 名年龄在 25 岁至 41 岁的成年人。直接测量身高，并在标准化条件下获得静息 12 导联心电图。使用多变量线性回归模型评估测量身高与心电图参数之间的关系。然后使用先前在 GIANT 联盟中确定的 655 个独立身高相关遗传变异进行孟德尔随机分析。中位年龄为 37 岁，中位身高为 1.71 米。中位 PR 间期、QRS 持续时间和 QTc 间期分别为 156、88 和 402 毫秒。经过多变量调整后，测量身高每增加 10 厘米，PR 间期的 β 系数（95%置信区间）为 4.17（2.65-5.69；P<0.0001），QRS 持续时间为 2.06（1.54-2.58；P<0.0001）。身高与 QTc 间期或 Sokolow-Lyon 指数无关。遗传决定的身高增加 10 厘米与 PR 间期增加 4.33 毫秒（0.76-7.96；P=0.02）和 QRS 持续时间增加 2.57 毫秒（1.33-3.83；P<0.0001）相关，但与 QTc 间期或 Sokolow-Lyon 指数无关。
在这项大型基于人群的研究中，我们发现测量身高和遗传决定身高与 PR 间期和 QRS 持续时间之间存在显著关联。我们的研究结果表明，成人身高是心脏传导改变的标志物，并且这些关系可能是因果关系。
