National Heart, Lung, and Blood Institute's Framingham Heart Study, MA (B.M.K., C.A., M.S.D., M.G.L., R.S.V.).
Department of Cardiology, Deutsches Herzzentrum München, Munich, Germany (B.M.K.).
Circ Arrhythm Electrophysiol. 2019 Jul;12(7):e007150. doi: 10.1161/CIRCEP.119.007150. Epub 2019 Jun 20.
The etiopathogenesis of electrocardiographic bundle branch and atrioventricular blocks is not fully understood. We investigated familial clustering of cardiac conduction defects and pacemaker insertion in the FHS (Framingham Heart Study). Additionally, we assessed familial clustering of pacemaker insertion in the Danish general population.
In FHS, we used multivariable-adjusted logistic regression models to investigate the association of parental atrioventricular block (PR interval, ≥0.2 s), complete bundle branch block (QRS, ≥0.12 s), or pacemaker insertion with the occurrence of cardiac conduction abnormalities in their offspring. The Danish nationwide administrative registries were interrogated to assess the relations of parental pacemaker insertion with offspring pacemaker insertion.
In FHS (n=371 cases with first-degree atrioventricular block, complete bundle branch block, or pacemaker insertion, and 1471 age- and sex-matched controls), individuals with at least 1 affected parent with a conduction defect had a 1.65-fold odds (odds ratio, 95% CI, 1.32-2.07) for manifesting an atrioventricular block and a 1.62-fold odds (95% CI, 1.08-2.42) for developing a complete bundle branch block. If at least 1 parent had any electrocardiographic conduction defect or pacemaker insertion, the offspring had a 1.62-fold odds (95% CI, 1.31-2.00) for experiencing any of these conditions. In Denmark (n=2 824 199 individuals; 5397 incident pacemaker implantations), individuals with at least 1 first-degree relative with history of pacemaker insertion had a multivariable-adjusted 1.68-fold (incidence rate ratio, 95% CI, 1.49-1.89) risk of undergoing a pacemaker insertion. If the affected relative was ≤45 years of age, the incidence rate ratio was markedly increased to 51.0 (95% CI, 32.7-79.9).
Cardiac conduction blocks and risk for pacemaker insertion cluster within families. A family history of conduction system disturbance or pacemaker insertion should trigger increased awareness of a similar propensity in other family members, especially so when the conduction system disease occurs at a younger age.
心电图束支和房室传导阻滞的病因学尚不完全清楚。我们研究了 FHS(弗雷明汉心脏研究)中心脏传导缺陷和起搏器植入的家族聚集性。此外,我们评估了丹麦普通人群中起搏器植入的家族聚集性。
在 FHS 中,我们使用多变量调整的逻辑回归模型来研究父母房室传导阻滞(PR 间期,≥0.2 秒)、完全束支传导阻滞(QRS,≥0.12 秒)或起搏器植入与子女心脏传导异常发生的关联。丹麦全国性行政登记处被查询,以评估父母起搏器植入与子女起搏器植入的关系。
在 FHS(n=371 例一级房室传导阻滞、完全束支传导阻滞或起搏器植入病例和 1471 例年龄和性别匹配的对照者)中,至少有 1 位受影响的父母有传导缺陷的个体发生房室传导阻滞的几率为 1.65 倍(比值比,95%可信区间,1.32-2.07),完全束支传导阻滞的几率为 1.62 倍(95%可信区间,1.08-2.42)。如果至少有 1 位父母有任何心电图传导缺陷或起搏器植入,那么子女发生这些情况的几率为 1.62 倍(95%可信区间,1.31-2.00)。在丹麦(n=2824199 人;5397 例新植入起搏器)中,至少有 1 位一级亲属有起搏器植入史的个体接受起搏器植入的多变量调整比值比为 1.68(发病率比,95%可信区间,1.49-1.89)。如果受影响的亲属年龄≤45 岁,则发病率比显著增加至 51.0(95%可信区间,32.7-79.9)。
心脏传导阻滞和起搏器植入的风险在家族中聚集。家族性传导系统疾病或起搏器植入史应引起对其他家庭成员类似倾向的更高认识,尤其是当传导系统疾病发生在较年轻时。