Bunch T Jared, Packer Douglas L, Jahangir Arshad, Locke G Richard, Talley Nicholas J, Gersh Bernard J, Roy Ranjini R, Hodge David O, Asirvatham Samuel J
Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Am J Cardiol. 2008 Nov 1;102(9):1207-11. doi: 10.1016/j.amjcard.2008.06.048. Epub 2008 Aug 27.
The mechanisms underlying the triggers and maintenance of atrial fibrillation (AF) are not fully understood. One potential unproved mechanism is that gastroesophageal reflux disease (GERD), in which acid reflux induces local and systemic inflammation, may increase triggered activity in the myocardium and pulmonary veins and increase AF risk. A self-report questionnaire was mailed to a random sample of 5,288 residents of Olmsted County, Minnesota, aged 25 to 74 years to assess the presence and frequency of GERD from 1988 to 1994. The long-term risk for AF over a period of 11.4 +/- 5.0 years was determined through review of clinical evaluations and the electrocardiographic database in those without previous AF. The average age was 53 +/- 17 years, and 2,571 subjects (49%) were man. Of these patients, 741 developed AF (cumulative probability of AF at 18 years 20%, 95% confidence interval [CI] 17% to 22%). Age (hazard ratio [HR] 1.09, 95% CI 1.08 to 1.10, p <0.001), male gender (HR 1.81, 95% CI 1.53 to 2.14, p <0.001), hypertension (HR 1.36, 95% CI 1.14 to 1.61, p = 0.0006), and heart failure (HR 1.74, 95% CI 1.16 to 2.60, p = 0.007) were independently associated with the risk of AF. The presence of any GERD was not associated with risk for AF (HR 0.81, 95% CI 0.68 to 0.96, p = 0.014) after adjustment for other risk factors. The frequency of GERD did not significantly affect the risk for AF, although patients with more frequent GERD had a slightly higher AF risk. Esophagitis increased the risk for AF (HR 1.94, 95% CI 1.35 to 2.78, p <0.001), but the association did not persist when accounting for other risk factors (p = 0.72). In conclusion, in this large population-based study of patients surveyed for GERD, no association was found with the presence or frequency of symptoms and AF. Patients with esophagitis were more likely to develop AF, although this association requires further study.
心房颤动（AF）触发和维持的潜在机制尚未完全明确。一种尚未证实的潜在机制是，胃食管反流病（GERD）中酸反流会引发局部和全身炎症，这可能会增加心肌和肺静脉的触发活动并增加房颤风险。向明尼苏达州奥尔姆斯特德县年龄在25至74岁的5288名居民随机抽取的样本邮寄了一份自我报告问卷，以评估1988年至1994年期间GERD的存在情况和发生频率。通过回顾此前无房颤患者的临床评估和心电图数据库，确定了11.4±5.0年期间房颤的长期风险。平均年龄为53±17岁，2571名受试者（49%）为男性。在这些患者中，741人发生了房颤（18年时房颤的累积概率为20%，95%置信区间[CI]为17%至22%）。年龄（风险比[HR]1.09，95%CI 1.08至1.10，p<0.001）、男性（HR 1.81，95%CI 1.53至2.14，p<0.001）、高血压（HR 1.36，95%CI 1.14至1.61，p = 0.0006）和心力衰竭（HR 1.74，95%CI 1.16至2.60，p = 0.007）与房颤风险独立相关。在对其他风险因素进行调整后，任何GERD的存在与房颤风险均无关联（HR 0.81，95%CI 0.68至0.96，p = 0.014）。GERD的发生频率对房颤风险没有显著影响，尽管GERD发作更频繁的患者房颤风险略高。食管炎会增加房颤风险（HR 1.94，95%CI 1.35至2.78，p<0.001），但在考虑其他风险因素后这种关联不再存在（p = 0.72）。总之，在这项针对GERD进行调查的大型人群研究中，未发现症状的存在或频率与房颤之间存在关联。食管炎患者更易发生房颤，尽管这种关联需要进一步研究。
