Kamel Hooman, Hunter Madeleine, Moon Yeseon P, Yaghi Shadi, Cheung Ken, Di Tullio Marco R, Okin Peter M, Sacco Ralph L, Soliman Elsayed Z, Elkind Mitchell S V
From the Department of Neurology, Feil Family Brain and Mind Research Institute (H.K.) and Division of Cardiology (P.M.O.), Weill Cornell Medical College, New York; Department of Neurology (M.H., Y.P.M., S.Y., K.C., M.S.V.E.) and Division of Cardiology (M.R.D.T.), Columbia College of Physicians and Surgeons, New York; Department of Biostatistics, Columbia Mailman School of Public Health, New York (K.C.); Department of Neurology, Human Genetics, and Public Health Sciences, Miller School of Medicine, University of Miami, FL (R.L.S.); Departments of Epidemiology and Prevention (E.Z.S.) and Internal Medicine-Cardiology (E.Z.S.), Epidemiological Cardiology Research Center, Wake Forest School of Medicine, Winston-Salem, NC; and Department of Epidemiology, Mailman School of Public Health, Columbia University, New York (M.S.V.E.).
Stroke. 2015 Nov;46(11):3208-12. doi: 10.1161/STROKEAHA.115.009989. Epub 2015 Sep 22.
Electrocardiographic left atrial abnormality has been associated with stroke independently of atrial fibrillation (AF), suggesting that atrial thromboembolism may occur in the absence of AF. If true, we would expect an association with cryptogenic or cardioembolic stroke rather than noncardioembolic stroke.
We conducted a case-cohort analysis in the Northern Manhattan Study, a prospective cohort study of stroke risk factors. P-wave terminal force in lead V1 was manually measured from baseline ECGs of participants in sinus rhythm who subsequently had ischemic stroke (n=241) and a randomly selected subcohort without stroke (n=798). Weighted Cox proportional hazard models were used to examine the association between P-wave terminal force in lead V1 and stroke etiologic subtypes while adjusting for baseline demographic characteristics, history of AF, heart failure, diabetes mellitus, hypertension, tobacco use, and lipid levels.
Mean P-wave terminal force in lead V1 was 4452 (±3368) μVms among stroke cases and 3934 (±2541) μVms in the subcohort. P-wave terminal force in lead V1 was associated with ischemic stroke (adjusted hazard ratio per SD, 1.20; 95% confidence interval, 1.03-1.39) and the composite of cryptogenic or cardioembolic stroke (adjusted hazard ratio per SD, 1.31; 95% confidence interval, 1.08-1.58). There was no definite association with noncardioembolic stroke subtypes (adjusted hazard ratio per SD, 1.14; 95% confidence interval, 0.92-1.40). Results were similar after excluding participants with a history of AF at baseline or new AF during follow-up.
ECG-defined left atrial abnormality was associated with incident cryptogenic or cardioembolic stroke independently of the presence of AF, suggesting atrial thromboembolism may occur without recognized AF.
心电图左心房异常与卒中相关,且独立于房颤(AF),这表明在无房颤的情况下可能发生心房血栓栓塞。如果属实,我们预期其与隐源性或心源性栓塞性卒中相关,而非与非心源性栓塞性卒中相关。
我们在北曼哈顿研究中进行了一项病例队列分析,该研究是一项关于卒中危险因素的前瞻性队列研究。从窦性心律参与者的基线心电图中手动测量V1导联的P波终末电势,这些参与者随后发生了缺血性卒中(n = 241),并从无卒中的参与者中随机选取了一个亚队列(n = 798)。采用加权Cox比例风险模型来检验V1导联P波终末电势与卒中病因亚型之间的关联,同时对基线人口统计学特征、房颤病史、心力衰竭、糖尿病、高血压、吸烟情况和血脂水平进行校正。
卒中病例中V1导联的平均P波终末电势为4452(±3368)μVms,亚队列中的平均P波终末电势为3934(±2541)μVms。V1导联的P波终末电势与缺血性卒中相关(每标准差调整后的风险比为1.20;95%置信区间为1.03 - 1.39),与隐源性或心源性栓塞性卒中的复合终点相关(每标准差调整后的风险比为1.31;95%置信区间为1.08 - 1.58)。与非心源性栓塞性卒中亚型无明确关联(每标准差调整后的风险比为1.14;95%置信区间为0.92 - 1.40)。在排除基线时有房颤病史或随访期间新发房颤的参与者后,结果相似。
心电图定义的左心房异常与新发隐源性或心源性栓塞性卒中相关,且独立于房颤的存在,这表明在未识别出房颤的情况下可能发生心房血栓栓塞。