Electrocardiographic left atrial abnormalities and risk of incident stroke in hypertensive patients with electrocardiographic left ventricular hypertrophy
Electrocardiographic left atrial abnormalities and risk of incident stroke in hypertensive patients with electrocardiographic left ventricular hypertrophy
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DOI：
10.1097/hjh.0000000000000989
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发表时间：
2016-09-01
影响因子：
4.9
通讯作者：
Devereux, Richard B.
中科院分区：
文献类型：
--
作者：
Okin, Peter M.;Kamel, Hooman;Devereux, Richard B.
背景资料：基于人群的研究中的最新发现表明，导联V1（PTFV 1）中的异常P波终末力（左心房异常（如纤维化、扩张和充盈压升高）的标志物）与缺血性卒中事件相关，即使在没有房颤的情况下也是如此。然而，PTFV 1是否预测高血压患者在血压降低过程中发生卒中还没有被检查。方法：检查与异常PTFV相关的卒中发生风险。7778例ECG左心室肥厚、无房颤病史、基线ECG为窦性心律且随访期间无房颤事件的高血压患者的基线ECG，结果集中于55 - 60岁的患者亚组，（n = 1879），因为在考克斯分析中PTFV 1和年龄之间存在显著的相互作用。异常PTFV 1定义为存在一个负的终端P波在导联V1与振幅x持续时间> 4000 V ms。结果：在平均随访4.8do0.9年，364例患者（4.7%）的总研究人群和45例患者（2.4%）在60岁或以下的患者亚组经历了明确的中风。在总体人群中，PTFV 1异常不是卒中事件的显著预测因子[风险比1.12，95%置信区间（CI）0.91-1.38，P=0.301]，但PTFV 1与60岁分层的年龄存在高度显著的相互作用（相互作用模型中PTFV 1异常的P=0.009，风险比2.30，95% CI 1.27-4.13，P=0.006）。对60岁或60岁以下患者亚组的进一步分析显示，基线PTFV 1异常的患者卒中发生率高于基线PTFV 1正常的患者：每1000人-年的发生率为7.8（95% CI 5.2-11.4）vs 3.4（95% CI 2.2-5.2; P=0.004）;卒中发生风险增加2倍以上单因素考克斯分析的风险比为2.31，95%CI为1.28-4.16，P=0.005;在多变量考克斯回归模型中，调整了该人群中卒中事件的其他重要预测因素（性别、卒中或短暂性脑缺血发作史、缺血性心脏病或糖尿病史、基线肌酐和治疗中SBP），PTFV 1异常仍与卒中发生风险增加2倍以上相关结论：PTFV 1异常（左房异常的标志物）与高血压患者发生卒中密切相关，与治疗中SBP和其他卒中发生的预测因子无关。在没有可检测到的房颤的情况下，这种相关性表明潜在的心房心脏病可能导致左心房血栓形成和随后的卒中，而不干预临床识别的房颤。
Background: Recent findings in population-based studies suggest that abnormal P wave terminal force in lead V1 (PTFV1), a marker of left atrial abnormalities such as fibrosis, dilatation and elevated filling pressures, is associated with incident ischemic stroke, even in the absence of atrial fibrillation. However, whether PTFV1 predicts incident stroke in hypertensive patients during blood pressure lowering has not been examined.Methods: Risk of incident stroke was examined in relation to abnormal PTFV., on a baseline ECG in 7778 hypertensive patients with ECG left ventricular hypertrophy, no history of atrial fibrillation, in sinus rhythm on their baseline ECG with no incident atrial fibrillation during follow-up, who were randomly assigned to losartan-based or atenolol-based treatment.Results focused on the subset of patients between 55 and 60 years old (n = 1879) because of a significant interaction between PTFV1 and age in Cox analyses. Abnormal PTFV1 was defined by the presence of a negative terminal P wave in lead V1 with amplitude x duration > 4000 V ms. Results: During mean follow-up of 4.8do0.9 years, 364 patients (4.7%) of the overall study population and 45 patients (2.4%) in the subset of patients aged 60 years or less experienced a definite stroke. In the overall population, abnormal PTFV1 was not a significant predictor of incident stroke [hazard ratio 1.12, 95% confidence interval (CI) 0.91-1.38, P=0.301], but there was a highly significant interaction of PTFV1 with age stratified at 60 (P=0.009, hazard ratio 2.30, 95% CI 1.27-4.13, P=0.006 for abnormal PTFV1 in the interaction model). Further analyses in the subset of patients aged 60 years or less revealed a higher incidence of stroke occurred in those with abnormal than normal baseline PTFV1: incidence rate per 1000 person -years, 7.8 (95% CI 5.2-11.4) vs 3.4 (95% CI 2.2-5.2; P=0.004); a greater than two -fold increased risk of incident stroke (hazard ratio 2.31, 95% CI 1.28-4.16, P=0.005) in univariate Cox analysis; and in multivariable Cox regression models that adjusted for other significant predictors of incident stroke in this population (sex, history of stroke or transient ischemic attack, ischemic heart disease or diabetes, baseline creatinine and in treatment SBP), that abnormal PTFV1 remained associated with a greater than two -fold increased risk of incident stroke (hazard ratio 2.06; 95% CI L14-3.74, P=0.017).Conclusion: Abnormal PTFV1, a marker of left atrial abnormality, was strongly associated with incident stroke in hypertensive patients, independent of in -treatment SBP and other predictors of incident stroke. This association, in the absence of detectable atrial fibrillation, suggests that an underlying atrial cardiopathy may cause left atrial thrombus formation and a subsequent stroke without intervening clinically recognized atrial fibrillation.