Abnormal P-wave terminal force in lead V(1) is a marker for atrial electrical dysfunction but not structural remodelling.
Abnormal P-wave terminal force in lead V(1) is a marker for atrial electrical dysfunction but not structural remodelling.
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DOI：
10.1002/ehf2.13488
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发表时间：
2021-10
影响因子：
3.8
通讯作者：
Wagner S
中科院分区：
文献类型：
--
作者：
Lebek S;Wester M;Pec J;Poschenrieder F;Tafelmeier M;Fisser C;Provaznik Z;Schopka S;Debl K;Schmid C;Buchner S;Maier LS;Arzt M;Wagner S
缺乏对心房心肌病和阵发性心房颤动患者的诊断和治疗选择。有趣的是，心电图导联V1 （PTFV1）的P波终末力异常与心房心肌病有关，但这种关系尚不清楚。我们研究了PTFV1作为功能、电和结构心房重构的标志物。56例急性心肌梗死患者和13例肾脏供者作为对照，前瞻性地接受了心脏磁共振成像，以评估PTFV1与功能重构（心房应变）之间的关系。为了进一步研究潜在的病理机制，我们收集了32例接受择期冠状动脉旁路移植术的患者的右心耳活检。PTFV1以V1导联负P波振幅和持续时间的乘积来评价，≥4000 ms*μV定义为异常。心脏钙/钙调素依赖性蛋白激酶II （CaMKII）的活性通过特定的HDAC4下拉试验来测定，作为电重构的替代方法。心房纤维化量化使用马松三色染色作为结构重塑的措施。进行多变量回归分析以解释潜在的混杂因素。急性心肌梗死患者中有16/56（29%）、肾供者中有3/13（23%）、冠状动脉搭桥术患者中有15/32 (47%)PTFV1异常。在急性心肌梗死患者中，PTFV1异常亚组左心房（LA）应变显著降低（LA库应变：32.28±12.86% vs. 22.75±13.94%,P = 0.018； LA导管应变：18.87±10.34% vs. 10.17±8.26%,P = 0.004）。PTFV1异常与LA导管应变呈负相关（系数B:−7.336,95%可信区间为−13.577 ~−1.095,P = 0.022），与临床协变量无关。PTFV1异常患者的CaMKII活性从（归一化到CaMKII表达）0.87±0.17显著升高至1.46±0.15 （P = 0.047）。PTFV1异常患者的增加与临床协变量无关（系数B: 0.542, 95%可信区间为0.057 ~ 1.027,P = 0.031）。PTFV1异常的患者心房纤维化明显降低，为12.32±1.63% (vs. 20.50±2.09%,P = 0.006)，提示PTFV1是电重构而非结构重构的标志物。PTFV1异常是心房功能受损和电重构的独立预测因子，但不是结构重构的预测因子。PTFV1可能是评估心房心肌病患者和房颤风险的一个有前途的工具。
There is a lack of diagnostic and therapeutic options for patients with atrial cardiomyopathy and paroxysmal atrial fibrillation. Interestingly, an abnormal P‐wave terminal force in electrocardiogram lead V1 (PTFV1) has been associated with atrial cardiomyopathy, but this association is poorly understood. We investigated PTFV1 as a marker for functional, electrical, and structural atrial remodelling. Fifty‐six patients with acute myocardial infarction and 13 kidney donors as control cohort prospectively underwent cardiac magnetic resonance imaging to evaluate the association between PTFV1 and functional remodelling (atrial strain). To further investigate underlying pathomechanisms, right atrial appendage biopsies were collected from 32 patients undergoing elective coronary artery bypass grafting. PTFV1 was assessed as the product of negative P‐wave amplitude and duration in lead V1 and defined as abnormal if ≥4000 ms*μV. Activity of cardiac Ca/calmodulin‐dependent protein kinase II (CaMKII) was determined by a specific HDAC4 pull‐down assay as a surrogate for electrical remodelling. Atrial fibrosis was quantified using Masson's trichrome staining as a measure for structural remodelling. Multivariate regression analyses were performed to account for potential confounders. A total of 16/56 (29%) of patients with acute myocardial infarction, 3/13 (23%) of kidney donors, and 15/32 (47%) of patients undergoing coronary artery bypass grafting showed an abnormal PTFV1. In patients with acute myocardial infarction, left atrial (LA) strain was significantly reduced in the subgroup with an abnormal PTFV1 (LA reservoir strain: 32.28 ± 12.86% vs. 22.75 ± 13.94%, P = 0.018; LA conduit strain: 18.87 ± 10.34% vs. 10.17 ± 8.26%, P = 0.004). Abnormal PTFV1 showed a negative correlation with LA conduit strain independent from clinical covariates (coefficient B: −7.336, 95% confidence interval −13.577 to −1.095, P = 0.022). CaMKII activity was significantly increased from (normalized to CaMKII expression) 0.87 ± 0.17 to 1.46 ± 0.15 in patients with an abnormal PTFV1 (P = 0.047). This increase in patients with an abnormal PTFV1 was independent from clinical covariates (coefficient B: 0.542, 95% confidence interval 0.057 to 1.027, P = 0.031). Atrial fibrosis was significantly lower with 12.32 ± 1.63% in patients with an abnormal PTFV1 (vs. 20.50 ± 2.09%, P = 0.006), suggesting PTFV1 to be a marker for electrical but not structural remodelling. Abnormal PTFV1 is an independent predictor for impaired atrial function and for electrical but not for structural remodelling. PTFV1 may be a promising tool to evaluate patients for atrial cardiomyopathy and for risk of atrial fibrillation.
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影响因子：
20.1
作者：
Kamel H;Healey JS
通讯作者：
Healey JS
影响因子：
5.5
作者：
Win, Theingi Tiffany;Venkatesh, Bharath Ambale;Volpe, Gustavo J.;Mewton, Nathan;Rizzi, Patricia;Sharma, Ravi K.;Strauss, David G.;Lima, Joao A.;Tereshchenko, Larisa G.
通讯作者：
Tereshchenko, Larisa G.
DOI：
10.1186/s12968-014-0060-6
发表时间：
2014-08-12
期刊：
Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance
影响因子：
--
作者：
Kowallick JT;Kutty S;Edelmann F;Chiribiri A;Villa A;Steinmetz M;Sohns JM;Staab W;Bettencourt N;Unterberg-Buchwald C;Hasenfuß G;Lotz J;Schuster A
通讯作者：
Schuster A
影响因子：
1.9
作者：
Huang, Zhuoshan;Zheng, Zhenda;Liu, Jinlai
通讯作者：
Liu, Jinlai
影响因子：
3.3
作者：
Dick, Anastasia;Schmidt, Bjoern;Baessler, Bettina
通讯作者：
Baessler, Bettina