Prolonged corrected QT interval in predicting atrial fibrillation: A systematic review and meta‐analysis

Zhang, Nixiao; Gong, Mengqi; Tse, Gary; Zhang, Zhiwei; Meng, Lei; Yan, Bryan P.; Zhang, Ling; Wu, Gang; Xia, Yunlong; Xin-Yan, Gan; Li, Guangping; Liu, Tong

doi:10.1111/pace.13292

Cited by 42 publications

(28 citation statements)

References 24 publications

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“…The cut‐off values of the QTc interval that could best predict procedural failure were identical in both studies (>448 ms). Several mechanisms have been proposed to explain these observations, including concomitant atrial cardiomyopathy, atrial torsades de pointes, atrio‐ventricular dyssynchrony secondary to QTc prolongation, and inflammatory reaction in both the atria and ventricles . Interestingly, in a series of over 1600 HCM patients from the Mayo Clinic, the authors found that the cut‐off value of QTc that could significantly predict death or SCD was 450 ms, almost identical to the value we calculated for predicting AF ablation outcome in HCM patients …”

Section: Discussionsupporting

confidence: 68%

“…The correlation between QTc and development of AF has also been investigated. A recent meta‐analysis based on pooled data of 309 676 individuals revealed that a prolonged QTc interval was associated with an increased risk of AF . Given the strong ties between AF and HCM, we investigated the impact of QTc interval on the outcomes of AF ablation in HCM patients.…”

Section: Discussionmentioning

confidence: 99%

“…A recent meta-analysis based on pooled data of 309 676 individuals revealed that a prolonged QTc interval was associated with an increased risk of AF. 16 Given the strong ties between AF and HCM, we investigated the impact of QTc interval on the outcomes of AF ablation in HCM patients. Our preliminary study was the first to demonstrate that the preprocedural QTc interval is an independent predictor of arrhythmia recurrence in HCM patients undergoing AF ablation.…”

Section: Qtc Interval Prolongation and Arrhythmia Recurrencementioning

confidence: 99%

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Depolarization and repolarization parameters on ECG predict recurrence after atrial fibrillation ablation in patients with hypertrophic cardiomyopathy

Wen

Zhu

Sun

et al. 2019

Cardiovasc electrophysiol

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Introduction The outcomes of atrial fibrillation (AF) ablation remain suboptimal. It is important to identify which AF patients will most likely benefit from ablation and who are more likely to show treatment failure, especially in those with structural heart disease such as hypertrophic cardiomyopathy (HCM). Methods and Results We enrolled 120 HCM patients who underwent primary AF ablation (48 with persistent AF). Preprocedural QTc was measured and corrected using the Bazett's formula, and the distribution of fragmentation of the QRS complex (fQRS) was recorded. Arrhythmia recurrence was defined as any kind of documented atrial tachyarrhythmia of more than 30 seconds. Overall, arrhythmia recurrence occurred in 69 patients after 13.4 months’ follow‐up. fQRS was present in 71 (59.17%) patients and was most commonly (81.69%) observed in the inferior leads. QTc more than 448 ms could predict arrhythmia recurrence with a sensitivity of 68.1% and specificity of 68.6%. Patients with QTc more than 448 ms (hazard ratio [HR]: 1.982; 95% confidence interval [CI]: 1.155‐3.402; P = .013) or those with fQRS+ (HR: 1.922; 95% CI: 1.151‐3.210; P = .012) were at an increased risk of recurrence. A combination of fQRS+ and QTc more than 448 ms was superior to fQRS or QTc alone in predicting arrhythmia recurrence. Conclusion In patients with HCM undergoing AF ablation, QTc prolongation, specifically >448 ms, and presence of fQRS are independent risk factors for arrhythmia recurrence at follow‐up. The combination of these two parameters has greater predictive value and would help to identify patients who are at the highest risk of procedural failure.

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Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Section: Qtc Interval Prolongation and Arrhythmia Recurrencementioning

confidence: 99%

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Depolarization and repolarization parameters on ECG predict recurrence after atrial fibrillation ablation in patients with hypertrophic cardiomyopathy

Wen

Zhu

Sun

et al. 2019

Cardiovasc electrophysiol

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“…55,56 One of the consequences is fibrosis, characterized by increased turnover of the extracellular matrix, producing conduction abnormalities that provide the necessary substrate for arrhythmogenesis. 57,58 A number of blood biomarkers 3,5-7,59-62 and electrocardiographic predictors 54,63,64 have been found in association with AF onset, development, and F I G U R E 1 Flow diagram of study selection process TA B L E 1 Characteristics of included studies for meta-analysis of association of galectin-3 and AF recurrence. Of these, galectin-3 plays a key role in acute and chronic pro-inflammatory responses and mediates activation of quiescent fibroblasts and synthesis of collagen.…”

Section: Discussionmentioning

confidence: 99%

Galectin‐3 and risk of atrial fibrillation: A systematic review and meta‐analysis

Gong

Cheung

Wang

et al. 2020

Clinical Laboratory Analysis

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Background Galectin‐3 is an inflammatory marker that is raised in myocardial fibrosis and inflammation. Recent studies have explored its role in predicting atrial fibrillation (AF) outcomes. The aim of this systematic review and meta‐analysis is to examine the association between serum concentration of galectin‐3 and AF. Methods PubMed, EMBASE, and the Cochrane Database were searched. A total of 280 studies were identified, of which 28 studies involving 10 830 patients were included in our meta‐analysis. Results Galectin‐3 is present at higher concentrations in patients with AF than those in sinus rhythm (mean difference [MD] = −0.68 ng/mL, 95% CI: −0.92, −0.44, Z = 5.61, P < .00001). Galectin‐3 levels were significantly higher in the persistent AF than in the paroxysmal AF group (MD = −0.94 ng/mL, 95% CI: −1.85, −0.03, Z = 2.04, P = .04). Higher galectin‐3 levels were associated with a 45% increase in the odds of developing AF (odds ratio [OR] = 1.45, 95% CI: 1.15, 1.83, Z = 3.11, P = .002) and risk of AF recurrence (hazard ratio [HR] =1.17, 95% CI: 1.06, 1.29, Z = 3.12, P = .002). Conclusions Our meta‐analysis found that galectin‐3 is significantly higher in patients with persistent AF than in those with paroxysmal AF, and can predict both AF development and recurrence after treatment.

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“…In the family with long QT syndrome 4 in which an ankyrin-B variant E1425G was identified, 12 of 21 patients with long QT syndrome showed paroxysmal AF (48,49). A recent meta-analysis showed that prolonged QTc is an independent risk predictor of AF (50). The underlying molecular mechanism for the association between prolonged QTc and QRS duration and AF is unknown, but the KI rats may serve as an animal model to explore such mechanisms in the future.…”

Section: Discussionmentioning

confidence: 99%

Mutation in NPPA causes atrial fibrillation by activating inflammation and cardiac fibrosis in a knock‐in rat model

et al. 2019

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Atrial fibrillation (AF) affects >30 million individuals worldwide. However, no genetic mutation from human patients with AF has been linked to inflammation. Here, we show that AF‐associated human variant p.Ile138Thr in natriuretic peptide A (NPPA) encoding the atrial natriuretic peptide (ANP) causes inflammation, fibroblast activation, atrial fibrosis, and AF in knock‐in (KI) rats. Variant p.Ile138Thr inhibits the interaction between ANP and its receptor natriuretic peptide receptor A and reduces intracellular cGMP levels. RNA sequencing and follow‐up analyses showed that mutant ANP (mANP) activates multiple innate immunity pathways, including TNF‐α, NF‐κB, and IL‐1β signaling. mANP induces differentiation of cardiac fibroblasts (CFs) to myofibroblasts and promotes CF proliferation and fibrosis. These results suggest that NPPA variant p.Ile138Thr causes AF by activating TNF‐α, NF‐κB, and IL‐1β signaling, inflammation, and fibrosis. Multiple computational programs suggest that p.Ile138Thr is damaging or deleterious. Based on the 2015 American College of Medical Genetics and Genomics Standards and Guidelines, p.Ile138Thr can be classified as a likely pathogenic variant. Variant p.Ile138Thr was found only in Asian people in the Genome Aggregation Database and Exome Aggregation Consortium database at an averaged frequency of 0.026%. An estimated 1.15 million Asian people carry the variant and might be at risk of AF. The KI rats may provide an inflammation‐based, genetic animal model for AF valuable for testing anti‐inflammation or other therapies for AF.—Cheng, C., Liu, H., Tan, C., Tong, D., Zhao, Y., Liu, X., Si, W., Wang, L., Liang, L., Li, J., Wang, C., Chen, Q., Du, Y., Wang, Q. K., Ren, X. Mutation in NPPA causes atrial fibrillation by activating inflammation and cardiac fibrosis in a knock‐in rat model. FASEB J. 33, 8878–8891 (2019). http://www.fasebj.org

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Prolonged corrected QT interval in predicting atrial fibrillation: A systematic review and meta‐analysis

Abstract: Prolonged QTc interval is associated with an increased risk of AF. And the potential mechanisms underlying this cause-and-effect relationship need further investigation.

Cited by 42 publications

References 24 publications

Depolarization and repolarization parameters on ECG predict recurrence after atrial fibrillation ablation in patients with hypertrophic cardiomyopathy

Depolarization and repolarization parameters on ECG predict recurrence after atrial fibrillation ablation in patients with hypertrophic cardiomyopathy

Galectin‐3 and risk of atrial fibrillation: A systematic review and meta‐analysis

Mutation in NPPA causes atrial fibrillation by activating inflammation and cardiac fibrosis in a knock‐in rat model

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