Investigation of the predictors of transition to persistent atrial fibrillation in patients with paroxysmal atrial fibrillation

BACKGROUND: Until now, no clinically useful indicators have existed that predict the transition from paroxysmal to persistent atrial fibrillation (AF). HYPOTHESIS: The current prospective study was conducted for identifying predictors of progression to persistent AF over the long term. METHODS: We studied 102 consecutive patients (mean age: 55 +/- 10 years: 75 men and 27 women) diagnosed with paroxysmal AF. Standard 12-lead electrocardiography, echocardiography, and P-wave-triggered signal-averaged electrocardiography (P-SAECG) were performed on all patients at the time of their entry into the study. RESULTS: The mean follow-up period was 61 +/- 13 months. Group 1 (n = 66) comprised patients in whom paroxysmal AF did not progress to persistent AF, and Group 2 (n = 36) comprised those who developed persistent AF. In Group 2 the patients were significantly older, and P-wave dispersion, filtered P-wave duration (FPD), and left atrial dimension were significantly higher than in Group 1 (p < 0.05). The root mean square voltage for the last 30 ms of the filtered P-wave was also significantly lower in Group 2 (p < 0.05). Multivariate logistic regression analysis using these five factors identified left atrial dimension (odds ratio [OR] 2.29; 95% confidence interval [CI] 1.16-4.54; p = 0.02) and FPD (OR 2.71; 95% CI 1.78-4.13; p < 0.01) as independent predictors of transition to persistent AF. Left atrial dimension > or = 40 mm predicted progression to persistent AF with a sensitivity of 64%, specificity of 76%, positive predictive value of 59%, negative predictive value of 79%, and an accuracy of 71%. An FPD > or = 150 ms predicted persistent AF with a sensitivity of 81%, specificity of 91%, positive predictive value of 88%, negative predictive value of 90%, and an accuracy of 87%. Filtered P-wave duration was a significantly more sensitive and specific predictor than left atrial dimension (p < 0.05). CONCLUSION: We conclude that FPD is a clinically useful predictor of progression from paroxysmal to persistent AF over the long term.     

Electroanatomic characteristics of atrial premature beats triggering atrial fibrillation in patients with persistent versus paroxysmal atrial fibrillation

APBs in Persistent Versus Paroxysmal AF. BACKGROUND: Although the electrical disconnection between the left atrium (LA) and pulmonary veins (PVs) by radiofrequency catheter ablation has been proven to be effective in controlling atrial fibrillation (AF), the recurrence rate is higher in patients with persistent AF (PeAF) than with paroxysmal AF (PAF). We hypothesized that the origin of the atrial premature beats (APBs) that trigger AF and the pattern of their breakthrough into the LA differ between PAF and PeAF. METHODS: We mapped 75 APBs (53 APBs triggering AF, 22 isolated APBs) from the LA and PVs in 26 patients with AF (age: 49.5 +/- 9.6, males: 23, PAF = 17, PeAF = 9), using a noncontact endocardial mapping (NCM) system. The location of the preferential conduction (PC) sites and their conduction velocity (CV) were compared. RESULTS: In patients with PeAF, the earliest activation (EA) site and exit of the PC were more frequently located on the LA side of the LA-PV junction as compared with PAF (P < 0.001). Eighty-one percent of the PCs were located in the area between the left and right superior PVs. The incidence of PCs was similar between the PeAF and PAF patients (P = NS). PCs were more commonly found with APBs inducing AF (63.3%) than with those not inducing AF (35.2%, P = 0.01). The CV of the PC was slower for PeAF than PAF (P < 0.001). The CV in the LA during sinus rhythm was also slower for PeAF than PAF (P < 0.01). CONCLUSION: PeAF was more frequently triggered by APBs from the LA side of the LA-PV junction than PAF and resulted in slower conduction than did PAF. These findings may help explain the higher potential for recurrence after electrical PV isolation in patients with PeAF.     

心脏起搏术后阵发性转为持续性心房颤动的影响因素分析

目的分析心脏起搏术后阵发性心房颤动(简称房颤)进展为持续性房颤的风险及可能影响因素。方法109例慢快综合征和30例快慢综合征患者,分别植入VVI(R)或DDD(R)起搏器。根据房颤进展情况分为持续性房颤组(进展组)和非持续性房颤组(非进展组)。分析心脏永久起搏术后房颤进展情况及影响因素。结果平均随访(5.1±2.2)年,51例进展为持续性房颤。单因素分析显示预测房颤进展的危险因素包括左房内径、未使用抗心律失常药物、VVI起搏、高房颤负荷及慢快综合征。多因素Logistic回归分析显示左房内径(HR=1.103,95%CI1.085~1.124,P0.05)、未使用抗心律失常药物(HR=1.975,95%CI 1.336~2.813,P0.001)、VVI起搏(HR=2.156,95%CI1.458~3.157,P0.001)及慢快综合征(HR=1.875,95%CI1.326~3.025,P0.001)是房颤进展的独立预测因素。Kaplan-Meier分析示慢快综合征进展为持续性房颤快于快慢综合征(P=0.034)。结论慢快综合征、左房内径、未使用抗心律失常药物、VVI起搏是阵发性房颤进展为持续性房颤的独立预测因素。     

阵发性心房颤动进展为持续性心房颤动前的血浆醛固酮水平

目的测定阵发性心房颤动(简称房颤)进展为持续性房颤前血浆醛固酮水平变化。方法选取本院心内科阵发性房颤患者91例,所有患者入选后行心脏超声、长程心电图和血生化检查,测定空腹清晨窦性心律时血清醛固酮浓度。结果随访18±6个月,86例完成随访,其中15例进展为持续性房颤。持续性房颤组在年龄、高血压、冠心病和心功能不全和醛固酮水平(302.7±78.3 pg/ml vs 234.3±69.6 pg/ml,P<0.01)与阵发性房颤组有差异。多因素回归分析显示年龄、左房内径、左室射血分数和醛固酮是阵发性房颤进展为持续性房颤的独立危险因素。结论阵发性房颤患者进展为持续性房颤前血清醛固酮水平升高。     

Characteristics and distribution of complex fractionated atrial electrograms in patients with paroxysmal and persistent atrial fibrillation

Introduction  

Substrate-based radiofrequency ablation for treatment of atrial fibrillation (AF) is still under development. The purpose of this study was to investigate the different characteristics and distribution of complex fractionated atrial electrograms (CFAE) in both atria in patients with paroxysmal and persistent AF.     

Endothelin system in human persistent and paroxysmal atrial fibrillation

INTRODUCTION: Activation of the endothelin system is an important compensatory mechanism that is activated during left ventricular dysfunction. Whether this system plays a role at the atrial level during atrial fibrillation (AF) has not been examined in detail. The purpose of this study was to investigate mRNA and protein expression levels of the endothelin system in AF patients with and without concomitant underlying valve disease. METHODS AND RESULTS: Right atrial appendages of 36 patients with either paroxysmal or persistent AF were compared with 36 controls in sinus rhythm. The mRNA amounts of pro-endothelin-1 (pro-ET-1), endothelin receptor A (ET-A), and endothelin receptor B (ET-B) were studied by semiquantitative polymerase chain reaction. Protein amounts of the receptors were investigated by slot-blot analysis. mRNA amounts of pro-ET-1 were increased (+40%; P = 0.002) only in AF patients with underlying valve disease. ET-A and ET-B receptor protein amounts were significantly reduced in patients with paroxysmal AF (-39% and -47%, respectively) and persistent AF with underlying valve disease (-28% and -30%, respectively) and in persistent AF without valve disease (-20% and -40%, respectively). ET-A mRNA expression was unaltered in paroxysmal and persistent AF, whereas ET-B mRNA was reduced by 30% in persistent AF with (P < 0.001) or without (P = 0.04) valve disease, but unchanged in paroxysmal AF. CONCLUSION: Substantial changes in gene expression of the endothelin system were observed in human atria during AF, especially in the presence of underlying valve disease. Alterations in endothelin expression associated with AF could play a role in the pathophysiology of AF and the progression of underlying heart disease.     

Characterization of conduction recovery across left atrial linear lesions in patients with paroxysmal and persistent atrial fibrillation

Background: Left atrial (LA) linear lesions are effective in substrate modification for atrial fibrillation (AF). However, achievement of complete conduction block remains challenging and conduction recovery is commonly observed. The aim of the study was to investigate the localization of gap sites of recovered LA linear lesions.
Methods and Results: Forty-eight patients with paroxysmal (n = 26) and persistent/permanent (n = 22) AF underwent repeat ablation after pulmonary vein (PV) isolation and LA linear ablation at the LA roof and/or mitral isthmus due to recurrences of AF or flutter. In 35 patients, conduction through the mitral isthmus line (ML) had recovered whereas roof-line recovery was observed in 30 patients. The gaps within the ML were distributed to the junction between left inferior PV and left atrial appendage in 66%, the middle part of the ML in 20%, and in 8% to the endocardial aspect of the ML while only 6% of lines showed an epicardial site of recovery. The RL predominantly recovered close to the right superior PV (54%) and less frequently in the mid roof or close to the left PV (both 23%). Reablation of lines required significantly shorter RF durations (ML: 7.24 ± 5.55 minutes vs 24.08 ± 9.38 minutes, RL: 4.24 ± 2.34 minutes vs 11.54 ± 6.49 minutes; P = 0.0001). Patients with persistent/permanent AF demonstrated a significantly longer conduction delay circumventing the complete lines than patients with paroxysmal AF (228 ± 77 ms vs 164 ± 36 ms, P = 0.001).
Conclusions: Gaps in recovered LA lines were predominantly located close to the PVs where catheter stability is often difficult to achieve. Shorter RF durations are required for reablation of recovered linear lesions. Conduction times around complete LA lines are significantly longer in patients with persistent/permanent AF as compared to patients with paroxysmal AF.     

阵发性心房颤动患者心房复极离散度的研究

目的　通过记录阵发性心房颤动 (房颤 )患者心房单相动作电位 (MAP) ,分析心房复极离散度与房颤发生的关系。方法　特发性阵发性房颤患者与无自发房颤病史的阵发性室上性心动过速患者各 1 5例 ,均接受心内电生理检查和 /或导管射频消融治疗。两根 MAP电极于右心房共取 4～ 1 0个不同部位进行同步的窦性心律基础刺激 (S1)及期前刺激 S2 时的 MAP记录。测量、计算心房复极离散度(RTd)及动作电位时限和局部冲动时间的离散度 (APDd、ATd)。　结果　窦性心律时房颤组最大 RTd显著大于对照组 (1 2 3 .69± 54.67) ms比 (64 .2 5± 2 3 .2 9) ms,(P<0 .0 1 )。其差异主要来源于 APDd(1 1 5.0 0± 4 6.90 ) ms比 (57.56± 3 3 .57) ms,(P<0 .0 1 ) ,ATd差异无显著性。随 S1、S2 的加入 ,各组局部激动时间和离散度逐渐增大 ,而动作电位时限逐渐缩短 ,且房颤组的这种改变程度显著大于对照组。在S1时无房颤发生 ,加入期前刺激时 ,大多数房颤组患者均多次诱发出短阵房颤。其诱发率及次数均显著高于对照组。　结论　研究结果表明 ,MAP记录技术是临床观察、分析心房复极离散度及其在阵发性房颤中的作用的较佳方法。心房复极离散度的增加是阵发性房颤发生的重要因素。期前刺激时动作电位时限的缩短和离散以及传导障碍在     

Chemoreflexsensitivity among patients with paroxysmal atrial fibrillation

Atrial fibrillation is the most common cardiac arrhythmia with typical complications of thromboembolisms. The autonomic nervous system is an important factor for the initiation of arrhythmias. A vagally or adrenergically hyperfunction could cause the initiation of paroxysmal atrial fibrillation (PAF). METHOD: We measured the chemoreflexsensitivity (CHRS) among 110 patients to determine a disturbed autonomic function as risk factor for PAF. We examined 45 patients with PAF (group A), 45 patients with sinus rhythm (group B) and 20 young volunteers (group C). The ratio between the difference of RR intervals in ECG and venous pO(2) was measured for the determination of CHRS. The margin of the CHRS was 3 ms/mmHg. RESULTS: Patients of group A had a significantly lower CHRS compared to group B (1.56+/-1.46 vs 6.29+/-3.71 ms/mmHg, p<0.0008) or group C (1.56+/-1.46 vs 6.35+/-4.29 ms/ mmHg, p<0.0003). A significant difference between group B and C could not be observed (6.29+/-3.71 vs. 6.35+/-4.29 ms/mmHg, p = n.s.). A specificity of 74% and a sensitivity of 71% was achieved for identifying patients with PAF by using a margin of 3 ms/mmHg for the CHRS. CONCLUSIONS: An analysis of CHRS seems to be an appropriate method to demonstrate a neurovegetative imbalance which might be one possible trigger mechanism of PAF. The predictive power has to be examined by prospective investigations of a larger patient population.     

Prevalence and characteristics of continuous electrical activity in patients with paroxysmal and persistent atrial fibrillation

Background: Complex fractionated atrial electrograms (CFAEs) may play a role in the genesis of atrial fibrillation (AF). One type of CFAE is continuous electrical activity (CEA). The prevalence and characteristics of CEA in patients with paroxysmal and persistent AF are unclear.
Methods and Results: In 44 patients (age = 59 ± 8 years) with paroxysmal (25) or persistent (19) AF, bipolar electrograms were systematically recorded for ≥5 seconds at 24 left atrial (LA) sites, including 8 antral sites, and 2 sites within the coronary sinus (CS). CEA was defined as continuous depolarization for > 1 second with no isoelectric interval. CEA was recorded at the LA septum (79%), antrum (66%), posterior (68%) and anterior walls (67%), roof (66%), base of the LA appendage (61%), inferior wall (61%), posterior mitral annulus (48%), CS (41%), and in the LA appendage (14%). Antral CEA was equally prevalent in patients with paroxysmal (63%) and persistent AF (70%, P = 0.12). In patients with paroxysmal AF, the prevalence of CEA was similar among antral and nonantral LA sites, except for the LA appendage. However, in patients with persistent AF, CEA was more prevalent at the nonantral (80%) than antral sites (70%, P = 0.03). CEA at nonantral sites except the CS was more prevalent in persistent than in paroxysmal AF (80% vs 57%, P < 0.001). The mean duration of intermittent episodes of CEA was longer in persistent than in paroxysmal AF (P < 0.001).
Conclusions: The higher prevalence and duration of CEA at nonantral sites in persistent than in paroxysmal AF is consistent with a greater contribution of LA reentrant mechanisms in persistent AF. However, the high prevalence of CEA at nonantral sites in paroxysmal atrial fibrillation (PAF) suggests that CEA alone is a nonspecific marker of appropriate target sites for ablation of AF. The characteristics of CEA that most accurately identify drivers of AF remain to be determined.     

Cholesterol paradox in patients with paroxysmal atrial fibrillation

Hypercholesterolemia is a major risk factor for coronary heart disease (CHD), but the associations among lipids, lipoproteins and paroxysmal atrial fibrillation (PAF) have not yet been reported. The associations among lipids, lipoproteins and PAF were examined in a case-control study, in which cases and controls were defined as those with/without definite ECG-detectable PAF, respectively. CHD patients were excluded from the study. The mean values of serum total cholesterol (TC), triglyceride (TG) and high density lipoprotein-cholesterol (HDL-C), after adjusting for age and gender, in patients with PAF were lower than those in patients without PAF (175 +/- 4 mg/dl vs. 190 +/- 3 mg/dl, 104 +/- 7 mg/dl vs. 123 +/- 6 mg/dl, 46.0 +/- 1.7 mg/dl vs. 51.8 +/- 1.4 mg/dl, respectively), as assessed by an analysis of covariance. After controlling for age and gender, TC, TG and HDL-C (all in quartiles) were inversely and linearly (p < 0.05) associated with the percentage of patients with PAF, as assessed by a multiple logistic regression analysis. The associations between TC or TG and PAF varied with the HDL-C level: significant when HDL-C was low (p < 0.05), but not when HDL-C was high. The odds ratio (relative risk of PAF) for patients with both low TC or TG and low HDL-C was 4.08 (95% CI: 1.81-9.57) times or 9. 40 (3.25-32.0) times higher (p < 0.01) than that for patients with high TC or TG and high HDL-C, respectively. In conclusion, low serum levels of TC and TG were found in PAF patients, while reduced HDL-C may cause PAF. Hypolipoproteinemia including low HDL-C may affect atrial vulnerability and cause atrial fibrillation.     

A noninvasive index of atrial remodeling in patients with paroxysmal and persistent atrial fibrillation: a pilot study

PurposeThis study aims to develop a noninvasive atrial remodeling index (RI) to separate patients presenting paroxysmal atrial fibrillation (ParAF) from those with sustained persistent atrial fibrillation (PerAF), that is, AF episodes interrupted 7 days or more after the onset.MethodsSignal-averaged P-wave duration (SAPWd) and left atrial anteroposterior diameter (LADd) were measured in 33 ParAF patients, in 26 sustained PerAF patients, and in 18 control subjects. By using SAPWd and LADd, a dichotomous (0/1) RI was created. A logistic regression model on the probability of having a sustained PerAF vs a ParAF episode was estimated, including the RI, sex, age, and cardiac comorbidities as covariates.ResultsSignal-averaged P-wave duration was significantly longer in sustained PerAF (153 ± 15 milliseconds) than in ParAF patients (142 ± 13 milliseconds, P < .001) and in both ParAF and sustained PerAF groups vs control group (123 ± 7 milliseconds, P < .001). Left atrial anteroposterior diameter was larger both in sustained PerAF (43 ± 6 mm) vs ParAF patients (38 ± 5 mm, P = .002) and in sustained PerAF group vs control group (38 ± 2 mm, P = .004), but no differences were observed between ParAF patients and controls (P = .6). A 12-fold increase (odds ratio, 11.8; 95% confidence interval, 2.2-63.5) in the odds of having a sustained PerAF vs a ParAF episode was observed in patients with RI equal to 1.ConclusionsP-wave duration and left atrium diameter enabled to define a noninvasive atrial RI to separate patients with ParAF from those with sustained PerAF. This could be a useful tool to select a suitable strategy for AF treatment.     

Progression of new onset to established persistent atrial fibrillation: an implantable device-based analysis with implications for clinical classification of persistent atrial fibrillation

Introduction  

The temporal patterns of onset of persistent atrial fibrillation (AF) recurrences leading to established persistent AF is currently unknown.     

Pharmacological cardioversion of persistent atrial fibrillation with and without a history of drug-resistant paroxysmal atrial fibrillation.

BACKGROUND: Suppression by antiarrhythmic drugs of the maintenance mechanisms could convert persistent atrial fibrillation (AF) to sinus rhythm (SR). Whether a history of drug-resistant paroxysmal AF (PAF) would affect the outcome of pharmacological conversion of persistent AF by bepridil or in combination with aprindine was evaluated in the present study. METHODS AND RESULTS: The study group comprised 51 consecutive patients (24 men, 61+/-8 years) undergoing pharmacological conversion of persistent AF lasting >1 month. Drug-resistant PAF was defined as AF and at least 2 ineffective antiarrhythmic drugs for suppression of AF recurrence. Fast Fourier transform analysis of fibrillation waves was used to measure fibrillation cycle length (FCL) from the peak frequency. Fifteen patients had a history of drug-resistant PAF (Group I), and the remaining 36 did not (Group II) before diagnosis of persistent AF. Ten patients (67%) in Group I and 26 patients (72%) in Group II were restored to SR by bepridil alone or in combination with aprindine after 29+/-15 days of drug administration. Before conversion to SR, bepridil increased the FCL more in Group II than in Group I. During a 12-month follow-up period, 4 of 10 patients in Group I and 2 of 26 patients in Group II (p<0.01) had recurrence of persistent AF with bepridil alone or in combination with aprindine. CONCLUSIONS: A history of drug-resistant PAF does not affect the efficacy of pharmacological conversion by bepridil or in combination with aprindine. However, recurrence of AF was significantly higher in patients with such a history.     

阵发性心房颤动患者心房内阻滞的评价

目的对阵发性心房颤动(房颤)患者心房内阻滞的情况进行评价.方法入选78例阵发性房颤患者和8创无阵发性房颤的射频消融患者,电生理检查时分别放置高位右心房、希氏束、冠状静脉窦电极导管作起搏和标测用,在高位右心房进行S1S2程序刺激,S1刺激固定于500ms,S2从450ms开始,-10ms扫描,记录不同刺激时心房内和心房间传导时间及心房不应期.结果S1刺激时阵发性房颤组和对照组S1-AHB间期分别为(56.7±15.4)ms和(60.8±14.2)ms;S1-ACSd间期在两组分别为(110.2±24.3)ms和(107.5±25.6)ms;差异均无显著性(P＞0.05).S2刺激时,心房内传导时间最长延长1倍以上的患者在两组分别为15/78例和11/80例,心房间传导最长延长1倍以上的患者在两组间分别为13/78例和9/80例,两组间差异无显著性(P＞0.05).心房不应期在两组分别为(218.0±28.2)ms和(216.0±24.7)ms,两者间差异无显著性(P＞0.05).结论多数阵发性房颤患者无明显的心房内阻滞和不应期改变,传导时间延长也并非特异地发生在阵发性房颤组,提示心房内阻滞和不应期缩短在阵发性房颤的发生中的作用尚不明确.     

Dispersion of atrial repolarization in patients with paroxysmal atrial fibrillation.

To study the role of the dispersion of atrial repolarization (DAR) in the genesis of atrial fibrillation (AF), monophasic action potentials (MAP) were recorded simultaneously from a catheter at the high lateral right atrium (HLRA) and a catheter moving around the high, middle and low lateral right atrium (RA) the high, anterior and posterior septal RA and the RA appendage in 15 patients with paroxysmal AF and 15 patients with atrioventricular nodal re-entry tachycardia (AVNRT) or concealed Wolff-Parkinson-White syndrome (WPW) without history of AF. After recordings during sinus rhythm (SR), MAPs were recorded during programmed stimulation (PS) via the HLRA catheter at a drive cycle length (CL) of 500 ms. Thus, MAPs were recorded simultaneously from 2 sites at a time and sequentially from 4 to 12 sites during SR, drive pacing and PS. Taking the MAP at the HLRA as reference, the dispersion of repolarization time (dispersion of RT) and its two components, the dispersions of activation time (dispersion of AT) and MAP duration (dispersion of MAP duration) among the 4 to 12 sites were calculated and taken as parameters of DAR. RESULTS: During SR and PS, the maximal dispersion of RT was significantly greater in AF than in control patients, 113+/-49 ms vs 50+/-28 ms (P<0.001) and 114+/-56 vs 70+/-43 ms (P<0.05) respectively. The increased dispersion of RT in the AF group was caused by increases in both dispersion of MAP duration and dispersion of AT. CONCLUSION: During SR and PS, DAR increased in patients with paroxysmal AF due to increases in dispersion of MAP duration and dispersion of AT, which suggests the involvement of both repolarization and conduction disturbances in the development of paroxysmal AF.