BACKGROUND AND PURPOSE: To investigate an association between left atrial (LA) structural and P wave dispersion (PWD) during sinus rhythm, and electrical remodeling in cryptogenic stroke (CS) patients. METHODS: Forty CS patients and 40 age- and sex-matched healthy controls were enrolled. P wave calculations were based on 12-lead electrocardiography (ECG) at a 50-mm/s-paper speed with an amplitude of 10 mm/mV. Difference between the maximum and minimum P wave duration was the P wave dispersion (PWD=Pmax-Pmin). LA deformation was evaluated by speckle tracking echocardiography within 3 days of the acute event. RESULTS: PWD was 30.1+/-7.0 ms and 27.4+/-3.5 ms in CS and control group (P=0.02), whereas LA maximum volume index [LAVImax] was 20.4+/-4.5 mL/m2 and 19.9+/-2.4 mL/m2 in CS and control group, respectively (P = 0.04). While global peak LA strain was [pLA-S] (LA reservoir function) 41.4 +/- 6.3% and 44.5 +/- 7.1% in CS and control group, (P = 0.04), global peak late diastolic strain rate values [pLA-SRa] (LA pump function) were 2.5 +/- 0.4% and 2.9 +/- 0.5% in CS and control group, respectively (P = 0.001). A mild and a strong negative correlation between global pLA-S and LAVImax (r=-0.49; P<0.01), and between PWD and global pLA-S (r = -0.52; P < 0.01), respectively, was observed in CS. CONCLUSIONS: Increased PWD is associated with impaired LA mechanical functions and enlargement, and involved in the pathophysiology of AF or an AF-like physiology in CS.
Atrial Remodeling* ; Echocardiography ; Electrocardiography ; Humans ; Physiology ; Stroke*

BACKGROUND AND OBJECTIVES: Conservation of the normal atrial size and architecture by preventing the structural atrial remodeling that's due to atrial fibrillation (AF) seems to be of prime importance for the management of AF patients. We attempted to assess the relevance of performing strain echocardiography for quantitatively assessing the left atrial (LA) status in AF patients. SUBJECTS AND METHODS: Tissue Doppler strain and 2-dimensional strain imaging were performed in 15 patients with chronic AF, in 15 patients with paroxysmal AF and in 15 healthy age-matched controls with using a GE vivid 7 dimension apparatus. The LA diameter, LA volume index and mitral inflow parameters were measured by standard echocardiography. Longitudinal peak strain and the strain rate were obtained from 2 different areas of the basal left atrial free wall and also the inter-atrial septum in the apical 4 chamber view with using the tissue Doppler strain. The mean peak systolic rate (Sm-SR), the peak early diastolic rate (Em-SR) and the peak late diastolic strain rate (Am-SR) were measured at the inter-atrial septum in the apical 4 chamber view with using the 2-dimensional strain imaging. RESULTS: The peak strain/rate, the Sm-SR and the Em-SR were significantly reduced in the AF group as compared with the normal controls, and they were especially reduced in the chronic AF group. There were no significant differences for the LA size and A wave velocity between the paroxysmal AF group and the normal group; however, the peak systolic strain/rate, the Em-SR and the Am-SR were significantly lower in the paroxysmal AF group than in the normal controls. CONCLUSION: The lower values of atrial Sm-SR, Em-SR and Am-SR revealed that active contraction and passive stretching of the LA wall may be impaired in some patients suffering with paroxysmal AF even before LA enlargement occurs, and this is possibly because of reduced atrial compliance. Our results indicated that strain echocardiography enabled quantitatively precise assessment of the LA contractile function and it can provide clinically useful information concerning the early reversible atrial functional changes in patients suffering with AF, and especially in the paroxysmal AF patients.
Atrial Fibrillation* ; Atrial Remodeling ; Compliance ; Echocardiography ; Humans ; Muscle Stretching Exercises

BACKGROUND AND OBJECTIVES: This study aimed to evaluate the impact of the CHA₂DS₂-VASc score on atrial fibrillation (AF) recurrence after a single catheter ablation procedure in patients with non-valvular AF. We also investigated the correlation between CHA₂DS₂-VASc score and atrial substrate. SUBJECTS AND METHODS: This study evaluated 151 patients who underwent catheter ablation of non-valvular AF. The study population was stratified into group 1 (<2, n=72) and group 2 (≥2, n=79) by CHA₂DS₂-VASc score. The CHA₂DS₂-VASc score was analyzed as a continuous and categorical value for evaluating its impact on AF recurrence after catheter ablation. The left atrial voltage data were analyzed by the categorical values of this score. RESULTS: Post-ablation recurrence (31.6% vs. 18.1%, p=0.046) was observed more frequently in group 2. The mean area of the lowvoltage zone was 75.64±24.81 cm² and 94.44±28.09 cm² in groups 1 and 2, respectively (p=0.005). The left atrial mean voltage in group 2 was 0.99±0.31 mV, significantly lower than that (1.49±0.67 mV, p=0.001) in group 1. The CHA₂DS₂-VASc score was the independent predictor with a modest predictive value for AF recurrence after catheter ablation. CONCLUSION: Our study showed that CHA₂DS₂-VASc score was associated with atrial remodeling and could be useful in stratifying post-ablation recurrence in patients with non-valvular AF.
Atrial Fibrillation* ; Atrial Remodeling* ; Catheter Ablation* ; Catheters* ; Humans ; Recurrence*

Atrial Fibrillation ; Atrial Remodeling ; Diagnostic Imaging ; Heart Atria ; Humans

Sympathetic remodeling after myocardial infarction is presented as denervation, sympathetic nerve sprouting and sympathetic hyperinnervation, and is closely related to ventricular tachyarrhythmias and even sudden cardiac death at convalescence in patients with myocardial infarction. This article reviews the anatomic structure, morphology and functional remodeling of cardiac sympathetic nerve, as well as its role in healed myocardial infarction identification, which may provide references for forensic research.
Atrial Remodeling ; Forensic Sciences ; Heart ; Humans ; Myocardial Infarction/pathology*

BACKGROUND AND OBJECTIVES: The cardiac autonomic nervous system is an emerging target for therapeutic control of atrial fibrillation (AF). We evaluated the effects of low-intensity autonomic nerve stimulation (LI-ANS) on atrial electrophysiology, AF vulnerability, and neural remodeling. SUBJECTS AND METHODS: Fourteen dogs were subjected to 3 hours rapid atrial pacing (RAP, 5 Hz) and concomitant high frequency LI-ANS (20 Hz, at voltages 40% below the threshold) as follows: no autonomic stimulation (control, n=3); or right cervical vagus nerve (RVN, n=6), anterior right ganglionated plexi (ARGP, n=3), and superior left ganglionated plexi (SLGP, n=2) stimulation. Programmed and burst atrial pacing were performed at baseline and at the end of each hour to determine atrial effective refractory period (ERP), window of vulnerability (WOV), and inducibility of sustained AF. RESULTS: Atrial ERP was significantly shortened by 3 hours RAP (in control group, DeltaERP=-47.9+/-8.9%, p=0.032), and RAP-induced ERP shortening was attenuated by LI-ANS (in LI-ANS group, DeltaERP=-15.4+/-5.9%, p=0.019; vs. control, p=0.035). Neither WOV for AF nor AF inducibility changed significantly during 3 hours RAP with simultaneous LI-ANS. There was no significant difference between the control and LI-ANS group in nerve density and sprouting evaluated by anti-tyrosine hydroxylase and anti-growth associated protein-43 staining. Among the various sites for LI-ANS, the ARGP-stimulation group showed marginally lower DeltaWOV (p=0.077) and lower nerve sprouting (p=0.065) compared to the RVN-stimulation group. CONCLUSION: Low-intensity autonomic nerve stimulation significantly attenuated the shortening of atrial ERP caused by RAP. ARGP may be a better target for LI-ANS than RVN for the purpose of suppressing atrial remodeling in AF.
Animals ; Atrial Fibrillation ; Atrial Remodeling ; Autonomic Nervous System ; Autonomic Pathways* ; Dogs ; Electrophysiology* ; Ganglion Cysts ; Vagus Nerve

BACKGROUND AND OBJECTIVES: Oxidative stress (OS) plays an important role in the pathophysiology of atrial fibrillation (AF) by amplifying the inflammatory cascade, wherein augmented inflammation facilitates the atrial electrical remodeling process. Few studies have investigated the possible link between systemic inflammation and OS in AF. SUBJECTS AND METHODS: A total of 220 consecutive patients with AF (117 patients) or healthy controls (103 patients) were enrolled. Among the 117 AF patients, 65 paroxysmal AF (PaAF) and 52 persistent AF (PeAF) patients were included. The level of 8-iso-prostaglandin F2α (8-iso-PGF2α) was measured as a marker of OS burden. We evaluated the correlations between 3 systemic inflammatory markers, high-sensitivity C-reactive protein (hsCRP), neutrophil to lymphocyte ratio (NLR), and red cell distribution width (RDW), and 8-iso-PGF2α. RESULTS: The 8-iso-PGF2α concentration in both PaAF and PeAF patients was higher than that of controls (p<0.001 and p=0.024, respectively). The NLR and RDW of PeAF patients were higher than those of both control and PaAF patients (p=0.041 and p=0.031 for NLR, p=0.057 and p=0.031 for RDW, respectively). There were no correlations between specific inflammatory markers and the 8-iso-PGF2α in AF. The 8-iso-PGF2α level decreased gradually with an increase in AF duration (p=0.008), contrary to the graded increase in hsCRP. Multiple regression analysis indicated that AF duration persisted as a significant determinant of 8-iso-PGF2α (β=−0.249, p=0.044). CONCLUSION: Systemic inflammatory marker levels were not proportional to the levels of 8-iso-PGF2α, an OS marker, in AF.
Atrial Fibrillation* ; Atrial Remodeling ; C-Reactive Protein ; Erythrocyte Indices ; Humans ; Inflammation ; Lymphocytes ; Neutrophils ; Oxidative Stress*

BACKGROUND: trial fibrillation (AF) causes electrical remodeling of the atrium that plays an important role in increasing atrial vulnerability and the perpetuation of AF. The regional variation and heterogeneities of AF-induced electrical remodeling in patients with AF remain unclear. The purpose of present study was to test the hypothesis that regional heterogeneity of the atrial electrical properties including sinus node dysfunction is more apparent in patients with chronic AF than in patients with paroxysmal AF. METHODS: The study group consisted of chronic AF (CAF, n=19), paroxysmal AF (PAF, n=19) and control group (CON, n=13). Monophasic action potential duration 90% (MAPD90) and atrial effective refractory period (AERP) were measured at 9 different sites in the right atrium using MAP catheter. Dispersion of MAPD90 and AERP were calculated from the difference between the maximum and minimum value at 9 sites, respectively. Intra-atrial conduction time (IACT) was calculated from the distance between the earliest activation and the latest one of the electrograms by 20-pole steerable catheter with 2-mm interelectrode distance which was positioned along the tricuspid annulus anterior to the crista terminalis. To evaluate sinus node function, post shock sinus node recovery time (PSRT) was measured. A rate corrected PSRT (PSRTc) was calculated from the difference between PSRT and basic sinus cycle length. RESULTS: MAPD90 significantly shortened in patients with CAF (227.0+/-32.6 ms) compared with PAF (246.8+/-38.3 ms, p<0.05) and CON (239.1+/-39.3 ms, p<0.05), but AERP was not significantly different among 3 groups. The regional changes and dispersion of MAPD90 and AERP in patients with CAF did not differ from those of PAF and CON. IACT was prolonged in CAF group (73.8+/-22.5 ms) compared with PAF (58.2+/-8.0 ms, p<0.05) and CON groups (51.6+/-12.3 ms, p<0.05). IACT in CAF group (73.8+/-22.5 ms) was significantly prolonged compared with CON groups (51.6+/-12.3 ms, p<0.05) and was longer than that of PAF groups (58.2+/-8.0 ms) without statistical significance. PSRTc was longer in CAF group (758.3+/-525.8 ms) than in PAF group (209.5+/-125.0 ms, p<0.05). CONCLUSION: Electrical changes defined as shortened MAPD90, prolonged IACT and PSRTc were more apparent in patients with CAF compared with PAF. However, these were neither accompanied by the regional variations nor dispersion of refractoriness of the atrium. These findings suggest that regional heterogeneities of electrical properties are not related to the chronicity of atrial fibrillation.
Action Potentials ; Atrial Fibrillation* ; Atrial Remodeling ; Catheters ; Heart Atria ; Humans ; Population Characteristics ; Shock ; Sick Sinus Syndrome ; Sinoatrial Node

BACKGROUND: Pacing-induced atrial electrical remodeling (AER) is characterized by shortening of atrial effective refractory period (A-ERP) and its altered rate adaptation. In paroxysmal atrial fibrillation (AF), periods of AF occur with interveneing normal sinus rhythm (NSR) when atria recover from the preceding AER. Previous episodes of AF may precondition the atrial myocardium and cause different time course of AER in subsequent episodes of AF. But the influence of the preceding AER on the subsequent AER has not been described. METHODS: Four mongrel dogs were anesthetized with enflurane. After thoracotomy, silicon band with 3 pairs of electrodes was sutured to the lateral wall of the left atrium. Atrial pacing was performed after 2 wks of recovery and autonomic blockade. Pacing protocol consisted of rapid atrial pacing (RAP) at 500 bpm (for 60 min) and recovery in NSR (for 60 min) which was repeated three times. A-ERP was measured every 10 min. The same pacing protocol was repeated after pretreatment with verapamil (0.1 mg/kg/hr). RESULTS: 1) With 60 min of RAP, A-ERP decreased significantly (126+/-6 ms vs. 105+/-7 ms, p<0.005). 2) After cessation of pacing, A-ERP returned to 98% of baseline value in 15 minutes. Recovery from AER occurred faster than AER (78 vs 21 ms/h). 3) After pretreatment with verapamil, RAP decreased A-ERP from 127+/-5 ms to 116+/-5 ms. AER, the reduction in A-ERP, was significantly attenuated by pretreatment with verapamil (deltaERp=17+/-7 vs. 9+/-0.2 %, p<0.05). 4) When RAPs were repeated, AER showed a tendency of acceleration, but it was not statistically significant (deltaERp=22 ms, 24 ms, 28 ms at the end of 60 min pacing for the 1st, 2nd, 3rd pacing). CONCLUSION: RAP induced AER in conscious dog atria and it was reduced by pretreatment with calcium channel blocking agent, verapamil. Upon repeated atrial stimulations, AER did not accelerate or decelerate when the atria recovered from the preceding AER.
Acceleration ; Animals ; Atrial Fibrillation ; Atrial Remodeling* ; Calcium ; Calcium Channels ; Dogs* ; Electrodes ; Enflurane ; Heart Atria ; Myocardium ; Silicones ; Thoracotomy ; Verapamil

Animals ; Atrial Fibrillation ; physiopathology ; Atrial Remodeling ; physiology ; Calcium ; metabolism ; Humans ; Inflammation ; etiology ; Ion Channels ; physiology ; MicroRNAs ; physiology ; Oxidative Stress