Background: Radiofrequency ablation (RFA)is an important treatment option for patients with atrial fibrillation (AF). During RFA, a significant amount of energy is delivered into the left atrium (LA), resulting in considerable LA-injury. The impact of this damage on mechanical and endocrine LA-function, however, is often disregarded.We therefore aimed to evaluate the endocrine- and mechanical function of the heart 4-months after RFA of AF.

Methods: In total 189 patients eligible for RFA of AF were studied. The levels of the N-terminal pro-B-natriuretic peptide (NT-proBNP) and the mid-regional fragment of the N-terminal pro-atrial natriuretic peptide (MR-proANP)were measured. The maximum LAvolume (LAVmax),the LAejection fraction (LAEF) and the LA peak longitudinal strain (PALS), were measured usingtransthoracic echocardiography. The measurements were performed before and 4-months after the intervention.

Results: 87 patients had a recurrence during a mean follow-up of 143±36 days.NT-proBNPand MR-proANPdecreased significantly at follow-up. This reduction was greater in patients who did not suffer any recurrence after RFA.The LAVmax decreased significantly, whereasthe PALS only improved in patients who did not suffer from any recurrence. On the other hand, LAEF did not change significantly after RFA of AF.

Conclusions: Despite extensiveablation during RFA of AF, the endocrine function of the heart improved 4-months after the index procedure. Patients with no arrhythmia recurrence showed a more pronounced improvement in their endocrinal function. Mechanically, the LAVmax was reduced, and the LA strain improved significantly.

n/a

Surgical resection of a left ventricular aneurysm in the setting of ventricular tachycardia (VT) was first described by Couch in 1959. The technique was further developed by Dor et al. with performance of endocardiectomy and complete myocardial revascularization. Despite an attempt to remove the arrhythmogenic substrate, however, recurrences of VT remain an issue. Furthermore, the surgical technique used entails limited access to the potential area of interest with regard to a percutaneous catheter ablation procedure. We present a case report of a 65-year-old man who was referred for catheter ablation due to recurrent episodes of VT. He had undergone a coronary artery bypass surgery 8 years previously. During surgery, resection of an apical thrombus and reconstruction of an apical aneurysm with a Fontan stitch and an endoventricular patch were performed. The mapping and ablation procedure was aided by intracardiac echocardiography. During mapping, the ablation catheter was noticed to enter the apical pouch from the inferoseptal border of the endoventricular patch. During the ablation procedure, one of the VTs was successfully ablated in the inferior aspect of the apical pouch. This report confirms that the arrhythmogenic substrate underneath an endoventricular patch may be accessed in some instances and that these complex catheter ablation procedures may benefit from the use of intracardiac echocardiography.

Background: Focal atrial tachycardias are tachycardias characterized by a radial spread of activation from a discrete area of the atrial myocardium. They account for 10-15% of supraventricular tachycardias and are generally poorly responsive to pharmacological treatment. The pathophysiologic substrate of these arrhythmias remains poorly understood. Computational studies suggest that a certain degree of intercellular uncoupling and anisotropy are important prerequisites for the development of focal arrhythmias. The anisotropy and intercellular uncoupling could promote focal arrhythmias by minimizing the suppressive effect of the surrounding atrial muscle on the pacemaking process in the focus. This hypothesis would be in agreement with the fact that fractionated electrograms, a marker of anisotropy and reduced intercellular coupling, are often recorded at the site of earliest activated site. Reduced intercellular coupling could be induced by factors enhancing the amount of intracardiac connective tissue, such as advancing age or cardiac disease states. Indeed, focal inflammatory processes have been reported in atrial specimens resected from patients with focal tachycardia undergoing arrhythmia surgery.

Methods: In a group of patients with paroxysmal and permanent atrial fibrillation we sought to assess whether there is a link between inflammation and the occurrence of atrial arrhythmia. We therefore analyzed different inflammatory markers (C-reactive protein and interleukin-6 and 8) in the systemic and pulmonary circulation as well as in the heart in these patients. In addition, we assessed the extent of intercellular uncoupling in the vicinity of tachycardia origin in patients with focal atrial tachycardia. We also assessed the impact of electrogram fractionation on the method of activation time determination, by comparing different methods for estimating activation time with regard to the appearance of the resultant activation maps and the location of the foci. We also assessed the observer variability in the estimation of activation time during mapping of these tachycardias.

Results: There was no evidence of elevated circulatory levels of inflammatory markers in patients with paroxysmal atrial fibrillation. However, patients with permanent atrial fibrillation had increased levels of inflammatory markers (interleukin-8) in the systemic circulation but not in the pulmonary circulation or in the heart. In patients with focal atrial tachycardia, a higher degree of electrogram fractionation existed in the region surrounding the earliest activation site and activated within the first 15 ms as compared with the remaining atrium. Moreover, within this region, from the periphery towards the earliest activated site, there was a gradual increase in electrogram fractionation as well as a gradual decrease in the peak-to-peak voltage. When comparing different methods for estimating local activation time we found that different methods can generate activation maps with different appearances and foci with different locations. However, regardless of the method of activation time determination, the foci tend to cluster within relatively large areas of low-amplitude fractionated electrograms. In addition we found significant observer variability in the estimation of the local activation time.

Conclusion: Patients with paroxysmal atrial fibrillation (and probably focal atrial tachycardia) do not have elevated levels of inflammatory markers. The increased levels of interleukin-8 in the systemic circulation suggest a link between long-lasting arrhythmia and inflammation. A relatively wide area of increased electrogram fractionation exists around the site of origin of focal atrial tachycardia. These findings suggest a sizeable atrial region with particular electrophysiological proprieties and raise the possibility of an anatomical substrate of the tachycardia. Increased electrogram fractionation can impact the process of activation determination, as suggested by the fact that different methods compute foci with different locations. In addition, there is significant observer variability in the estimation of local activation time in these patient.

AIMS: Elevated levels of C-reactive protein and other inflammatory markers have been reported in some patients with atrial fibrillation (AF). Whether this finding is related to AF per se or to other conditions remains unclear. In addition, the source of inflammatory markers is unknown. Therefore, in the present study, we sought to assess the extent and the source of inflammation in patients with AF and no other concomitant heart or inflammatory conditions.

METHODS AND RESULTS: The study group consisted of 29 patients referred for radiofrequency catheter ablation: 10 patients with paroxysmal AF, 8 patients with permanent AF, and 10 control patients with Wolf-Parkinson-White (WPW) syndrome and no evidence of AF (mean age 54 +/- 11 vs. 57 +/- 13 vs. 43 +/- 16). No patient had structural heart diseases or inflammatory conditions. High-sensitive C-reactive protein, interleukin-6 (IL-6), and interleukin-8 (IL-8) were assessed in blood samples from the femoral vein, right atrium, coronary sinus, and the left and right upper pulmonary veins. All samples were collected before ablation. Compared with controls and patients with paroxysmal AF, patients with permanent AF had higher plasma levels of IL-8 in the samples from the femoral vein, right atrium, and coronary sinus, but not in the samples from the pulmonary veins (median values in the femoral vein: 2.58 vs. 2.97 vs. 4.66 pg/mL, P = 0.003; right atrium: 2.30 vs. 3.06 vs. 3.93 pg/mL, P = 0.013; coronary sinus: 2.85 vs. 3.15 vs. 4.07, P = 0.016). A high-degree correlation existed between the IL-8 levels in these samples (correlation coefficient between 0.929 and 0.976, P < 0.05). No differences in the C-reactive protein and IL-6 levels were noted between the three groups of patients.

CONCLUSION: The normal levels of C-reactive protein and IL-6, along with the elevated levels of IL-8 in patients with permanent AF but not in those with paroxysmal AF, suggest a link between a low-grade inflammatory reaction and long-lasting AF. The elevated IL-8 levels in the peripheral blood, right atrium, and coronary sinus but not in the pulmonary veins suggest a possible source of inflammation in the systemic circulation.

BACKGROUND Disease progression in patients with nonischemic cardiomyopathy (NICM) is poorly understood. OBJECTIVE To assess left ventricular(LV) scar progression and dilatation by using endocardial electroanatomic mapping. METHODS We studied 13 patients with NICM and recurrent ventricular tachycardia. Two detailed sinus rhythm endocardial voltage maps(265 +/- 122 points/map) were obtained after a mean of 32 months(range 9-77 months). The scar area, defined by low bipolar (BI; less than 1.5 mV) and unipolar(UNI; less than 8.3 mV) endocardial voltage, and the LV volume were measured and compared. A scar difference of greater than 6% of the LV surface and an increase in LV volume of greater than= 20 mL were considered beyond measurement error. RESULTS Six (46%) patients had an increase in scar area beyond boundaries of prior ablation. Five patients had an increase in UNI and 1 patient had an increase in both BI and UNI areas. The increase in BI area represented 16% and the increase in UNI area represented 6.5%-46.2% of the LV surface. A significant decrease in LV ejection fraction was found only in patients with scar progression (from 39% +/- 8%:p = .0003) (LV volume increase ranging between 9% and 23%) was noted in 3 patients, all of whom had scar progression. CONCLUSIONS Progressive scarring with an increase in the area of UNI and less commonly BI electrogram abnormality is seen in 46% of the patients with NICM and ventricular tachycardia and is associated with LV dilatation and decrease in LV ejection fraction. The prominent UNI abnormality suggests predominantly midmyo-cardial or epicardial scarring.

Background: Different algorithms of estimating local activation time (LAT) can be usedduring the mapping of focal atrial tachycardia (FAT).

Objective: The impact of these algorithms on the reproducibility of LAT measurementand the location of the focus.

Methods: Fifteen patients (48 ± 17 yrs) with FAT were studied. Three independentobservers reviewed 1438 bipolar electrograms and successively assigned the LAT on thepeak amplitude (Bi-peak), the steepest downslope (Bi-dslope), and the onset (Bi-on) ofthe electrograms. The reproducibility of LAT measurement was estimated.

Results: The mean interobserver absolute differences in LAT for the three algorithmswere 1.47 ± 2.75 ms (Bi-peak) vs. 2.15 ± 3.89 ms (Bi-dslope) vs. 2.87 ± 3.47 (Bi-on) (p <0.0001). The corresponding intraobserver differences were 2.29 ± 3.74 ms (Bi-peak) vs2.47 ± 4.17 ms (Bi-dslope) vs 3.16 ± 4.49 ms (Bi-on) (p < 0.0001). The interobserverdifferences in the location of the focus were 3.57 ± 3.81 mm (Bi-peak) vs 5.47 ± 4.98mm (Bi-dslope) vs 6.57 ± 6.94 mm (Bi-on) (p = 0.03), with differences of up to 13 mm(Bi-peak), 16 mm (Bi-dslope), and 25 mm (Bi-on). However, regardless of the method ofLAT determination, the foci computed by the three observers clustered within regions oflow-amplitude fractionated electrograms.

Conclusions: Significant observer variability exists among the three algorithms, whichtend to compute different LAT and foci with different locations. However, the foci aresituated in regions of low voltage fractionated electrograms.

The present study sought to assess the extent of gender differences in electrophysiologic parameters in patients with atrioventricular nodal reentrant tachycardia (AVNRT). The study population consisted of 203 patients (women/men ratio 2:1) who underwent slow pathway ablation. Patients with associated heart disease experienced the first episode of tachycardia at a significantly older age than patients with lone AVNRT (women 50 ± 18 vs 29 ± 15 years, p <0.0001, men 45 ± 20 vs 31 ± 17 years, p = 0.01). Sinus cycle length (797 ± 142 vs 870 ± 161 ms, p = 0.0001), HV interval (41 ± 7 vs 45 ± 8 ms, p = 0.0001), atrioventricular (AV) block cycle length (348 ± 53 vs 371 ± 75 ms, p = 0.01), slow pathway effective refractory period (ERP) (258 ± 46 vs 287 ± 62 ms, p = 0.006), and tachycardia cycle length (354 ± 58 vs 383 ± 60 ms, p = 0.001) were shorter in women. No gender differences were noted in fast pathway ERP and ventriculoatrial (VA) block cycle length. In women, an AV block cycle length <350 ms along with a VA block cycle length <400 ms predicted tachycardia induction without the need for autonomic intervention, with a positive predictive value of 93% (sensitivity 71%, specificity 82%). No such cut-off values could be found in men. The acute success rate (100% vs 98%) and the recurrence rate (3% vs 6%) were similar for the 2 genders. In conclusion, in patients with lone AVNRT, the onset of symptoms occurred at a younger age than in patients with concomitant heart disease. Women had shorter slow pathway refractory periods, AV block cycle lengths, and tachycardia cycle lengths. No gender differences were noted in the fast pathway ERP. Therefore, women have a wider "tachycardia window" (i.e., the difference between the fast and slow pathway refractory periods), a finding that may explain their greater incidence of AVNRT. © 2006 Elsevier Inc. All rights reserved.

The term "nonischemic cardiomyopathy" (NICM) designates a myocardial disease characterized by mechanical and/or electrical dysfunction in the absence of significant coronary artery disease, valvular heart disease, hypertension, or congenital heart disease. Although sustained ventricular tachycardia (VT) occurs in only 5% of patients with NICM, it is an important cause of sudden cardiac death. In this review we summarize the current understanding of the anatomic and electrophysiologic substrates of VT in the different types of NICM. In addition, we discuss recent progress and experience with catheter ablation of VT in these patients. 

Purpose

Different methods can be used to estimate activation time during the mapping of focal atrial tachycardia. The present study aimed to compare activation maps generated by three widely used methods of determining activation time.

Methods

Fourteen patients (mean age 48 ± 17 years) with focal atrial tachycardia were investigated. Mapping was performed with the CARTO system. All patients underwent successful ablation. Local activation time was successively defined as the peak amplitude (Bi-peak), the steepest downslope (Bi-dslope), and the onset (Bi-on) of the bipolar electrograms.

Results

The three methods of activation time determination were highly correlated with one another but generated foci with different locations. The distances between the foci generated by the different methods were 4.36 ± 4.91 mm (Bi-peak–Bi-dslope), 7.21 ± 5.11 mm (Bi-peak–Bi-on), and 7.21 ± 5.87 mm (Bi-dslope–Bi-on) (p = 0.26). Also, the three methods generated foci with different diameters: 3.13 ± 2.17 mm for Bi-peak, 2.81 ± 0.78 for Bi-dslope, and 2.54 ± 0.14 mm for Bi-on (p = 0.60). However, the foci tended to cluster within relatively wide regions of low-amplitude fractionated electrograms. The surface of these regions was 3.81 ± 2.34 cm² (Bi-peak), 3.38 ± 2.12 cm² (Bi-dslope), and 4.76 ± 3.01 cm² (Bi-on) (p = 0.34).

Conclusion

The three methods of activation time determination, although highly correlated with one another, may generate foci of different sizes and in different locations. However, the foci tend to cluster within relatively large areas of low-amplitude fractionated electrograms. These findings suggest a sizeable atrial region with particular electrophysiological proprieties and raise the possibility of an anatomical substrate of the tachycardia. During mapping, this region can be roughly delineated by all three methods of activation time estimation. However, details concerning the activation pattern within the region and the location of the focus vary among the methods.

P values of P < 0.0001 should have been given in the abstractfor the increase within the region activated during the first15 ms of both the incidence of bipolar electrograms with multiplenegative deflections and of the incidence of unipolar electrogramswith multiple negative deflections.

In the section ‘Characteristics of electrograms in theregion surrounding the earliest activation site and in the remainingatrium’ the P value for bipolar voltage should be P <0.0001, not P < 0001. In the same section the P value forthe decrease of unipolar and bipolar peak-to-peak voltage shouldbe P < 0.0001, not P < 0001.

Aims: Fractionated electrograms are often noted during mapping of focal atrial tachycardia (FAT). This finding suggests poor cell-to-cell coupling, which is thought to be an important prerequisite in the process of ectopic impulse initiation and propagation. The purpose of the present study was to assess the electrogram fractionation in the vicinity of the earliest activation site and in the remaining atrium in these patients.

Methods and results: Thirteen patients with FAT (age 48 ± 17 years) who underwent catheter ablation were investigated. Mapping was performed with the CARTO system. Electrogram fractionation was assessed on the basis of the number of negative deflections, both in the region surrounding the earliest activation site and in the remaining atrium. Unipolar and bipolar peak-to-peak voltage and bipolar electrogram duration were also studied. All patients underwent successful radiofrequency ablation. A higher degree of electrogram fractionation existed in the region surrounding the earliest activation site and activated within the first 15 ms when compared with the remaining atrium (incidence of bipolar electrograms with multiple negative deflections: 88 vs. 79%, P < 0.0001; incidence of unipolar electrograms with multiple negative deflections: 56 vs. 43%, P = 0.0001). The peak-to-peak voltage in the region activated within the first 15 ms was less than that in the remaining atrium (bipolar voltage: 1.33 ± 0.99 vs. 1.61 ± 1.11 mV, P < 0.001; unipolar voltage: 1.75 ± 0.92 vs. 1.95 ± 1.11 mV, P = 0.0188). There were no significant differences in bipolar electrogram duration. Within the region activated during the first 15 ms, from the periphery to the earliest activation site, there was a gradual increase in electrogram fractionation (incidence of bipolar electrograms with multiple negative deflections gradually increasing from 82 to 100% and incidence of unipolar electrograms with multiple negative deflections increasing from 56 to 90%), as well as a gradual decrease in peak-to-peak voltage (bipolar voltage gradually decreasing from 1.47 ± 1.06 to 0.89 ± 0.54 mV, P < 0.0001; unipolar voltage gradually decreasing from 1.89 ± 0.94 to 1.30 ± 0.63 mV, P < 0.0001). Irregular, closely spaced isochrones were also noted in the region activated during the first 15 ms. The area of this region was 4.88 ± 3.59 cm².

Conclusion: Increased electrogram fractionation exists within a relatively wide region around the tachycardia origin when compared with the remaining atrium. Moreover, this region is electrically heterogeneous, as suggested by the fact that the degree of electrogram fractionation increases gradually whereas the electrogram voltage decreases gradually towards the earliest activation site. These findings suggest that a non-discrete atrial region with gradually changing electrophysiological properties may underlie the substrate of FAT.

Premature ventricular complex (PVC) is common in the general population. Symptoms vary from none to pronounced. The prognostic significance of PVCs depends on the presence of underlying structural heart disease. The clinical evaluation in patients with PVC aims at excluding structural heart disease and usually involves transthoracic echocardiogram and Holter. Patients without structural heart disease usually have a good prognosis. Frequent PVCs may cause impaired left ventricular function, which usually is reversible after treatment with drugs or ablation. A 12-lead ECG provides important information about PVC localization, however anatomical factors such as the hearts localization in the thorax as well as electrode placement and pharmacological treatment may affect the ECG appearance. In symptomatic patients with or without left ventricular impairment, pharmacological treatment or catheter ablation is indicated. However, in most cases the main goal is to reasure the patient of the good prognosis. To summarize, treatment of choice depends on symptoms, comorbidities, left ventricular function and patients choice.

BACKGROUND: Anatomic studies have reported the presence of shared myocardial fibers between approximately half of ipsilateral pulmonary veins (IPVs).

OBJECTIVE: The purpose of this study was to assess the prevalence of electrical connection between IPVs and the impact of antral isolation with or without carina ablation on IPV connection.

METHODS: Thirty consecutive patients undergoing atrial fibrillation (AF) ablation (14 redo) were included. Wide antral pulmonary vein isolation (PVI) was performed with or without carina lesions. For each PV set, IPV electrical connection was assessed before and after PVI by pacing and recording from the ostium of both IPVs using a circular mapping catheter and the ablation catheter. Adenosine was given after PVI to assess for acute PV reconnection.

RESULTS: Before PVI without preceding AF ablation procedure, all the PVs had ipsilateral connection albeit frequently via the left atrium. After PVI, 65.6% of the IPVs were connected without carina ablation vs 17.7% if prior carina ablation (P = .001). Left vs right IPVs were connected in 57.1% and 72.2% of the cases without carina ablation, respectively, vs 30% and 0% of cases with carina ablation (P = .19 and P = .001). When transient PV reconnection was demonstrated during adenosine challenge, connected IPVs uniformly demonstrated simultaneous reconnection.

CONCLUSION: Electrical connection between IPVs is uniformly demonstrated before any ablation. Two-thirds of the IPVs are connected after antral PVI, and carina ablation decreases IPV connection. Connected IPVs consistently show the same response to adenosine challenge; therefore, a single catheter positioned in either of the IPVs with electrical connection is sufficient to confirm reconnection in both veins.

INTRODUCTION: Capture of the myocardial sleeves of the pulmonary veins (PV) during PV pacing is mandatory for assessing exit block after PV isolation (PVI). However, previous studies reported that a significant proportion of PVs failed to demonstrate local capture after PVI. We designed this study to evaluate the prevalence and the clinical significance of loss of PV capture after PVI.

METHODS AND RESULTS: Thirty patients (14 redo) undergoing antral PVI were included. Before and after PVI, local PV capture was assessed during circumferential pacing (10 mA/2 milliseconds) with a circular multipolar catheter (CMC), using EGM analysis from each dipole of the CMC and from the ablation catheter placed in ipsilateral PV. Pacing output was varied to optimize identification of sleeve capture. All PVs demonstrated sleeve capture before PVI, but only 81% and 40% after first time and redo PVI, respectively (P < 0.001 vs. before PVI). In multivariate analysis, absence of spontaneous PV depolarizations after PVI and previous PVI procedures were associated with less PV sleeve capture after PVI (40% sleeve capture, P < 0.001 for both). Loss of PV local capture by design was coincident with the development of PV entrance block and importantly predicted absence of acute reconnection during adenosine challenge with 96% positive predictive value (23% negative predictive value).

CONCLUSION: Loss of PV local capture is common after antral PVI resulting in entrance block, and may be used as a specific alternate endpoint for PV electrical isolation. Additionally, loss of PV local capture may identify PVs at very low risk of acute reconnection during adenosine challenge.