Atrial tissue characterisation using electroanatomic voltage mapping and cardiac magnetic resonance imaging

Atrial fibrillation (AF) recurrence after catheter ablation (CA), often due to incomplete lesions, remains a challenge. In this study, we evaluate the role of cardiac magnetic resonance (CMR) in characterizing lesion formation and guiding re-ablation strategies in patients with paroxysmal AF undergoing radiofrequency catheter ablation (RFCA). This prospective, single-center study enrolled patients undergoing first-time RFCA for paroxysmal AF. Pre-ablation CMR was performed for functional, anatomical, and fibrosis assessment. Repeat CMR 3 months post-ablation was performed to quantify fibrosis using Image Intensity Ratio (IIR) and detect lesion gaps, defined as ≥ 3mm discontinuities in late gadolinium enhancement (LGE). AF recurrence was monitored for 18 months. 25 patients (20% female) were enrolled. 8/25 patients (32%) experienced AF recurrence. Post-ablation CMR showed significantly increased atrial fibrosis, though only in 2/25 patients (8%) complete circumferential pulmonary vein (PV) lesions were observed. Fibrosis burden did not differ significantly between patients with and without recurrence. Among 6 patients undergoing repeat ablation, 3 with LGE-defined gaps in circumferential lesions were successfully treated with a single re-isolation procedure. In contrast, 3 patients with extensive lesions and minimal or no gaps required multiple repeat procedures and additional ablation at extra-pulmonary vein sites. CMR can be a useful tool to assess post-ablation lesions and detect gaps after RFCA for paroxysmal AF. This may help distinguish recurrence due to insufficient initial ablation from other arrhythmogenic triggers, thereby guiding tailored and effective re-ablation strategies.

Funding Acknowledgements Type of funding sources: None. Background The recent introduction of Omnipolar Technology (OT) has the potential to improve ventricular substrate characterization. In fact, the amplitude of omnipolar electrograms is less dependent of the propagation direction of the recorded wavefront than that of bipolar electrograms, potentially increasing the sensitivity for the detection of viable myocardium by electroanatomical voltage mapping (EVM). Purpose To assess the presence and extension of dense scar regions and low-voltage areas in omnipolar voltage (OV) maps of the left ventricle (LV) as compared to standard bipolar endocardial maps and cardiac magnetic resonance (CMR)-derived pixel signal intensity (PSI) maps, among patients undergoing EVM-guided endomyocardial biopsy (EMB). Methods The study included 10 patients undergoing LV substrate mapping and EVM-guided EMB at our institution using the Advisor HD Grid mapping catheter. Before the procedure, contrast enhanced-CMR was obtained for each patient and PSI maps were derived from late gadolinium enhancement sequences with the ADAS-VT software. Scar core and border zone areas were measured in PSI endocardial (10-40% of wall thickness) maps and compared to dense scar regions (<0.5 mV) and low-voltage areas (0.5-1.5 mV) measured by standard bipolar endocardial mapping and OV endocardial mapping, respectively. Continuous variables were checked for normality with the Shapiro-Wilk test, and are reported as mean±standard deviation or median [1st-3rd quartile], as appropriate. Statistical comparisons among the three types of mapping (PSI mapping, standard bipolar, and OV) were performed with Friedman test with post-hoc sign test, as appropriate. P values<0.05 were considered statistically significant, and all analyses were performed with the software RStudio. Results The indication for EVM-guided EMB was a clinical suspicion of arrhythmogenic or inflammatory cardiomyopathy in all cases. Dense scar regions and low voltage areas detected by OV (dense scar: 2.2 [1.2-6.9] cm2; low voltage areas: 8±3.8 cm2) and standard bipolar mapping (dense scar: 3.4 [2.3-9.6] cm2; low voltage areas: 8.4±4 cm2) were similar to scar core and border zone areas shown by PSI maps (scar core: 1.6[0.6-2.9] cm2; border zone: 3.9[3.7-7.6] cm2; all p=NS). However, dense scar regions were less widespread with OV mapping that with standard bipolar mapping (Friedman test p=0.07; adjusted p=0.006, Figure). The diagnostic yield of EMB measured 80%, whereas mean procedural and fluoroscopy times were 136±30 min and 11±4 min, respectively. Conclusion OV mapping allowed a refinement of endocardial substrate maps of the LV as compared to standard bipolar mapping, by reducing the dependency of electrogram amplitude on the direction of propagation, thus allowing the detection of viable myocardium even in bipolar scar regions. Therefore, OV mapping may soon become a preferred approach for EVM-guided EMB.

Funding Acknowledgements ICMR Aims Association of atrial fibrillation (AF) is a common cause of morbidity and mortality in patients with rheumatic heart disease (RHD). Association of Atrial Fibrillation with inflammation is well delineated in nonvalvular AF as compared to Rheumatic AF. This study evaluated the presence of atrial inflammation, in patients with AF and rheumatic mitral stenosis (MS), using cardiac MRI and its correlation with inflammatory markers. Methods and Results Twenty RHD patients with predominant mitral stenosis were recruited for the study. Ten patients had persistent AF, three had paroxysmal AF and seven were in sinus rhythm. Patients with AF had lower mitral valve areas. Cardiac MRI showed evidence of late gadolinium enhancement (LGE) in the atrial wall in 61.54% (8/13) of patients with AF as compared with only 20% (1/5; p < 0.05) of patients in sinus rhythm. Mean levels of IL-6 were also significantly higher in patients with AF (10.62 ± 5.92 pg/mL versus 4.37 ± 2.68 pg/mL; P= 0.017). IL6 with a cutoff of ≥ 6.5 pg/mL was associated with a sensitivity of 76.92 % and specificity of 71.43 % for prediction of AF. There was also significant association between high IL-6 levels and LGE on MRI (13.13 ± 5.75 pg/mL vs 5.29 ± 3.23pg/mL; P < 0.05) Conclusion Patients with MS who developed AF show evidence of atrial inflammatory sequelae in the form of fibrosis as suggested by LGE on cardiac MRI. Systemic inflammation in the form of elevated IL-6 levels correlated significantly with atrial fibrosis and AF. Table 1: MS patients with or without AF Clinical Features Rhythm P-Value NSR (n = 7) AF (n = 13) Mean Valve Area (cm2) 1.28 ± 0.35 0.83 ± 0.26 < 0.01 Mean Diastolic Gradient (mmHg) 6.29 ± 2.2 11.92 ± 5.65 <0.01 Wilkin Score 7 ± 0.816 8.46 ± 1.66 0.04 LVEF % (non indexed) 59.57 ± 1.13 58.77 ± 2.89 0.49 LA Volume with MRI (ml) 127.50 ± 51.32 284.33 ± 133.12 <0.01 Inflammatory Markers hs-CRP (mg/L) 5.59 ± 3.89 3.94 ± 3.47 0.34 IL6 (pg/mL) 4.37 ± 2.68 10.62 ± 5.92 0.017 sCD-40L (ng/mL) 3.72 ± 3.73 4.77 ± 2.80 0.48 Atrial LGE 0 (0%) 8 (61.5%) 0.04 Abstract P89 Figure. Image 1: Cardiac MRI showing LGE

Searching for the Key to Foreseeing Left Atrial Fibrosis in Atrial Fibrillation: Could This Be Simple and Reliable with MRI?

This study aims to examine the association of clinical co-morbidities with the presence of left atrial (LA) late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR). Previous studies have established the severity of LA LGE to be associated with atrial fibrillation (AF) recurrence following AF ablation. We sought to determine whether baseline clinical characteristics were associated with LGE extent among patients presenting for an initial AF ablation. The cohort consisted of 179 consecutive patients with no prior cardiac ablation procedures who underwent pre-procedure LGE-CMR. The extent of LA LGE for each patient was calculated using the image intensity ratio, normalized to the mean blood pool intensity, corresponding to a bipolar voltage ≤0.3 mV. The association of LGE extent with baseline clinical characteristics was examined using non-parametric and multivariable models. The mean age of the cohort was 60.9 ± 9.6 years and 128 (72%) were male. In total, 56 (31%) patients had persistent AF. The mean LA volume was 118.4 ± 41.6 mL, and the mean LA LGE extent was 14.1 ± 10.4%. There was no association with any clinical variables with LGE extent by quartiles in the multivariable model. Extent of LGE as a continuous variable was positively, but weakly associated with LA volume in a multivariable model adjusting for age, body mass index, AF persistence, and left ventricular ejection fraction (1.5% scar/mL, P = 0.038). In a cohort of patients presenting for initial AF ablation, the presence of pre-ablation LA LGE extent was weakly, but positively associated with increasing LA volume.

Left atrial low-voltage areas predict atrial fibrillation recurrence after catheter ablation in patients with paroxysmal atrial fibrillation

BackgroundLeft atrial volume (LAV) and low voltage areas (LVAs) are acknowledged markers for worse rhythm outcome after ablation of atrial fibrillation (AF). Some studies reported the importance of increased right atrial volume (RAV) as a predictor for arrhythmia recurrences in AF patients.ObjectiveTo investigate association between the LAV/RAV ratio and LVAs presence.MethodsPatients undergoing first AF ablation were included. LVAs were assessed peri‐procedurally using high‐density 3D maps and defined as <0.5 mV. All patients underwent pre‐procedural cardiovascular magnetic resonance imaging. LAV (biplane) and RAV (monoplane 4‐chamber) were assessed prior to ablation, and the LAV/RAV ratio was calculated.ResultsThe study population included 189 patients (age mean 63 ± 10 years, 33% women, 57% persistent AF, 22% LVAs). There were 149 (79%) patients with LAV > RAV. In univariable analysis LAV > RAV was associated with LVAs (OR 6.803, 95%CI 1.395–26.514, p = .016). The association remained robust in multivariable model after adjustment for persistent AF, CHA2DS2‐VASc score, and heart rate (OR 5.981, 95%CI 1.256–28.484, p = .025). Using receiver operator curve analysis, LAV > RAV (AUC 0.668, 95%CI 0.585–0.751, p = .001) was significant predictor for LVAs. In multivariable analysis, after adjustment for age, persistent AF, and renal function, RAV≥LAV was threefold higher in males (OR 3.040, 95%CI 1.050–8.802, p = .04).ConclusionsLAV > RAV is useful for the prediction of electro‐anatomical substrate in AF. LAV > RAV was associated with LVAs presence, while male sex remained associated with RAV≥LAV and less LVAs.

Background Atrial fibrillation (AF) is related to left atrial fibrosis, but its identification by late magnetic resonance imaging (LGE) with gadolinium (LGE) persists in controversy due to heterogeneous results in its correlation with the electroatomic map (EAM) and the difficulty of perform histological studies in humans. Purpose We try to examine the point-by-point association between high density EAM and LGE-MRI using an automatic and reproducible method. Methods A LGE-MRI was performed in 16 patients prior to ablation. Three different areas were established depending on the intensity of normalized enhancement for each patient according to their blood group with the image intensity ratio (IIR) (healthy &amp;lt;1.20, border area (BZ) ≥1.20 &amp;lt;1.32 and scar ≥1.32). The high density electroanatomic maps of the left atrium (LA) were projected onto the MRI, obtaining an automatic correlation point by point. Results The study obtained significant differences (p &amp;lt; 0.001) between voltage (mV) and CV (mm/ms) among healthy, BZ and scar areas, as well a significant inverse correlation (p &amp;lt; 0.001) between voltage and IIR (R=-0.39). It obtained too a significant correlation between CV and IIR (R=-0.24), but this showed a greater correlation in those patients who have the least dilated LA (p = 0.02). Conclusions LGE-MRI and EAM showed good correlation in delineating potential pathologic substrate in AF, but left atrium dilation could reduce the performance of the CMR in this task. Conduction velocity could be more sensitive than voltage and LGE-MRI to detect incipient substrate in AF. Voltage and conduction velocity values Area /IIR Velocity (mm/ms) Voltage (mV) I / &amp;lt;.20 1.036(0.913-1.158) 1.593(1.489-1.696) 2 / ≥1.20 and &amp;lt;1.32 0.722(0.590-0.850) 0.792 (0.649-0,935) 3 / ≥1.32 0.623(0.473-0,733) 0.444(0.245-0.642) Voltage and conduction velocity values in the three areas of the LGE-RMN. Abstract Figure. Correlation among voltage, VC and LA

Funding Acknowledgements Type of funding sources: Private company. Main funding source(s): Abbott Background Pulmonary vein isolation (PVI) is a recommended approach for all atrial fibrillation (AF) ablation procedures, but PVI alone does not cure all AF. Supplementary substrate modification beyond PVI has mixed results. Identifying low voltage zones and ablating those targets in addition to PVI may be beneficial. Electroanatomic mapping is critical to identify subjects that may require further substrate modification. The amount of low voltage area may be predictive of the optimal treatment approach. Purpose This was a prospective, multicenter, interventional study of a high-density grid-style mapping catheter (HD Grid) to characterize left atrial (LA) low voltage substrate during sinus rhythm (SR) and AF in subjects undergoing de novo radiofrequency (RF) ablation for paroxysmal AF (PAF), early persistent AF (PsAF) (7 days-3 months) or non-early PsAF (&amp;gt;3 months-12 months) using a PVI only approach. Methods High-density voltage maps were collected with HD Grid during both SR and AF prior to ablation. Differences in low voltage area between (1) SR and AF and (2) simultaneous orthogonal bipole wave configuration (HDW) and standard along-the-spline linear electrode configuration (SD) were investigated. Results Three hundred subjects, enrolled at 18 centers in Europe and Israel, underwent PVI only RF ablation for PAF (N=113), early PsAF (N=79), and non-early PsAF (N=108). The average age was 62.0 ± 9.5 years and 70.3% (211/300) were male. SR maps and AF maps were available and evaluated in HDW and SD for 196 subjects (65.3%) (63 PAF, 65 early PsAF, 68 non-early PsAF). Mean LA surface area was 108.8 cm² and mean mapped surface area ranged from 83.2 to 89.5 cm². HDW maps showed less low voltage area compared to SD in all subgroups, both in AF and in SR (Figure). For example, in AF with a low voltage cutoff of 0.5 mV, mean low voltage area was 49.8 cm² using SD and only 45.6 cm² using HDW (p&amp;lt;.0001). Similarly, in SR with a low voltage cutoff of 0.5 mV, mean low voltage area was 16.1 cm² using SD and only 12.6 cm² using HDW (p&amp;lt;.0001). HDW showed significantly less low voltage area than SD in SR for all measured voltage cutoffs from 0.1 mV to 1.5 mV. On average, non-early PsAF subjects had a larger low voltage area than early PsAF subjects and PAF subjects in both SR and AF. In SR HDW, non-early PsAF subjects had 15.6 cm² under 0.5 mV, early PsAF subjects had 12.4 cm², and PAF subjects had 9.2 cm² (p=.0316). In AF HDW, non-early PsAF subjects had 56.6 cm² under 0.5 mV, early PsAF had 42.8 cm² and PAF subjects had 35.4 cm² (p&amp;lt;.0001). Conclusion Non-early PsAF subjects had the largest low voltage area on average compared to both early PsAF and PAF subjects in this study. Using HD grid, HDW provided better low voltage area characterization compared to SD in both SR and AF. The final results of this study will suggest whether an HDW substrate characterization of low voltage area can predict recurrences after a single PVI-only strategy procedure.

Veltmann C, Schimpf R, Steitner F, Hu D, Pfeiffer R, Borggrefe M, Wolpert C, Antzelevitch C. Electrocardiographic identification of SCN5A mutation carriers in a large European family. Europace Journal 2009, 11(Supplement 2), Abstract 34.Wijnmaalen AP, Van Der Geest RJ, Siebelink HJ, Kroft L, Bax JJ, Reiber JH, Schalij MJ, Zeppenfeld K. Integration of MRI derived 3D scar maps with electroanatomical mapping during catheter ablation of scar-related ventricular tachycardia late after myocardial infarction. Europace Journal 2009, 11(Supplement 2), Abstract 35.Algalarrondo VA, Dinanian SD, Juin CJ, Adams DA, Slama MS. Paroxystic AV block and prophylactic pacing in familial amyloid polyneuropathy. Europace Journal 2009, 11(Supplement 2), Abstract 36.# Electrocardiographic identification of SCN5A mutation carriers in a large European family {#article-title-2} Veltmann C, Schimpf R, Steitner F, Hu D, Pfeiffer R, Borggrefe M, Wolpert C, Antzelevitch C. Electrocardiographic identification of SCN5A mutation carriers in a large European family. Europace Journal 2009, 11(Supplement 2), Abstract 34.Wijnmaalen AP, Van Der Geest RJ, Siebelink HJ, Kroft L, Bax JJ, Reiber JH, Schalij MJ, Zeppenfeld K. Integration of MRI derived 3D scar maps with electroanatomical mapping during catheter ablation of scar-related ventricular tachycardia late after myocardial infarction. Europace Journal 2009, 11(Supplement 2), Abstract 35.Algalarrondo VA, Dinanian SD, Juin CJ, Adams DA, Slama MS. Paroxystic AV block and prophylactic pacing in familial amyloid polyneuropathy. Europace Journal 2009, 11(Supplement 2), Abstract 36.The loss-of-function SCN5A missense mutation E1784K leads to the Brugada and/or Long QT phenotype and to cardiac conduction disease. The aim of the present study was to perform a genotype-phenotype correlation in a large family with the E1784K mutation and to identify electrocardiographic markers capable of differentiating between mutation carriers and non-carriers. Methods: We screened a large 33-member European family. The work-up included the medical and family history (n=33), a baseline ECG (n=27), sodium blocker challenge (n=23) and genetic screening (n=27). Results: 27 members (28±15 years of age; 16 males, 11 females) were genotyped. In 17 of 27 patients (8 males, 9 females) a E1784K missense mutation was identified in SCN5A. Mutation carriers revealed significantly longer PR and QT intervals and QRS duration compared to non-carriers. (PQ: 195ms vs. 155ms, P<0.003; QT: 466ms vs. 415ms, P<0.0001, QRS: 100ms vs. 80ms; P<0.002). Using ROC analysis, QTc ≥ 445 ms was identified as a good predictor of a positive genotype (sensitivity 88%, specificity 100%). No patient showed a spontaneous Brugada type I ECG. 4 patients displayed a Brugada type II and III ECG. Out of 23 ajmaline tests 12 were positive, 8 negative und 3 were prematurely terminated due to QRS prolongation and premature ventricular contractions. All non-carriers revealed a negative ajmaline test (n=8). In 15 of 17 patients with positive genotype, ajmaline challenge was performed. 12 tests (80%) were positive and 3 tests were prematurely terminated. Conclusions: Our results indicate E1784K-SCN5A carriers have significantly longer PR, QT and QRS durations. 80% of mutation carriers and none of non-carriers display a Type I ST segment elevation characteristic of Brugada syndrome following challenge with sodium channel blockers. QTc interval ≥ 445 predicted the presence of the E1784K mutation. All non-carriers displayed normal ECG parameters. # Integration of MRI derived 3D scar maps with electroanatomical mapping during catheter ablation of scar-related ventricular tachycardia late after myocardial infarction {#article-title-3} Veltmann C, Schimpf R, Steitner F, Hu D, Pfeiffer R, Borggrefe M, Wolpert C, Antzelevitch C. Electrocardiographic identification of SCN5A mutation carriers in a large European family. Europace Journal 2009, 11(Supplement 2), Abstract 34.Wijnmaalen AP, Van Der Geest RJ, Siebelink HJ, Kroft L, Bax JJ, Reiber JH, Schalij MJ, Zeppenfeld K. Integration of MRI derived 3D scar maps with electroanatomical mapping during catheter ablation of scar-related ventricular tachycardia late after myocardial infarction. Europace Journal 2009, 11(Supplement 2), Abstract 35.Algalarrondo VA, Dinanian SD, Juin CJ, Adams DA, Slama MS. Paroxystic AV block and prophylactic pacing in familial amyloid polyneuropathy. Europace Journal 2009, 11(Supplement 2), Abstract 36.Background: The current used gold standard to guide substrate based ablation of scar-related ventricular tachycardia (VT) relies on electroanatomical endocardial and epicardial voltage mapping (EAM). Integration of the complex 3-dimensional (3D) scar geometry derived from contrast enhanced magnetic resonance imaging (CE-MRI) with EAM may provide supplementary substrate information. This study aimed to assess the feasibility of integrating CE-MRI derived data with EAM during radiofrequency catheter ablation (RFCA) of scar-related VT. Methods: 15 patients (14 male, 64±9yr) referred for RFCA of VT late after myocardial infarction underwent CE-MRI using a 1.5 T MRI system. Endocardial and epicardial contours of the CE-MRI were used to create 3D surface meshes of the left ventricle (LV), the aortic cusps and the left main (LM) origin. The vertices of the meshes were color coded based on the transmural extend of scar at a particular intramural location. Prior to ablation the MRI derived scar maps were imported into the CARTO-merge system. Bipolar endocardial EAM of the LV and aortic cusps were obtained and the LM location was marked. Areas with bipolar electrograms <1.5mV were defined as scar. Registration of the MRI derived scar maps and electroanatomical voltage maps was performed using the LM as landmark and the CARTO surface registration algorithm. Results: The average number of LV EAM points was 258±42. Merging of MRI derived scar data with voltage maps was successful in all patients with an average registration error of 3.8±0.6mm. There was a good agreement between regions of transmural scar defined by MRI and EAM. In 5 (33%) patients the subendocardial scar area identified by CE-MRI was larger than the scar area defined by EAM. Conclusions: Integration of MRI derived scar maps with EAM during VT ablation is feasible and accurate. CE-MRI derived scar maps identify intramural scar undetected by EAM and may provide important supplementary substrate information. # Paroxystic AV block and prophylactic pacing in familial amyloid polyneuropathy {#article-title-4} Veltmann C, Schimpf R, Steitner F, Hu D, Pfeiffer R, Borggrefe M, Wolpert C, Antzelevitch C. Electrocardiographic identification of SCN5A mutation carriers in a large European family. Europace Journal 2009, 11(Supplement 2), Abstract 34.Wijnmaalen AP, Van Der Geest RJ, Siebelink HJ, Kroft L, Bax JJ, Reiber JH, Schalij MJ, Zeppenfeld K. Integration of MRI derived 3D scar maps with electroanatomical mapping during catheter ablation of scar-related ventricular tachycardia late after myocardial infarction. Europace Journal 2009, 11(Supplement 2), Abstract 35.Algalarrondo VA, Dinanian SD, Juin CJ, Adams DA, Slama MS. Paroxystic AV block and prophylactic pacing in familial amyloid polyneuropathy. Europace Journal 2009, 11(Supplement 2), Abstract 36.Introduction: Familial amyloid polyneuropathy (FAP) is a dominantly inherited disease caused by mutated transthyretin. FAP cardiopathy is characterized by conduction disorders, denervation, and hypertrophic cardiomyopathy. Because of the risk of high degree atrioventricular (AV) block, prophylactic pacing can be suggested for high risk patients: in case of infra nodal AV block (HV interval > 70ms or between 60ms and 70ms with ECG abnormalities) or in case of unexplained syncope. By using pacing systems wich preserve physiological AV conduction, our purpose was to estimate prevalence of AV block and pacing dependance for high risk FAP patients. Methods: In a cohort of 29 FAP patients with conduction disorders leading to prophylactic pacing, we studied AV conduction using the AAI Safe R system (ELA medical). Datas were collected by using the Holter memories of pacemakers. Results: Patients were 50±15 years old and were followed during 13.7±11.9 months after pace maker insertion (12080 days cumulated). Before pace maker insertion, ECG was normal in 23% of cases. Electrophysiologic study showed 118±12ms for AH interval and 62±6ms for HV interval. Average percentage of ventricular pacing was 15±25%and 31±34% for atrial pacing. If 58% of patients (17/29) had less than 5% needs of ventricular pacing, we noted AV blocks episods for all patients but three (90%). Frequency of AV conduction disorders was 356±514 events per month (epm) and was distributed in 17±56 epm for type III AV block, 288±483 epm for type II AV block, 39±61epm for type I AV block and 1±4 for pauses. Percentage of ventricular pacing was positively correlated to frequency of AV block (R = 0.9, P<0.0001), to AH interval (R = 0.7, P = 0.003) and negatively to HV interval (R = -0.63, P = 0.007). During the study, sustained atrial arrhythmias occurred in two patients. No sustained ventricular arrhythmias were noted. Conclusion: Patients with FAP cardiopathy can present unpredictable paroxystic high degrees AV blocks. For patients with high risk of conduction disorders (HV interval >70ms, HV interval between 60ms and 70ms with ECG abnormalities or in case of unexplained syncope), prophylactic pacemaker insertion should be performed. Pacemaker features designed to promote spontaneous atrioventricular conduction allow a good AV conduction monitoring in FAP patients. Pre operative impairment of the nodal conduction is correlated to the rate of ventricular pacing with this stimulation mode.

Background/Introduction Left atrium LVAs are associated with impaired myocardial substrate and are known to contribute to the persistence of atrial fibrillation (AF). Understanding the significance of LVAs not only aids in refining ablation strategies but also enhances patient selection and risk stratification. Thus, identifying patients with LVA by using non-invasive methods such as a predictive risk score is an important endeavor. Purpose We sought to create and validate a simple and easy to use risk score as a clinical tool for identifying LVAs in patients undergoing AF catheter ablation. Methods Consecutive patients who underwent radiofrequency pulmonary vein isolation (PVI) for paroxysmal or persistent AF were included in this study. A sequential high-density 3D bipolar voltage map was constructed in all patients during sinus rhythm (SR), guided by a 3D electroanatomic mapping system. The cutoff value for LVA was defined as a bipolar voltage ≤ 0.5 mV measured in SR. LVA as percentage of the mapped left atrial surface in SR was also calculated. A novel low voltage area (LVA) prediction score, the P.A.L.A.H. risk score, was established. It includes P wave duration (PWD) on an electrocardiogram (PWD&amp;gt;120ms -1pt), Age (age &amp;gt;65 y/o-1pt, age&amp;gt;75y/o-2 pts), Left atrial diameter (LAD) (LAD&amp;gt;40mm-1pt), Arterial Hypertension (Arterial Hypertension- 1pt), Heart Failure (HF) (HF-2pt). Patients in the study were categorized into five distinct groups based on their P.A.L.A.H. score, which ranged from 0 to 5. Results One hundred and four consecutive patients (104) were included in our study [(age: 60.12±11.05 years; 50 men (48%)]. Sixty patients (60; 57.7%) suffered from paroxysmal AF. The highest P.A.L.A.H. score recorded was 5 (2.1±1.40). Regarding the LVA, significant differences between each value of P.A.L.A.H score and LVA value (p&amp;lt;0.0001) and LVA percentage (p&amp;lt;0.0001) were recorded (Figure 1,2). Conclusion(s) The P.A.L.A.H. score was significantly associated with the presence and extent of LVAs in patients undergoing AF catheter ablation. This relationship suggests that the P.A.L.A.H. score may serve as an important tool for risk stratification and clinical decision-making.P.A.L.A.H. score and LVAs percentage P.A.L.A.H. score and LVA value

Introduction: Atrial remodeling, characterized by changes in atrial structure and function, is central to the development and maintenance of atrial fibrillation (AF). Besides left atrial (LA) remodeling, right atrial (RA) remodeling may also contribute to AF perpetuation, and its presence may affect clinical outcome of AF ablation. Bi-atrial remodeling in patients with AF is rarely assessed and data on the presence of RA fibrosis, the relationship between RA and LA fibrosis, and possible association of RA remodeling with AF recurrence after ablation is limited. Methods: 110 AF patients undergoing initial pulmonary vein isolation (PVI) were included in the present study. Patients were in sinus rhythm during cardiac magnetic resonance (CMR) imaging performed prior to ablation. LA and RA volumes and function (volumetric and strain) were derived from cine CMR images. The extent of LA and RA fibrosis was assessed from 3D late gadolinium enhancement images. AF recurrence was followed-up for 12 months after PVI using either 12 lead ECGs or Holter monitoring. Results: Arrhythmia recurrence was observed in 39 patients (36%) after the 90-day blanking period, occurring at a median of 181 (IQR: 122-286) days. RA remodeling parameters were not significantly different between patients with AF recurrence as compared to patients without AF recurrence after ablation, whereas LA remodeling parameters were (volume, emptying fraction and strain). LA fibrosis had a strong correlation with RA fibrosis (r=0.88, P &lt;0.001). Both, LA and RA fibrosis was not different between patients with and without AF recurrence. Conclusions: RA remodeling parameters were not predictive of AF recurrence after AF ablation. Bi-atrial fibrotic remodeling is present in AF patients and the amount of LA fibrosis had a strong correlation with the amount of RA fibrosis. The presence of bi-atrial fibrotic tissue may be an expression of disease state although no relation with AF recurrence after AF ablation was found.

Although atrial arrhythmias may have genetic causes, very few data are available on evaluation of the arrhythmic substrate in genetic atrial diseases in humans. In this study, we evaluate the nature and evolution of the atrial arrhythmic substrate in a genetic atrial cardiomyopathy. Repeated electroanatomic mapping and tomographic evaluations were used to investigate the evolving arrhythmic substrate in 5 patients with isolated arrhythmogenic atrial cardiomyopathy, caused by Natriuretic Peptide Precursor A (NPPA) gene mutation. Atrial fibrosis was assessed using late gadolinium enhancement magnetic resonance imaging (LGE-MRI). The substrate of atrial tachycardia (AT) and atrial fibrillation (AF) was biatrial dilatation with patchy areas of low voltage and atrial wall scarring (in the right atrium: 68.5% ± 6.0% and 22.2% ± 10.2%, respectively). The evolution of the arrhythmic patterns to sinus node disease with atrial standstill (AS) was associated with giant atria with extensive low voltage and atrial scarring areas (in the right atrium: 99.5% ± 0.7% and 57.5% ± 33.2%, respectively). LGE-MRI-proven biatrial fibrosis (Utah stage IV) was associated with AS. Atrial conduction was slow and heterogeneous, with lines of conduction blocks. The progressive extension and spatial distribution of the scarring/fibrosis were strictly associated with the different types of arrhythmias. The evolution of the amount and distribution of atrial scarring/fibrosis constitutes the structural substrate for the different types of atrial arrhythmias in a pure genetic model of arrhythmogenic atrial cardiomyopathy.

In patients with atrial fibrillation (AF), extensive atrial tissue fibrosis identified by delayed enhancement magnetic resonance imaging has been associated with early recurrence of AF after catheter ablation. We present a case of a patient with extensive atrial fibrosis and AF recurrence.The study of late gadolinium enhancement with cardiac magnetic resonance imaging in patients with AF could be a valuable noninvasive tool for the selection of patients suitable for successful catheter ablation.

We sought to investigate the overlap between late gadolinium enhancement (LGE) in cardiac magnetic resonance (CMR) and electro-anatomical maps (EAM) of patients with non-ischaemic dilated cardiomyopathy (NIDCM) and how it relates with the outcomes after catheter ablation of ventricular arrhythmias (VA). We identified 50 patients with NIDCM who received CMR and ablation for VA. Late gadolinium enhancement was detected in 16 (32%) patients, mostly in those presenting with sustained ventricular tachycardia (VT): 15 patients. Low-voltage areas (<1.5 mV) were observed in 23 (46%) cases; in 7 (14%) cases without evidence of LGE. Using a threshold of 1.5 mV, a good and partially good agreement between the bipolar EAM and LGE-CMR was observed in only 4 (8%) and 9 (18%) patients, respectively. With further adjustments of EAM to match the LGE, we defined new cut-off limits of median 1.5 and 5 mV for bipolar and unipolar maps, respectively. Most VT exits (12 out of 16 patients) were found in areas with LGE. VT exits were found in segments without LGE in two patients with VT recurrence as well as in two patients without recurrence, P = 0.77. In patients with VT recurrence, the LGE volume was significantly larger than in those without recurrence: 12% ± 5.8% vs. 6.9% ± 3.4%; P = 0.049. In NIDCM, the agreement between LGE and bipolar EAM was fairly poor but can be improved with adjustment of the thresholds for EAM according to the amount of LGE. The outcomes were related to the volume of LGE.