Image Integration to Identify Histologic and Electroanatomic Ventricular Scar: A Clinicopathological Study Comparing 2 Image Integration Systems.

Noninvasive assessment of the ventricular arrhythmogenic substrate using electrocardiographic imaging during sinus rhythm: The NIAVAS study.

Late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) imaging distinguishes between intrinsic postinfarction scar and radiofrequency ablation lesion related scar (dark core lesions [DCLs]) in patients with prior ventricular tachycardia (VT) ablation procedures. To combine LGE-CMR and electroanatomic mapping data to describe the relationship between DCLs and recurrent VT among patients undergoing repeat ablations for postinfarction VT. Consecutive patients with repeat ablation for postinfarct VT with LGE-CMR before the repeat procedures were studied. Prior ablation procedures and implantable cardiac defibrillator electrograms were analyzed to determine new versus previously documented VT. DCLs were identified on preprocedure LGE-CMR and registered to electroanatomic maps. A control group of patients undergoing repeat ablation procedures without imaging was included. Nineteen study patients and 14 control patients were followed for 2.6 (1.6-5.6) years (31 [94%] men, age 65.8 ± 8.4 years, ejection fraction 24.7 ± 10.3, p > 0.10 for all). DCLs corresponded to unexcitable tissue during repeat procedures (area 22.4 ± 15.1 vs. 22.9 ± 16.8 cm3 , correlation coefficient = .93). Most VT target sites (39/50 [78%]) were in close proximity (<1 cm) to DCLs. Most DCL related VTs 32/39 (82%) were new VTs. Patients with LGE-CMR imaging incorporated into their ablation procedures had improved 24-month survival from VT (64% vs. 38%, log rank p < 0.02). LGE-MRI can identify prior ablation lesions corresponding to nonexcitable tissue during repeat ablation procedures for postinfarction VT. VT target sites are often located in close proximity to the DCL area that may function as a fixed border for reentry circuits. Registration of DCL from prior ablation may facilitate repeat ablation procedures.

Intracardiac Echocardiography for the Detection of Arrhythmogenic Periaortic Ventricular Tachycardia Substrate: Multimodality Core Lab Analysis.

Cardiac Magnetic Resonance-Guided Ventricular Tachycardia Substrate Ablation

Advanced postprocessing of late gadolinium enhancement cardiac magnetic resonance (CMR) and computed tomography (CCT) imaging increasingly guides ventricular tachycardia ablation. However, a direct comparison between 2 widely adopted platforms, ADAS 3D LV (Adas3D Medical) and inHEART (IHU Liryc/Inria), is lacking. This study aimed to compare CMR- and CCT-derived ventricular substrate models generated by ADAS 3D and inHEART in patients with ischemic and nonischemic cardiomyopathy undergoing ventricular tachycardia ablation. Patients who underwent both CCT and late gadolinium enhancement CMR before ablation were retrospectively included. ADAS 3D models were generated on-site, whereas inHEART models were processed remotely. Substrate models were evaluated using a custom scoring system incorporating quantitative (scar mass, transmurality) and qualitative parameters (wall thickness, scar delineation, and conduction corridors). Electroanatomic maps (EAMs) assessed correspondence between low-voltage and ablation regions, with imaging-defined corridors. 16 patients (n = 8 ischemic, n = 8 nonischemic) were analyzed; 12 had detailed EAM data. Scar core and border zone measurements were comparable between platforms in both subgroups (all P > .05). ADAS 3D showed slightly higher visualization scores, particularly in nonischemic cardiomyopathy, although differences were not statistically significant. Spatial concordance between imaging-derived scar and EAM-defined ablation areas was good to excellent in 10 of 12 cases. ADAS 3D and inHEART demonstrated high concordance in scar quantification and substrate characterization, with comparable performance across cardiomyopathy types. Given their complementary strengths, platform choice should be guided by procedural goals, imaging availability, operator experience, and institutional context, as each system offers distinct advantages. Prospective studies are needed to evaluate the impact on procedural success and long-term outcomes.

Nonischemic cardiomyopathy (NICM) is responsible for approximately one-third of heart failure and is associated with significant morbidity and mortality. Recent data suggested the lack of mortality reduction from adding a defibrillator to cardiac resynchronization therapy (CRT) in all patients with NICM. Myocardial fibrosis detected by cardiac magnetic resonance late gadolinium enhancement (CMR-LGE) can help risk stratify patients who would benefit from adding a defibrillator to CRT in this patient population. We aim to assess the relationship between the presence of myocardial fibrosis detected by CMR-LGE and the rate of major arrhythmic events (MAE) that included sustained ventricular tachycardia (VT), appropriate cardiac resynchronization therapy-defibrillator (CRT-D) intervention, ventricular fibrillation (VF), and sudden cardiac death (SCD) in patients with NICM undergoing CRT and to compare all-cause mortality and heart failure improvement between patients receiving cardiac resynchronization therapy-pacing (CRT-P) versus those receiving CRT-D based on the presence of myocardial fibrosis. All consecutive patients with NICM satisfying a guideline-directed indication for CRT implantation were included in the study after excluding patients who refused to consent, patients with acute decompensated heart failure, and those contraindicated for a cardiac magnetic resonance (CMR). Patients were divided into two groups based on the presence of fibrosis in cardiac MRI: the LGE/CRT-D group and the No LGE/CRT-P group. They were then followed for 1 year. Sixty patients were enrolled. Sixteen patients (26.6%) developed MAE during the study duration, among those patients, seven had myocardial fibrosis (receiving CRT-D as per protocol), while nine had no myocardial fibrosis (receiving CRT-P as per protocol), (41.2%vs. 20.9%, p = 0.045). The presence of CMR-LGE, regardless of the extent and distribution, predicted MAE with an odds ratio of 2.6 (CI = 1.78-8.9, p = 0.04). The presence of ≥7.5% of myocardial fibrosis by CMR was associated with 54% sensitivity and 100% specificity for MAE in the study population. All-cause mortality was significantly higher in the No LGE/CRT-P group versus the LGE/CRT-D group (15 [34.9%] vs. 2 [11.8%], p = 0.076). In patients with NICM candidates for biventricular pacing, the presence of LGE on CMR, irrespective of the extent or segmental pattern, is independently associated with an MAE and is associated with worse heart failure outcomes. However, the absence of LGE did not rule out MAE, and implanting CRT-P based on lack of fibrosis may result in higher all-cause mortality.

Introduction: Recently, in patients with hypertrophic cardiomyopathy (HCM), an abnormal serum concentration of cardiac troponin (cTn), which is a sensitive marker of myocyte injury, was reported to be an independent predictor of the adverse outcome. In addition, late gadolinium-enhancement (LGE) cardiac magnetic resonance (CMR) imaging, which has been used to uniquely characterize the extent of myocardial fibrosis, has prognostic value in HCM. However, the relationship between myocyte injury, fibrosis, and clinical events/manifestations remains unclear. Hypothesis: A combined analysis using cTn and LGE by CMR may help to identify the clinical events/manifestations in patients with HCM. Methods: Eighty-seven HCM patients receiving regular outpatient treatment underwent CMR (cine and LGE imaging). LV myocardial fibrosis mass index (FMI) was quantified and the distribution/pattern of LGE was analyzed using 17 segment model. Serum cTnI was measured within a week around CMR testing. cTnI elevation was defined as ≥ 0.05ng/mL. Clinical events were defined as heart failure (HF) admission, ventricular tachycardia (VT), atrial fibrillation, and syncope. Results: In total patients, mean age was 65.7 ± 15.0 years old and female patients were 41.4%. HF and VT events were observed in 22 (25%) and 16 (18%) patients, respectively. Both elevated cTnI and higher FMI were associated with the combined clinical events (P&lt;0.01 and P&lt;0.05, respectively). Elevated cTnI was associated not with HF (P=0.06), but with VT (P&lt;0.001). In contrast, higher FMI was associated with HF (P=0.01), but not with VT (P=0.67). A grouping according to both cTnI and FMI showed the good stratification for clinical events as shown in the figure. Conclusions: In HCM patients, both cTn and FMI were significant markers for clinical events in HCM patients. In particular, elevated cTn was strongly associated with VT. Combined analysis of cTn and CMR may be useful in clinical practice for HCM.

Percutaneous coronary intervention (PCI) in acute myocardial infarction (AMI) is sometimes complicated by microvascular damage and hemorrhage. Hemoglobin degradation products have magnetic susceptibility effects which help in detecting hemorrhagic AMI by T₂ -weighted cardiac magnetic resonance (CMR) images. To investigate the possibility to detect intramyocardial hemorrhage after AMI and to assess its contribution to the delayed hypoenhanced core on late gadolinium enhancement (LGE) CMR, a feature traditionally referred to as microvascular obstruction. Consecutive patients with AMI who underwent PCI and CMR were investigated. Hypointense zones T₂ -weighted images were labelled as "hemorrhagic" AMI. Areas of late hypoenhancement on LGE CMR were considered as regions of persistent microvascular damage (PMD). Only transmural AMI were considered. A total number of 108 transmural AMI patients were eventually enrolled and divided into two groups according to the presence of hypoenhancement on T₂ images. Thirty-two patients showed an hypointense stria within the high signal intensity zone on T₂ -weighted images; all these patients showed midmural PMD on LGE. Among the remaining 76 patients, only 14 (18.4%) showed PMD in the subendocardial region. The angiographic outcome was worse in patients with hemorrhagic AMI, with a lower prevalence of TIMI 3 (65.6% vs. 96.1%, P = 0.017) and higher prevalence of myocardial blush grade 0 (84.4% vs. 13.2%, P < 0.001) post-PCI. T₂ -weighted CMR in reperfused AMI allows identification of hemorrhage, related to PMD areas on LGE images and to a worse reperfusion profile on angiography. These features open new avenues of investigation for prognostic assessment of reperfused AMI.

to evaluate the diagnostic accuracy of late iodine enhancement (LIE) in cardiac computed tomography (CCT) compared to late gadolinium enhancement (LGE) in cardiac magnetic resonance (CMR) for myocardial tissue characterization. EMBASE, PubMed/MEDLINE, and CENTRAL were searched for studies reporting the accuracy of LIE with LGE as the gold standard of reference. QUADAS-2 tool was used to assess the risk of bias. A bivariate random-effects model was used to analyze, pool, and plot the diagnostic performance measurements across studies. Pooled sensitivity, specificity, positive (+LR) and negative (-LR) likelihood ratio, diagnostic odds ratio (DOR), and hierarchical summary ROC curve (HSROC) were computed. Prospero registration number: CRD42023484045. Fourteen studies involving 526 patients and 5758 myocardial segments were included. At the patient level, LIE in CCT showed a pooled sensitivity of 0.96 (95% CI: 0.88-0.99), specificity of 0.95 (95% CI: 0.88-0.98) and the HSROC AUC of 0.98 (95% CI: 0.97-0.99). The +LR was 20.97 (95% CI: 7.54-58.38) and the -LR was 0.04 (95% CI: 0.01-0.13), resulting in a DOR of 535 (95% CI: 94-3024). At the segment level, sensitivity was 0.86 (95% CI: 0.79-0.91), specificity was 0.98 (95% CI: 0.96-0.99), and the HSROC AUC was 0.97 (95% CI:0.95-0.98). The +LR was 55.08 (95% CI: 19.94-152.16) and the -LR was 0.14 (95% CI: 0.09-0.22) with a DOR of 388 (95% CI: 113-1333). Dual-energy CCT improved segment-level sensitivity to 0.93 (95% CI: 0.88-0.96). LIE in CCT shows excellent diagnostic accuracy when compared to LGE in CMR for myocardial tissue characterization, suggesting its potential as a promising alternative to CMR. Question How does myocardial tissue characterization by late iodine enhancement (LIE) on cardiac CT (CCT) compare to late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR)? Findings LIE in CCT demonstrates excellent diagnostic accuracy, with high sensitivity and specificity at both patient and segment levels, using LGE in CMR as the reference. Clinical relevance LIE in CCT provides a reliable alternative to LGE in CMR, especially for patients for whom CMR is not available or feasible or is contraindicated, thus improving access to myocardial tissue characterization.

BackgroundMyocardial fibrosis is frequently identified in patients with hypertrophic cardiomyopathy (HCM). The aim of this study was to investigate the role of myocardial fibrosis detected by late gadolinium-enhancement (LGE) cardiovascular magnetic resonance (CMR) as a potential arrhythmogenic substrate in HCM. We hypothesized that the extent of LGE might be associated with the inducibility of ventricular tachyarrhythmias (VT) during programmed ventricular stimulation (PVS).MethodsWe evaluated retrospectively LGE CMR of 76 consecutive HCM patients, of which 43 presented with one or more risk factors for sudden cardiac death (SCD) and were therefore clinically classified as high-risk patients. Of these 43 patients, 38 additionally underwent an electrophysiological testing (EP). CMR indices and the extent of LGE, given as the % of LV mass with LGE were correlated with the presence of risk factors for SCD and the results of EP.ResultsHigh-risk patients had a significant higher prevalence of LGE than low-risk patients (29/43 [67%] versus 14/33 [47%]; p = 0.03). Also the % of LV mass with LGE was significantly higher in high-risk patients than in low-risk patients (14% versus 3%, p = 0.001, respectively). Of the 38 high- risk patients, 12 had inducible VT during EP. LV function, volumes and mass were comparable in patients with and without inducible VT. However, the % of LV mass with LGE was significantly higher in patients with inducible VT compared to those without (22% versus 10%, p = 0.03). The prevalence of LGE was, however, comparable between HCM patients with and those without inducible VT (10/12 [83%] versus 15/26 [58%]; p = 0.12). In the univariate analysis the % of LV mass with LGE and the septal wall thickness were significantly associated with the high-risk group (p = 0.001 and 0.004, respectively). Multivariate analysis demonstrated that the extent of LGE was the only independent predictor of the risk group (p = 0.03).ConclusionsThe extent of LGE in HCM patients correlated with risk factors of SCD and the likelihood of inducible VT. Furthermore, LGE extent was the only independent predictor of the risk group. This supports the hypothesis that the extent of fibrosis may serve as potential arrhythmogenic substrate for the occurrence of VT, especially in patients with clinical risk factors for SCD.

The majority of ventricular tachycardias (VTs) occurs in patients with structural heart disease, predominantly coronary heart disease. Implantable cardioverter defibrillators (ICDs) are first-line therapy in patients with VT and structural heart disease. In patients who receive an ICD after a spontaneous sustained VT, recurrent VT episodes or an electrical storm are major problems. In addition, in patients with an ICD implanted for primary prevention of sudden cardiac death, 20% will experience at least one VT episode within 3-5 years after ICD implantation. Catheter ablation has a high acute success rate in eliminating clinical VT. However, several factors make catheter ablation of VT more difficult than ablation of supraventricular tachyarrhythmias. (1) The infarct region is often large. (2) The induced VT can be unstable or hemodynamically only poorly tolerated and therefore "unmappable". (3) Though most commonly located in the subendocardium, the critical VT zone can occasionally be epicardial or intramural in location. (4) In many cases, several reentrant circuits may coexist making ablation of a single form of VT a palliative procedure which does not obviate the risk of sudden death. Thus, catheter ablation of sustained VT in the setting of structural heart disease can only be considered an adjunctive therapy which, in general, will require ICD therapy. Numerous "modern" mapping technologies have been developed, which have increased success rates of catheter ablation of VT in patients with and without structural heart disease. The aim of the present article is to review current three-dimensional mapping systems in comparison to conventional mapping and to describe a reasonable, tailored approach for the individual patient with VT.

21 - Myocardial Viability

We read with much interest the recent publication by Sood et al., which addresses the effect of catheter ablation (CA) for ventricular tachycardia (VT) on left ventricular ejection fraction (LVEF) in patients with structural heart disease (SHD). This study contributes crucial information on the safety and efficacy of CA in this susceptible group, given the known association between VT and the advancement of heart failure. While the study deserves praise for its findings, we would like to highlight several noteworthy advantages and disadvantages for future reference [1]. The research answers a clinically relevant query, Does CA impair cardiac function in patients with structural heart disease? The authors show that CA does not cause LVEF to drop; it also highlights that those with significantly low baseline LVEF (≤ 20) can show significant improvement, just like earlier research has shown that ventricular function can be restored, and VT burden can be reduced with early ablation [2]. In order to enhance interpretability and capture the heterogeneity of SHD, patients are stratified into ischemic (ICM) and non-ischemic cardiomyopathy (NICM) groups. The study's therapeutic usefulness is further enhanced by the use of multivariate analysis to identify predictors of LVEF change, such as pre-ablation LVEF and renin-angiotensin system usage. While it has strengths, the study has various methodological limitations. First of all, there is not a control group. Without a non-ablation comparison group, it cannot be definitively concluded if LVEF changes were due to CA or the natural course of SHD. Secondly, there is variability in follow-up duration. While the mean follow-up was more than 3 years, some post-ablation echocardiographic evaluations were as early as 137 days. This brief interval could potentially underestimate long-term LVEF changes or delayed remodeling effects [3]. Thirdly, there are potential confounding factors. Key LVEF determinants like CRT-D therapy, drug compliance, and intensification of neurohormonal blockade were not systematically addressed. All these variables potentially independently affect post-ablation LVEF as earlier reported [4]. This research supports that CA is an effective therapeutic agent for patients with VT and SHD and can provide functional recovery in severely ill patients. Further, the established correlation between VT non-recurrence and LVEF improvement indicates the potential of CA to modify the disease course. Further studies should aim to use randomized controlled designs to isolate the effect of ablation on cardiac function, determine whether earlier intervention results in more LVEF improvement, and use advanced imaging modalities, such as cardiac MRI to predict responders according to scar burden and tissue viability [5]. In conclusion, the Sood et al. study provides meaningful real-world evidence for the functional safety of VT ablation among patients with SHD, especially in those with end-stage LV dysfunction. Methodological limitations like not having a comparison group and bias from possible confounders confine conclusions to the definitive category. These findings are worthy of being validated further by prospective and controlled trials based on standardized imaging and extended durations of follow-up. The authors declare no conflicts of interest. This article is linked to Sood et al. paper. To view this article, visit https://doi.org/10.1002/joa3.70042.

Catheter ablation (CA) of ventricular tachycardia (VT) in patients with nonischemic dilated cardiomyopathy can be challenging because of the complexity of underlying substrates. We sought to determine the long-term outcomes of endocardial and adjuvant epicardial CA in nonischemic dilated cardiomyopathy. We examined 282 consecutive patients (aged 59±15 years, 80% males) with nonischemic dilated cardiomyopathy who underwent CA. Ablation was guided by activation/entrainment mapping for tolerated VT and pacemapping/targeting of abnormal electrograms for unmappable VT. Adjuvant epicardial ablation was performed for recurrent VT or persistent inducibility after endocardial-only ablation. Epicardial ablation was performed in 90 (32%) patients. Before ablation, patients failed a median of 2 antiarrhythmic drugs), including amiodarone, in 166 (59%) patients. The median follow-up after the last procedure was 48 (19-67) months. Overall, VT-free survival was 69% at 60-month follow-up. Transplant-free survival was 76% and 68% at 60- and 120-month follow-up, respectively. Among the 58 (21%) patients with VT recurrence, CA still resulted in a significant reduction of VT burden, with 31 (53%) patients having only isolated (1-3) VT episodes in 12 (4-35) months after the procedure. At the last follow-up, 128 (45%) patients were only on β-blockers or no treatment, 41 (15%) were on sotalol or class I antiarrhythmic drugs, and 62 (22%) were on amiodarone. In patients with nonischemic dilated cardiomyopathy and VT, endocardial and adjuvant epicardial CA is effective in achieving long-term VT freedom in 69% of cases, with a substantial improvement in VT burden in many of the remaining patients.

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.