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Magnetic resonance imaging (MRI) in patients with left ventricular (LV) leads may cause tissue or lead heating, dislodgment, venous damage, or lead dysfunction.The purpose of this study was to determine the safety of MRI in patients with LV pacing leads.Prospective data on patients with coronary sinus LV leads undergoing clinically indicated MRI at 3 institutions were collected. Patients were not pacemaker-dependent. Scans were performed under pacing nurse, technician, radiologist, and physicist supervision using continuous vital sign, pulse oximetry, and ECG monitoring and a 1.5-T scanner with specific absorption rate1.5 W/kg. Devices were interrogated pre- and post-MRI, programmed to asynchronous or inhibition mode with tachyarrhythmia therapies off (if present), and reprogrammed to their original settings post-MRI.MRI scans (n = 42) were performed in 40 patients with non-MRI conditional LV leads between 2005 and 2013 (mean age 67 ± 9 years, n = 16 [40%] women, median lead implant duration 740 days with interquartile range 125-1173 days). MRIs were performed on the head/neck/spine (n = 35 [83%]), lower extremities (n = 4 [10%]), chest (n = 2 [5%]), and abdomen (n = 1 [2%]). There were no overall differences in pre- and post-MRI interrogation LV lead sensing (12.4 ± 6.2 mV vs 12.9 ± 6.7 mV, P = .38), impedance (724 ± 294 Ω vs 718 ± 312 Ω, P = .67), or threshold (1.4 ± 1.1 V vs 1.4 ± 1.0 V, P = .91). No individual LV lead changes required intervention.MRI scanning was performed safely in non-pacemaker-dependent patients with coronary sinus LV leads who were carefully monitored during imaging without clinically significant adverse effect on LV lead function.

Surrogate electro-anatomic-derived geometries are used as the three-dimensional (3D) basis for mapping of cardiac arrhythmias. While merged computed tomography (CT) imaging may provide stellar pulmonary vein (PV) and left atrial (LA) anatomy, the applied scans must be obtained prior to ablation, and may not reflect physiologic conditions at the time of intervention. Patient-specific, ultrasound-derived 3D imaging has been developed as an alternative basis for new generation electro-anatomic mapping. An electro-anatomic sensor positioned at the tip of the phased-array intracardiac ultrasound catheter, provides the means to specify both location and orientation of each image as the 'context' for creating the 3D volumes for co-registration with electro-anatomic mapping. Specific anatomic details such as the pulmonary veins, membranous fossa, papillary muscles, or valve structures derived from real-time imaging can also be integrated into each segmented volume. This presentation reviews the basis and methods for this novel multi-modality image fusion for the creation of robust, nearly real-time anatomic images for guiding electro-anatomic mapping and ablation without requiring pre-acquired CT image sets, with accompanying limitations.

1.1 Document Development Process #### 1.1.1 Writing Committee Organization The writing committee was selected to represent the American College of Cardiology (ACC) and the Heart Rhythm Society (HRS) and included a cardiovascular training program director, an electrophysiology (EP) program

The idiopathic inflammatory myopathies (IIM) are systemic connective tissue diseases in which autoimmune pathology is suspected to promote chronic muscle inflammation and weakness. We have performed low to high resolution genotyping to characterize the allelic profiles of HLA-A, -B, -Cw, -DRB1, and -DQA1 loci in a large population of North American Caucasian patients with IIM representing the major clinicopathologic groups (n = 571). We confirmed that alleles of the 8.1 ancestral haplotype were important risk markers for the development of IIM, and a random forests classification analysis suggested that within this haplotype, HLA-B*0801, DRB1*0301 and/ or closely linked genes are the principal HLA risk factors. In addition, we identified several novel HLA factors associated distinctly with 1 or more clinicopathologic groups of IIM. The DQA1*0201 allele and associated peptide-binding motif (KLPLFHRL) were exclusive protective factors for the CD8+ T cell-mediated IIM forms of polymyositis (PM) and inclusion body myositis (IBM) (pc0.005). In contrast, HLA-A*68 alleles were significant risk factors for dermatomyositis (DM) (pc = 0.0021), a distinct clinical group thought to involve a humorally mediated immunopathology. While the DQA1*0301 allele was detected as a possible risk factor for IIM, PM, and DM patients (p0.05), DQA1*03 alleles were protective factors for IBM (pc = 0.0002). Myositis associated with malignancies was the most distinctive group of IIM wherein HLA Class I alleles were the only identifiable susceptibility factors and a shared HLA-Cw peptide-binding motif (AGSHTLQWM) conferred significant risk (pc = 0.019). Together, these data suggest that HLA susceptibility markers distinguish different myositis phenotypes with divergent pathogenetic mechanisms. These variations in associated HLA polymorphisms may reflect responses to unique environmental triggers resulting in the tissue pathospecificity and distinct clinicopathologic syndromes of the IIM.

Background: Patients with atrial fibrillation (AF) are at higher risk of developing all forms of dementia. The mechanisms behind the association of AF and dementia are unknown. One possibility is that exposure to chronic microbleeds results in repetitive cerebral injury that is manifest by cognitive decline. We hypothesize that AF patients receiving antiplatelet therapy will display higher rates of dementia if coupled with a higher percentage of time exposed to over-anticoagulation. Methods: Chronically anticoagulated patients receiving warfarin (target INR 2-3) for AF and managed by the Intermountain Healthcare Clinical Pharmacist Anticoagulation Service (CPAS) with no history of dementia or stroke/TIA and receiving antiplatelet therapy were included. The primary outcome was the presence of dementia defined by neurology determined ICD-9 codes. Percent time with an INR above 3.0 was determined. Multivariable Cox hazard regression was utilized to determine dementia incidence by percentage categories of supratherapeutic INR. Results: A total of 1031 patients were studied. Of these, the categories of the mean percent time with an INR >3.0 were 25% (n=240). Patients with a higher percent of time with supratherapeutic INRs were more likely to have valvular heart disease, renal failure (Cr>2.0), a higher percent of CHADS 3-6 scores, and a prior bleed. Dementia was diagnosed in 2.7% of patients with supratherapeutic INR levels 25%, p=0.05. Those with a supratherapeutic INR >25% of the time were at an increased dementia risk throughout follow-up. After multivariate adjustment, those with levels >25% had significantly higher rates of dementia compared to those with levels Discussion: In AF patients receiving antiplatelet and anticoagulant therapies, the percent of time exposed to over anticoagulation increases risk of dementia. These data support the possibility of chronic cerebral injury from microbleeds as a mechanism that underlies the association of AF and dementia.

Background: Risk stratification tools are needed to better select candidates for catheter ablation of atrial fibrillation (AF). Both the CHADS2 and CHADS2-VASC scores have utility in predicting AF-related outcomes and guiding anticoagulation treatment. We sought to determine if these risk scores predict long-term outcomes after AF ablation and if one risk score provides comparative superior performance. Methods: CHADS2 and CHADS2-VASC scores were calculated in 2179 AF ablation patients enrolled into Intermountain Heart Collaborative Study. CHADS2 and CHADS2-VASC were categorized by recursive partitioning categories as CHADS2: 0-1, 2-4, and >4 and CHADS2-VASC: 0-2, 2-5, >5. Patient outcomes were analyzed over 5 years for AF/Aflutter recurrence and MACE (death, stroke, heart failure hospitalization and AF/Aflutter recurrence). Results: Average age was 65.7±10.5 years and 61.1% were male. Both scores incrementally predicted risk of AF recurrence, stroke, heart failure, and death at 5 years (Figure). Increasing CHADS2 (hazard ratio [HR] =1.19, p Conclusion: Both the CHADS2 and CHADS2-VASC scores were excellent in stratifying patients for 5-year outcomes after AF ablation. However, the CHADS2-VASC score was superior to CHADS2 when accounting for all baseline variables for predicting both AF recurrence and AF-related morbidities.

AF ablation in the patients involving PV stumps from prior lobectomy and pneumonectomy has not been described in literature. We describe a multicenter experience of all patients with residual PV stumps after lung resection undergoing AF ablation. 14 patients with lung resection (for tumors in 9

There is limited data on the impact of very low left ventricular ejection fraction (LVEF) on mortality after catheter ablation of ventricular tachycardia (VT). Multicenter, retrospective analysis of all consecutive patients undergoing VT ablation at 4 high volume centers between 2007 and 2010. We

Background. ICD implantation for primary prevention of sudden death in patients with ischemic cardiomyopathy and left ventricular dysfunction is well established. However debate exists between the relationship between ischemia and the proarrhythmic state. Persistent ischemia may counter antiarrhythmic (AA) drug and/or device efficacy. Furthermore, the extent to which revascularization mitigates this influence of ischemia on efficacy is unknown. Methods . 704 patients enrolled in the MUSTT trial were studied. Ischemia was determined by the presence of angina within 6 weeks of enrollment and ≥ 2 reversible thallium defects. Revascularization was characterized as CABG or PTCA within 1 year of enrollment or the use of thrombolytics with the sentinal myocardial infarction (MI). We compared groups who were randomized to background medical treatment (BG Rx) verses those who were randomized to AA drug therapy in addition to EP testing (EP AARx). Results . 507 (81%) patients had ≤2 vessel CAD, whereas the remaining 19% had 3 vessel disease. 268 patients reported angina within 6 weeks of study enrollment. Thallium imaging revealed 0–1 defects in 458 (65%) and ≥2 in another 246 (35%). Those with ≥ 2 defects on Thallium and angina within 6 weeks of device implant had a significantly lower 5-year freedom from mortality in the EP AARx and BG Rx cohorts (Table ). Patients with EP AARx had an 8% lower mortality than those with BG Rx therapy alone if they received thrombolytics. However, if they did not receive thrombolytics, their mortality rate was 5% higher than the BG Rx group. Conclusion . Outcomes are worse in patients on antiarrhythmic therapy with ischemic factors compared to those on background therapy alone, particularly in the setting of recent angina. A proarrhythmic effect from antiarrhythmic drug therapy in patients with ischemia may underlie the higher mortality. ICD therapy mitigates the negative long-term effect of ischemia on mortality in those treated with AA therapy. Five Year Freedom from Mortality

Objective To investigate possible associations of HLA polymorphisms with idiopathic inflammatory myopathy (IIM) in African Americans, and to compare this with HLA associations in European American IIM patients with IIM. Methods Molecular genetic analyses of HLA–A, B, Cw, DRB1, and DQA1 polymorphisms were performed in a large population of African American patients with IIM (n = 262) in whom the major clinical and autoantibody subgroups were represented. These data were compared with similar information previously obtained from European American patients with IIM (n = 571). Results In contrast to European American patients with IIM, African American patients with IIM, in particular those with polymyositis, had no strong disease associations with HLA alleles of the 8.1 ancestral haplotype; however, African Americans with dermatomyositis or with anti–Jo-1 autoantibodies shared the risk factor HLA–DRB1*0301 with European Americans. We detected novel HLA risk factors in African American patients with myositis overlap (DRB1*08) and in African American patients producing anti–signal recognition particle (DQA1*0102) and anti–Mi-2 autoantibodies (DRB1*0302). DRB1*0302 and the European American–, anti–Mi-2–associated risk factor DRB1*0701 were found to share a 4–amino-acid sequence motif, which was predicted by comparative homology analyses to have identical 3-dimensional orientations within the peptide-binding groove. Conclusion These data demonstrate that North American IIM patients from different ethnic groups have both shared and distinct immunogenetic susceptibility factors, depending on the clinical phenotype. These findings, obtained from the largest cohort of North American minority patients with IIM studied to date, add additional support to the hypothesis that the myositis syndromes comprise multiple, distinct disease entities, perhaps arising from divergent pathogenic mechanisms and/or different gene–environment interactions.

The idiopathic inflammatory myopathies (IIM) are systemic connective tissue diseases defined by chronic muscle inflammation and weakness associated with autoimmunity. We have performed low to high resolution molecular typing to assess the genetic variability of major histocompatibility complex loci (HLA-A, -B, -Cw, -DRB1, and -DQA1) in a large population of European American patients with IIM (n = 571) representing the major myositis autoantibody groups. We established that alleles of the 8.1 ancestral haplotype (8.1 AH) are important risk factors for the development of IIM in patients producing anti-synthetase/anti-Jo-1, -La, -PM/Scl, and -Ro autoantibodies. Moreover, a random forests classification analysis suggested that 8.1 AH-associated alleles B*0801 and DRB1*0301 are the principal HLA risk markers. In addition, we have identified several novel HLA susceptibility factors associated distinctively with particular myositis-specific (MSA) and myositis-associated autoantibody (MAA) groups of the IIM. IIM patients with anti-PL-7 (anti-threonyl-tRNA synthetase) autoantibodies have a unique HLA Class I risk allele, Cw*0304 (pcorr = 0.046), and lack the 8.1 AH markers associated with other anti-synthetase autoantibodies (for example, anti-Jo-1 and anti-PL-12). In addition, HLA-B*5001 and DQA1*0104 are novel potential risk factors among anti-signal recognition particle autoantibody-positive IIM patients (pcorr = 0.024 and p = 0.010, respectively). Among those patients with MAA, HLA DRB1*11 and DQA1*06 alleles were identified as risk factors for myositis patients with anti-Ku (pcorr = 0.041) and anti-La (pcorr = 0.023) autoantibodies, respectively. Amino acid sequence analysis of the HLA DRB1 third hypervariable region identified a consensus motif, 70D (hydrophilic)/71R (basic)/74A (hydrophobic), conferring protection among patients producing anti-synthetase/anti-Jo-1 and -PM/Scl autoantibodies. Together, these data demonstrate that HLA signatures, comprising both risk and protective alleles or motifs, distinguish IIM patients with different myositis autoantibodies and may have diagnostic and pathogenic implications. Variations in associated polymorphisms for these immune response genes may reflect divergent pathogenic mechanisms and/or responses to unique environmental triggers in different groups of subjects resulting in the heterogeneous syndromes of the IIM.

Objective To define the apparent changes in ventricular fibrillation (VF) as cause of out-of-hospital cardiac arrest. (OHCA) Methods Retrospective analysis of prospectively acquired observational data of OHCA in a population-controlled setting with a single emergency medical service (EMS) system between 1991-2004. Results In the study period there were 338 all-cause arrests, with 203 (57%) in homes, 85 (24%) in public locations, and 69 (19%) in other locations (hotels, nursing homes). VF incidence during 1991-1997 was 24/100 000/person-yr and during 1998-2004 it was 11/100 000/person-yr (p

Genetic predisposition to dementia has been strongly sought, but risk loci remain elusive. Atrial fibrillation (AF), a known risk factor for cerebrovascular accidents (CVA), was recently linked with dementia, especially in a younger population. Two chromosomal loci, 4q25 and 16q22, are associated

Limited data is available on the role of percutaneous left ventricular assist devices (pLVADs) during ablation of unstable VT. Multicenter observational study of all consecutive pts undergoing VT ablation with either intra aortic balloon pump (IABP) or pLVAD. We compared the baseline