Temporal Association of Atrial Fibrillation with Device Based Heart Failure Status in Patients with CRT

Temporal Association of Atrial Fibrillation with Device Based Heart Failure Status in Patients with CRT

S82 Journal of Cardiac Failure Vol. 25 No. 8S August 2019 Electrophysiology/Arrhythmias 215 Temporal Association of Atrial Fibrillation with Device B...

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S82 Journal of Cardiac Failure Vol. 25 No. 8S August 2019

Electrophysiology/Arrhythmias 215 Temporal Association of Atrial Fibrillation with Device Based Heart Failure Status in Patients with CRT John P. Boehmer1, Jeff S. Healey2, Michael R. Gold3, Rezwan Ahmed4, Yi Zhang4, Pramodsingh H. Thakur4, Paul W. Jones4, Alessandro Capucci5; 1Penn State Hershey Medical Center, Hershey, PA; 2Population Health Research Institute, McMaster University, Hamilton, ON, Canada; 3Medical University of South Carolina, Charleston, SC; 4Boston Scientific, St. Paul, MN; 5Marche Polytechnic University of Ancona, Ancona, Italy Background: Atrial Fibrillation (AF) is common in Heart Failure (HF). Whether AF triggers or is triggered by worsening HF is debated, although both are likely. Recently, a device based multisensory algorithm (HeartLogic) was developed that detected worsening HF events with high sensitivity. Daily sensor measurements provide detailed information about HF condition around the time of AF progression. We sought to investigate whether HF status impacted the risk of AF and if AF onset changed the risk of HF. Methods: The MultiSENSE study followed 900 CRT-D patients for 1 year and collected HF diagnostic sensor data including heart sounds, respiration, thoracic impedance, heart rate and activity. Patients were grouped by the longest daily atrial high rate event (AHRE) burden (24 hours, 6min to < 24 hrs, and <= 6min). HF risk was separately evaluated during the period from enrollment to AHRE and after AHRE via time to event analysis. Sensor data was aligned to the first 24-hr AF day analyzed from -60 to +60 days. For patients with no AHRE, a randomly selected day was chosen as the first AHRE day. AF risk was evaluated separately with and without sensor data via cox proportional hazard ratios. Results: Out of 900 patients, 98 had AHRE >24 hrs, 141 had AHRE <24 hrs, and 630 had AHRE < 6 min (no AHRE). HF risk was not significantly different in the three groups from enrollment to first AHRE but was significantly different post AHRE (p<0.001), suggesting AHRE leading to higher risk of HF. HeartLogic Index was significantly elevated in the 60 days after first 24 AHRE episode compared to 60 days pre-AHRE (19.2 post 24-hr AHRE vs 9.5 pre; p <0.001), whereas patients without AHRE had lower and unchanged HeartLogic Index (5.9 post random day vs 5.8 pre; p =0.26). Besides history of AF, baseline NT-proBNP and device based S3 prior to AHRE onset were independent predictors for the risk of AHRE (NT-proBNP: HR 1.25, 95% CI 1.07 - 1.46, p = 0.004); (S3: HR 3.31, 1.45 - 7.59, p=0.005), suggesting worsened HF status led to high risk of AHRE. Conclusion: Device based sensors reflect the worsening of HF status preceding and following AF onset. AF onset significantly increases the risk of HF events while HF status (NT-proBNP and S3) is also an important factor in predicting the risk of AF, suggesting the bidirectional interactions between AF and HF.

and 2) variables associated with improvement or persistence of LV systolic dysfunction. Results: 92 pts were identified matching our entry criteria having a mean LVEF of 31.2§9.2%. Among these, 37 (40%) exhibited persistent LV systolic dysfunction (LVEF 34.3 § 8.2%) after a follow-up of 27 § 35 months. The LVEF normalized in the remaining 55 pts (LVEF 57.1§4.2%) supporting probable tachycardia-induced CMP. We observed no significant differences among clinical, laboratory or ECG variables between those pts whose LVEF normalized vs. those with a persistent CMP. Echocardiographic data from the index hospitalization demonstrated that pts with persistent CMP had an increased left atrial volume index (LAVI) compared to those with normalization in their LVEF (51.6 § 19.2 ml/m2 vs 37.7 § 10.4 ml/m2, respectively, p <0.01). No significant differences were observed in LV chamber size or wall thickness measurements. Conclusion: The incidence of persistent LV systolic dysfunction was present in 40% of pts presenting with AF with RVR and acute HFrEF supporting that a substantial number have a primary CMP rather than a reversible, tachycardiainduced CMP. These data support early intervention in these pts with guideline directed medical therapy. Greater LAVI on echocardiography may help identify pts with a primary CMP presenting with a new atrial tachyarrhythmia, heart failure and a reduced LVEF.

217 Anticoagulation with Warfarin versus Novel Oral Anticoagulants in Atrial Fibrillation in Amyloid Transthyretin Amyloidosis Cardiomyopathy: A Retrospective Cohort Study Lindsey R. Mitrani, Jeffeny De Los Santos, Stephen Helmke, Angelo B. Biviano, Mathew S. Maurer; Columbia University, New York, NY Introduction: Transthyretin amyloid (TTR) cardiomyopathy arises from deposits of amyloid fibrils in the myocardium. Due to disarray of the fibrils, incidence of atrial fibrillation (AF) is increased in patients with TTR amyloidosis. The backbone of therapy for AF includes anticoagulation with warfarin or novel oral anticoagulants (NOACs). Hypothesis: Treatment with NOACs will have superior outcomes of thrombotic events and major bleeding when compared to warfarin. Methods: We conducted a chart review of 290 patients with TTR cardiac amyloid. Of 290 patients, 159 presented with AF at diagnosis and 64 developed AF during follow-up. Of 223 total patients with AF, 79 received warfarin, two received enoxaparin, 119 received NOACs, four switched from warfarin to NOACs, and 21 stopped or did not receive anticoagulation. We defined thrombotic events as stroke or TIA, while major bleed included hemorrhage requiring admission to the hospital or transfusion. We defined labile INR as values outside of therapeutic range of 2-3 forty percent of the time. To examine outcomes, we calculated relative risk and fisher’s exact test for incident cases. Results: In TTR patients, 14 patients had a thrombotic event with 100% of those patients having or developing AF. For thrombotic events, there was no statistical difference between NOACs and warfarin (1.23/100 person-years CI: 0.35- 4.42). For major bleeds, there was no statistical difference between NOACs and warfarin (0.87/100 person-years CI: 0.33-2.26). For patients treated with warfarin, 50% had labile INRs, and of the patients on warfarin with an event and major bleed, 100% had labile INRs. Conclusion: TTR amyloid patients with AF are at increased risk for stroke compared to TTR patients without AF. There was no statistical difference for events and major bleed comparing patients who received warfarin to NOACs. Patients receiving warfarin were at risk for labile INRs, and all patients with major bleeds and events in the warfarin group had labile INRs.

218 216 Incidence of Primary, Dilated Rather Than Tachycardia-Induced Cardiomyopathy among Patients Presenting with New Onset Atrial Arrhythmia and Heart Failure with Reduced Ejection Fraction Hayaan Kamran, Sarju Ganatra, Philip Formica, Sachin P. Shah, David M. Venesy, Richard D. Patten; Lahey Hospital and Medical Center, Burlington, MA Background: Tachycardia-induced cardiomyopathy (CMP) is an established cause of left ventricular (LV) systolic dysfunction and heart failure (HF) that is reversible upon treatment of the tachyarrhythmia. The incidence of a primary, dilated CMP among patients (pts) presenting with presumed tachycardia-induced CMP, and the features that distinguish them are not well established. Methods: We examined the records of 476 consecutive pts presenting with new atrial fibrillation or flutter (AF) and a rapid ventricular rate (RVR) coupled with acute HF with reduced LV ejection fraction (HFrEF - LVEF 45%). We sought to determine the number of pts with a sustained, presumed primary CMP (persistent LVEF  45%) rather than one that is reversible. Pts with clinically relevant coronary artery disease, severe valvular disease or other suspected/known cause of CMP were excluded. Clinical variables, ECGs and follow up echocardiography were examined to establish: 1) the number of pts with improvement in LVEF vs. those with persistently depressed LVEF (LVEF  45%);

Impact of Centrifugal-Flow Ventricular Assist Devices on Right Ventricular Pacing Function Daniel R. Musikantow, Marc Miller, Anelechi Anyanwu, Aishe Cuca, Noah Moss; Icahn School of Medicine at Mount Sinai, New York City, NY Background: Transvenous Cardiac Defibrillators (ICDS) are frequently present at the time of Ventricular Assist Device (VAD) implantation. Many of these patients have underlying rhythms which depend on the pacing function of these devices or derive benefit from cardiac resynchronization therapy. Furthermore, adequate ventricular lead function is critical for the detection and treatment of tachyarrhythmias. Previous studies have shown decreased right ventricular sensing thresholds in patients undergoing earlier generation axial-flow VAD placement. Heartmate 3 (HM3) and Heartware (HVAD) are two of the newer-generation VADs whose unique use of a magnetically-levitated rotor and intrapericardial placement may result in increased interference with nearby right ventricular device leads. Methods: A retrospective analysis of all patients with a PPM or ICD who underwent implantation of an HM3 or HVAD between 2015-2019 was performed. We examined the device interrogations of patients immediately before and after device implantation, as well as a third most recent interrogation if available. A significant change in ventricular pacing threshold was defined as an increase in 2V in either of the post VAD interrogations. Results: 52 patients with HM3 and 16 patients with HVADs who had ICDs in place at the time of LVAD implant were identified, 46 of whom had both pre and post VAD interrogation reports available. 10 patients (21%) met the criteria for significant