- Email: [email protected]
Box Change Data for Audits
S132
Heart, Lung and Circulation 2012;21:S1–S142
CSANZ 2012 Abstracts
ABSTRACTS
and solid MES accounted for 89% and 11% of total signals, respectively. There was no difference in MES count or composition between PAF and PeAF pts (Table). Type of AF, number of cardioversions, AF/SR during ablation, CHADS2 score, and age were not predictive of increased MES count. No pt experienced a clinical embolic event. Conclusions: MES in PAF and PeAF pts undergoing PVI are primarily gaseous. Solid events comprise a small but significant proportion of MES, and occur in the absence of overt neurologic complication. These MES may be responsible for silent cerebral microinfarction and subtle neurocognitive sequelae associated with PVI. PAF (n = 37) Total MES (median, IQR) Gaseous MES (median, IQR) Solid MES (median, IQR) LA access time (mins) Ablation time (min) Cardioversions (n)
234 (397) 221 (374) 30 (47) 159 ± 45 49 ± 18 0.3 ± 1.1
PeAF (n = 18) 299 (266) 254 (234) 29 (40) 175 ± 42 58 ± 24 1.5 ± 2.3
p NS NS NS NS NS 0.02
http://dx.doi.org/10.1016/j.hlc.2012.05.331 322 Obesity and the Risk of Atrial Fibrillation: A Systematic Review and Meta-Analysis C. Wong ∗ , A. Brooks, M. Sun, T. Sullivan, D. Lau, D. Leong, A. Ganesan, K. Roberts-Thomson, G. Wittert, P. Sanders Centre for Heart Rhythm Disorders, University of Adelaide and Royal Adelaide Hospital, Australia Background: A number of studies have suggested that obesity is an emerging risk factor for atrial fibrillation (AF). Methods: Electronic databases were searched for published studies up until December 2011. Studies were included if they assessed the incidence or prevalence of AF in relation to body mass index (BMI). Data were pooled using random effects meta-analysis. When data were reported as a series of dose-specific relative risks compared to a reference BMI category, these were transformed into risk estimates per unit of BMI via the Hartemink method to allow pooling. Studies reporting hazard ratios (HR) and odds ratios (OR) were considered separately. Results: Twenty-nine studies were identified. Four studies were not considered for pooled analysis due to already-included reports from the same study cohort. Three studies did not report sufficient data to convert categorical to continuous relative risks. Of the remaining studies, pooled analysis of eight studies reporting HR data revealed a significant association between BMI and incident AF (HR per unit of BMI 1.053 [95% CI 1.043–1.063]). Pooled analysis of fourteen studies reporting OR data similarly revealed a significant association between BMI and prevalent AF (OR per unit of BMI 1.034 [95% CI 1.020–1.048]). Conclusions: For every unit increase in BMI, there is a 5.3% increased risk of developing AF. These findings suggest that weight control may be a reasonable public health strategy to combat the growing AF epidemic. http://dx.doi.org/10.1016/j.hlc.2012.05.332
323 Pacemaker Battery Longevity Projections/Box Change Data for Audits J. England Blue Mountains District Anzac Memorial Hospital, Australia The most common question patients ask at a pacemaker follow up clinic is “How long will my battery last?” The remaining pacemaker or AICD voltage is recorded and projected against the calculated ERI voltage to give the time to replacement – 5 years for AICD and 8–10 years for a pacemaker. Several pacemakers have failed prematurely well before the manufacturers projections on tender to the implanting hospital. Fluorosis malfunction of the Medtronic P1501DR “EnRhythm” caused failure requiring replacement under warranty at around two years. EnTrust voltage may drop suddenly around ERI. Small can design led to failure of the St Jude Identity DR 5370 at three years independent of whether the patient was V paced 100% of the time or less than 5% of the time, Identity ADXSR5180 may fail around five years. We reviewed routine box changes retrospectively for all pacemaker and AICD brands and the pool results: 73 Pacemaker box changes battery longevity. . .7.3. . .years 17 Defibrillator box changes battery longevity. . .3.9. . .years Box changes occurred early due to high output voltages (safety margins) related to high implant lead thresholds or subsequent partial dislodgement. Lead noise and insulation malfunction led to premature loss of power or sudden failure with Fidelis and Riata leads. There is the need to implement the National Cardiac Implanted Devices Registry (2007 NSW Clinical Excellence Report recommendations). The Registry can assess each individual device’s battery longevity and compare the same pacemaker/AICD implanted at different hospitals, public and private/audit premature box changes. http://dx.doi.org/10.1016/j.hlc.2012.05.333 324 Patients with Lone Atrial Fibrillation Harbor Diffuse Ventricular Fibrosis L. Ling 1,∗ , A. Taylor 1 , A. Ellims 1 , L. Iles 1 , A. Teh 1,2,3 , G. Lee 1,2,3 , M. Wong 1,2,3 , D. Kaye 1 , J. Kalman 2,3 , P. Kistler 1,2,3 1 Alfred
Hospital and Baker IDI, Australia Melbourne Hospital, Australia 3 University of Melbourne, Australia 2 Royal
Introduction: Atrial fibrillation (AF) can induce tachycardia-mediated cardiomyopathy (TMC) characterised by left ventricular (LV) dilatation, systolic dysfunction, and diffuse fibrosis. Delayed enhancement on cardiac magnetic resonance imaging (CMR) provides spatial information on focal scar. Diffuse ventricular
Heart, Lung and Circulation 2012;21:S1–S142
CSANZ 2012 Abstracts
ABSTRACTS
and solid MES accounted for 89% and 11% of total signals, respectively. There was no difference in MES count or composition between PAF and PeAF pts (Table). Type of AF, number of cardioversions, AF/SR during ablation, CHADS2 score, and age were not predictive of increased MES count. No pt experienced a clinical embolic event. Conclusions: MES in PAF and PeAF pts undergoing PVI are primarily gaseous. Solid events comprise a small but significant proportion of MES, and occur in the absence of overt neurologic complication. These MES may be responsible for silent cerebral microinfarction and subtle neurocognitive sequelae associated with PVI. PAF (n = 37) Total MES (median, IQR) Gaseous MES (median, IQR) Solid MES (median, IQR) LA access time (mins) Ablation time (min) Cardioversions (n)
234 (397) 221 (374) 30 (47) 159 ± 45 49 ± 18 0.3 ± 1.1
PeAF (n = 18) 299 (266) 254 (234) 29 (40) 175 ± 42 58 ± 24 1.5 ± 2.3
p NS NS NS NS NS 0.02
http://dx.doi.org/10.1016/j.hlc.2012.05.331 322 Obesity and the Risk of Atrial Fibrillation: A Systematic Review and Meta-Analysis C. Wong ∗ , A. Brooks, M. Sun, T. Sullivan, D. Lau, D. Leong, A. Ganesan, K. Roberts-Thomson, G. Wittert, P. Sanders Centre for Heart Rhythm Disorders, University of Adelaide and Royal Adelaide Hospital, Australia Background: A number of studies have suggested that obesity is an emerging risk factor for atrial fibrillation (AF). Methods: Electronic databases were searched for published studies up until December 2011. Studies were included if they assessed the incidence or prevalence of AF in relation to body mass index (BMI). Data were pooled using random effects meta-analysis. When data were reported as a series of dose-specific relative risks compared to a reference BMI category, these were transformed into risk estimates per unit of BMI via the Hartemink method to allow pooling. Studies reporting hazard ratios (HR) and odds ratios (OR) were considered separately. Results: Twenty-nine studies were identified. Four studies were not considered for pooled analysis due to already-included reports from the same study cohort. Three studies did not report sufficient data to convert categorical to continuous relative risks. Of the remaining studies, pooled analysis of eight studies reporting HR data revealed a significant association between BMI and incident AF (HR per unit of BMI 1.053 [95% CI 1.043–1.063]). Pooled analysis of fourteen studies reporting OR data similarly revealed a significant association between BMI and prevalent AF (OR per unit of BMI 1.034 [95% CI 1.020–1.048]). Conclusions: For every unit increase in BMI, there is a 5.3% increased risk of developing AF. These findings suggest that weight control may be a reasonable public health strategy to combat the growing AF epidemic. http://dx.doi.org/10.1016/j.hlc.2012.05.332
323 Pacemaker Battery Longevity Projections/Box Change Data for Audits J. England Blue Mountains District Anzac Memorial Hospital, Australia The most common question patients ask at a pacemaker follow up clinic is “How long will my battery last?” The remaining pacemaker or AICD voltage is recorded and projected against the calculated ERI voltage to give the time to replacement – 5 years for AICD and 8–10 years for a pacemaker. Several pacemakers have failed prematurely well before the manufacturers projections on tender to the implanting hospital. Fluorosis malfunction of the Medtronic P1501DR “EnRhythm” caused failure requiring replacement under warranty at around two years. EnTrust voltage may drop suddenly around ERI. Small can design led to failure of the St Jude Identity DR 5370 at three years independent of whether the patient was V paced 100% of the time or less than 5% of the time, Identity ADXSR5180 may fail around five years. We reviewed routine box changes retrospectively for all pacemaker and AICD brands and the pool results: 73 Pacemaker box changes battery longevity. . .7.3. . .years 17 Defibrillator box changes battery longevity. . .3.9. . .years Box changes occurred early due to high output voltages (safety margins) related to high implant lead thresholds or subsequent partial dislodgement. Lead noise and insulation malfunction led to premature loss of power or sudden failure with Fidelis and Riata leads. There is the need to implement the National Cardiac Implanted Devices Registry (2007 NSW Clinical Excellence Report recommendations). The Registry can assess each individual device’s battery longevity and compare the same pacemaker/AICD implanted at different hospitals, public and private/audit premature box changes. http://dx.doi.org/10.1016/j.hlc.2012.05.333 324 Patients with Lone Atrial Fibrillation Harbor Diffuse Ventricular Fibrosis L. Ling 1,∗ , A. Taylor 1 , A. Ellims 1 , L. Iles 1 , A. Teh 1,2,3 , G. Lee 1,2,3 , M. Wong 1,2,3 , D. Kaye 1 , J. Kalman 2,3 , P. Kistler 1,2,3 1 Alfred
Hospital and Baker IDI, Australia Melbourne Hospital, Australia 3 University of Melbourne, Australia 2 Royal
Introduction: Atrial fibrillation (AF) can induce tachycardia-mediated cardiomyopathy (TMC) characterised by left ventricular (LV) dilatation, systolic dysfunction, and diffuse fibrosis. Delayed enhancement on cardiac magnetic resonance imaging (CMR) provides spatial information on focal scar. Diffuse ventricular