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Inappropriate therapy and fatal proarrhythmia by an implantable cardioverter defibrillator
Session 31 AB30-6 INAPPROPRIATE THERAPY AND FATAL PROARRHYTHMIA BY AN IMPLANTABLE CARDIOVERTER DEFIBRILLATOR Dirk Vollmann, MD, Lars Lu¨thje, MD and Christina Unterberg, MD. Department of Cardiology, Go¨ttingen, Germany. A case of noise oversensing, inappropriate therapy and fatal proarrhythmia in a young patient with an implantable cardioverter defibrillator (ICD) is presented. A 38-year-old man with a dilated cardiomyopathy received a Medtronic Gem III dual-chamber ICD in 2000 because of symptomatic ventricular tachycardias. During the last follow-up in June 2003 no evidence for device dysfunction was found. Two months later, the patient received multiple consecutive shocks and finally lost consciousness. His wife made an emergency call, but the patient died after a prolonged attempt at resuscitation. Interrogation of the explanted device revealed inappropriate detection of VF and shock delivery due to oversensing of electrical noise during sinus rhythm. The 6. shock delivered during one episode of oversensing induced true VF (Figure; top:Atip/Aring; middle:Vtip/Vring; bottom: marker annotations; arrows: true ventricular potentials), and the patient died because the sequence of programmable therapies had ended with this last, proarrhythmic discharge. Automatic device measurements revealed a sudden increase in ventricular pacing impedance from 780⍀ on the day before to ⬎2000⍀ just prior to the fatal event, indicating that failure (conductor fracture /insulation defect) of the implanted defibrillation lead (Medtronic model 6944) was the presumable cause for fatal ICD therapy in this case.
ABSTRACT SESSION 31: CLINICAL ELECTROPHYSIOLOGY/PHARMACOLOGY IV: Clinical EP of Ventricular Arrhythmias Friday, May 6, 2005 8:15 a.m.–9:45 a.m. AB31-1 RISING PREVALENCE OF PULSELESS ELECTRICAL ACTIVITY: WHAT DETERMINES OCCURRENCE OF PEA VS. VF IN THE GENERAL POPULATION? Celia Dervan, Eric C. Stecker, Kalpana Narapasetty, Carmen Miu, Catherine Vickers, Justin Waltz, Ron Mariani, Kyndaron Reinier, Karen Gunson, Jonathan Jui, John H. McAnulty and Sumeet S. Chugh. Oregon Health and Science University, Portland, OR. Background: Recent studies have reported a steadily rising prevalence of pulse-less electrical activity among cases of primary cardiac arrest but rates of successful resuscitation remain very low. We compared cases of sudden cardiac death (SCD) presenting with primary pulseless electrical activity (PEA) to those presenting with VF in a community-based study. Methods and Results: The Oregon Sudden Unexplained Death Study (Ore-SUDS) is an ongoing prospective, population-based study of sudden cardiac death (SCD) among residents of Multnomah County OR (Pop. 660,486). During 2002 and 2003, a total of 720 SCDs were identified, of which 453 underwent attempted resuscitation (63%). Of these, the presenting arrhythmia was VF in 43%, PEA in 21% and asystole in 31%. Initial resuscitation was successful (return of spontaneous circulation, ROSC) in 37% of VF, 20% of PEA and 9% of asystole cases (p⫽0.003; ROSC in 14% overall). For a subset of patients with detailed medical records, we performed a comparison of multiple clinical variables between PEA (n⫽29) and those presenting with VF (n⫽75). The response time (time between 911 call received and arrival of first responders) did not differ
S61 significantly between PEA vs.VF (mean 5.8 vs. 6.3 min, p⫽0.29). PEA cases were older than VF (Mean age 71 vs. 65 yr, p⫽0.004), more likely to be female (50% vs 33%, p⫽0.006) and less likely to have known coronary artery disease (24% vs. 57%, p⫽0.002). Overall, 45% of PEA had known lung disease (COPD, asthma or idiopathic pulmonary fibrosis) versus only 20% of VF (p⫽0.01). There were no significant differences in clinical history of congestive heart failure, diabetes mellitus, hypertension, obesity, cerebral vascular accident, peripheral vascular disease, hypercholesterolemia, obstructive sleep apnea and syncope. Conclusions: Cases of primary PEA were distinguishable from VF by older age, female gender and presence of lung disease- but not by response time. Future PEA-targeted advances in resuscitation may benefit from a renewed focus on hypoxia, hypercapnia and respiratory acidosis. AB31-2 THE FORTUITOUS INDIVIDUAL WITH A BRUGADA-LIKE ELECTROCARDIOGRAM Pedro Brugada, MD, PhD, Josep Brugada, MD, PhD and Ramo´n Brugada, MD. Cardiovascular Center, Aalst, Belgium, Hospital Clinic, Barcelona, Spain and Masonic Medical Research Laboratory, Utica, NY. Background: Brugada syndrome (BrS) is a genetic disease that may lead to ventricular fibrillation (VF) and sudden death (SD). Symptomatic patients (pts) receive an implantable cardioverter defibrillator (ICD), however, there exist no data on how to approach asymptomatic pts with an ECG of BrS and no family history of SD or BrS (fortuitous cases). Methods and Results: In a prospective multicenter study we identified 724 pts with a coved type ECG of BrS. Of them 168 (23%) were asymptomatic, non-familial, fortuitous cases. ECG and pharmacologic testing of firstdegree living relatives (161 of 168 families) was negative for BrS. Mean age was 44 ⫾ 12 ys, 82% were males. The ECG was spontaneously abnormal in 155 (92%). Programmed ventricular stimulation (PVS) induced a sustained polymorphic ventricular tachycardia in 36 (29%) of the 125 (75%) tested individuals. Thirty-six individuals (28 inducible, 8 noninducible) received an ICD. During a mean follow-up of 28 ⫾ 42 months there were 5 SD and 7 VF (near SD) terminated by an implanted defibrillator. All 5 SD occurred in individuals (n⫽ 43) who did not undergo PVS and had no ICD. Individuals who underwent PVS and were inducible, usually (77%) received an ICD and all survived. Conclusions: Fortuitous, asymptomatic individuals with an ECG of BrS have a substantial risk (6%) of (aborted) SD during a short mean follow-up period of 28 months. The best predictor of an arrhythmic event is the outcome of PVS. The best predictor of SD is the lack of an electrophysiologic study. These data indicate that full investigation to assess the arrhythmic risk and to define a therapeutic approach is required in the fortuitous individual with BrS. AB31-3 CLINICAL PRESENTATION OF THE PATIENTS WITH SHORT QT SYNDROME Carla Giustetto, MD, Christian Wolpert, MD, Olli M. Anttonen, MD, Pascal Sbragia, MD, Giampiero Leone, MD, Rainer Schimpf, MD, Martin Borggrefe, MD, Jean F. Leclercq, MD, Michel Haı¨ssaguerre, MD and Fiorenzo Gaita, MD. Ospedale Civile, Asti, Italy, University Hospital, Mannheim, Germany, Oulu University Hospital, Oulu, Finland, Hopital Nord, Marseille, France, Ospedale Regionale, Aosta, Italy and Hoˆpital Cardiologique du Haut Le´ve`que, Bordeaux, France. Background: Short QT syndrome is a recently described genetic arrhythmogenic disorder. Little is known about its clinical presentation as only a few cases have been described. Methods: Clinical history, physical examination, ECGs, echocardiogram, exercise testing, Holter ECG, electrophysiologic study, cardiac MRI and
ABSTRACT SESSION 31: CLINICAL ELECTROPHYSIOLOGY/PHARMACOLOGY IV: Clinical EP of Ventricular Arrhythmias Friday, May 6, 2005 8:15 a.m.–9:45 a.m. AB31-1 RISING PREVALENCE OF PULSELESS ELECTRICAL ACTIVITY: WHAT DETERMINES OCCURRENCE OF PEA VS. VF IN THE GENERAL POPULATION? Celia Dervan, Eric C. Stecker, Kalpana Narapasetty, Carmen Miu, Catherine Vickers, Justin Waltz, Ron Mariani, Kyndaron Reinier, Karen Gunson, Jonathan Jui, John H. McAnulty and Sumeet S. Chugh. Oregon Health and Science University, Portland, OR. Background: Recent studies have reported a steadily rising prevalence of pulse-less electrical activity among cases of primary cardiac arrest but rates of successful resuscitation remain very low. We compared cases of sudden cardiac death (SCD) presenting with primary pulseless electrical activity (PEA) to those presenting with VF in a community-based study. Methods and Results: The Oregon Sudden Unexplained Death Study (Ore-SUDS) is an ongoing prospective, population-based study of sudden cardiac death (SCD) among residents of Multnomah County OR (Pop. 660,486). During 2002 and 2003, a total of 720 SCDs were identified, of which 453 underwent attempted resuscitation (63%). Of these, the presenting arrhythmia was VF in 43%, PEA in 21% and asystole in 31%. Initial resuscitation was successful (return of spontaneous circulation, ROSC) in 37% of VF, 20% of PEA and 9% of asystole cases (p⫽0.003; ROSC in 14% overall). For a subset of patients with detailed medical records, we performed a comparison of multiple clinical variables between PEA (n⫽29) and those presenting with VF (n⫽75). The response time (time between 911 call received and arrival of first responders) did not differ
S61 significantly between PEA vs.VF (mean 5.8 vs. 6.3 min, p⫽0.29). PEA cases were older than VF (Mean age 71 vs. 65 yr, p⫽0.004), more likely to be female (50% vs 33%, p⫽0.006) and less likely to have known coronary artery disease (24% vs. 57%, p⫽0.002). Overall, 45% of PEA had known lung disease (COPD, asthma or idiopathic pulmonary fibrosis) versus only 20% of VF (p⫽0.01). There were no significant differences in clinical history of congestive heart failure, diabetes mellitus, hypertension, obesity, cerebral vascular accident, peripheral vascular disease, hypercholesterolemia, obstructive sleep apnea and syncope. Conclusions: Cases of primary PEA were distinguishable from VF by older age, female gender and presence of lung disease- but not by response time. Future PEA-targeted advances in resuscitation may benefit from a renewed focus on hypoxia, hypercapnia and respiratory acidosis. AB31-2 THE FORTUITOUS INDIVIDUAL WITH A BRUGADA-LIKE ELECTROCARDIOGRAM Pedro Brugada, MD, PhD, Josep Brugada, MD, PhD and Ramo´n Brugada, MD. Cardiovascular Center, Aalst, Belgium, Hospital Clinic, Barcelona, Spain and Masonic Medical Research Laboratory, Utica, NY. Background: Brugada syndrome (BrS) is a genetic disease that may lead to ventricular fibrillation (VF) and sudden death (SD). Symptomatic patients (pts) receive an implantable cardioverter defibrillator (ICD), however, there exist no data on how to approach asymptomatic pts with an ECG of BrS and no family history of SD or BrS (fortuitous cases). Methods and Results: In a prospective multicenter study we identified 724 pts with a coved type ECG of BrS. Of them 168 (23%) were asymptomatic, non-familial, fortuitous cases. ECG and pharmacologic testing of firstdegree living relatives (161 of 168 families) was negative for BrS. Mean age was 44 ⫾ 12 ys, 82% were males. The ECG was spontaneously abnormal in 155 (92%). Programmed ventricular stimulation (PVS) induced a sustained polymorphic ventricular tachycardia in 36 (29%) of the 125 (75%) tested individuals. Thirty-six individuals (28 inducible, 8 noninducible) received an ICD. During a mean follow-up of 28 ⫾ 42 months there were 5 SD and 7 VF (near SD) terminated by an implanted defibrillator. All 5 SD occurred in individuals (n⫽ 43) who did not undergo PVS and had no ICD. Individuals who underwent PVS and were inducible, usually (77%) received an ICD and all survived. Conclusions: Fortuitous, asymptomatic individuals with an ECG of BrS have a substantial risk (6%) of (aborted) SD during a short mean follow-up period of 28 months. The best predictor of an arrhythmic event is the outcome of PVS. The best predictor of SD is the lack of an electrophysiologic study. These data indicate that full investigation to assess the arrhythmic risk and to define a therapeutic approach is required in the fortuitous individual with BrS. AB31-3 CLINICAL PRESENTATION OF THE PATIENTS WITH SHORT QT SYNDROME Carla Giustetto, MD, Christian Wolpert, MD, Olli M. Anttonen, MD, Pascal Sbragia, MD, Giampiero Leone, MD, Rainer Schimpf, MD, Martin Borggrefe, MD, Jean F. Leclercq, MD, Michel Haı¨ssaguerre, MD and Fiorenzo Gaita, MD. Ospedale Civile, Asti, Italy, University Hospital, Mannheim, Germany, Oulu University Hospital, Oulu, Finland, Hopital Nord, Marseille, France, Ospedale Regionale, Aosta, Italy and Hoˆpital Cardiologique du Haut Le´ve`que, Bordeaux, France. Background: Short QT syndrome is a recently described genetic arrhythmogenic disorder. Little is known about its clinical presentation as only a few cases have been described. Methods: Clinical history, physical examination, ECGs, echocardiogram, exercise testing, Holter ECG, electrophysiologic study, cardiac MRI and