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© 2015 American Medical Association. All rights reserved. Supplementary Online Content Tseng ZH, Hayward RM, Clark NM, et al. Sudden death in patients with cardiac implantable electronic devices. JAMA Intern Med. Published online June 22, 2015. doi:10.1001/jamainternmed.2015.2641. eTable. Details of Investigation for SCDs With Cardiovascular Implantable Electronic Devices eFigure 1. Case 5 eFigure 2. Case 1 eFigure 3. Case 2 eFigure 4. Case 3 eFigure 5. Case 4 eFigure 6. Case 15 eFigure 7. Case 18 eFigure 8. Case 19 eFigure 9. Case 20 eFigure 10. Case 21 This supplementary material has been provided by the authors to give readers additional information about their work. Downloaded From: https://jamanetwork.com/ by a Non-Human Traffic (NHT) User on 04/24/2021

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Page 1: Supplementary Online Content€¦ · SC ICD Acute RCA thrombus. Cardiomegaly, cirrhosis, COPD Extended VF with undersensing leading to a delay in interval counts that delayed therapy

©2015AmericanMedicalAssociation.Allrightsreserved.

Supplementary Online Content

Tseng ZH, Hayward RM, Clark NM, et al. Sudden death in patients with cardiac implantable electronic devices. JAMA Intern Med. Published online June 22, 2015. doi:10.1001/jamainternmed.2015.2641. eTable. Details of Investigation for SCDs With Cardiovascular Implantable Electronic Devices eFigure 1. Case 5 eFigure 2. Case 1 eFigure 3. Case 2 eFigure 4. Case 3 eFigure 5. Case 4 eFigure 6. Case 15 eFigure 7. Case 18 eFigure 8. Case 19 eFigure 9. Case 20 eFigure 10. Case 21 This supplementary material has been provided by the authors to give readers additional information about their work.

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eTable 1. Details of Investigation for SCDs with Cardiovascular Implantable Electronic Devices 

 Case  Patient Details  Device  Autopsy Findings  Device Interrogation  Terminal Rhythm  Adjudicated COD  Device Concern 

1  70♂ with CHB, AF  DC PPM  No MI or other acute COD  Sudden battery depletion from 2.62V (5 weeks prior to death) to 2.17V (day of death). See eFigure 2.  

Presumed profound bradycardia/asystole  Arrhythmic  Yes (Battery; Hardware 

failure) 

2  42♂ with CHB, HCM, syncope  DC PPM  Hypertrophic CM with 3.0 cm 

septum. No acute MI  Normal PPM function with VF at time of death. See eFigure 3.   VF  Arrhythmic Yes (ICD was indicated at time of PPM; Improper 

device selection) 

77♀ with sick sinus syndrome, advanced AV block, CAD s/p MI, CVA, 

Alzheimer's dz 

DC PPM  No MI; acute bronchopneumonia  No VT/VF. Rapid rise in RV lead impedance (650‐>1620 ohms) 1wk prior to death concerning for lead fracture. See eFigure 4.   PEA  Pneumonia  Yes (RV lead; Possible 

hardware failure) 

4  60♂ with CHB, AF  DC PPM 

Rectal adenocarcinoma, cardiomegaly, 30% LAD stenosis, and severe myocardial fibrosis. No MI or acute COD 

Increase in RV lead impedance 2 days prior to death. PMVT/VF at the time of death. See eFigure 5.   PMVT/VF  Arrhythmic  Yes (RV lead; Hardware 

failure) 

5  26♂ with 2nd deg. HB, L‐TGA s/p mechanical TVR  DC PPM  Massive pulmonary hemorrhage  Normal PPM function w/o recorded events at time of death. See eFigure 

1.   PEA  Massive pulmonary hemorrhage  No 

6  87♀ with 2nd deg. HB, AF, CAD s/p MI  DC PPM  Intracranial hemorrhage  Acute increase in RV lead impedance (380‐>1340 ohms) post‐mortem.  AF w/ RVR ‐>Asystole  Intracranial 

hemorrhage  No 

7  98♀ with CHB, AF  DC PPM  Pulmonary edema and scar from remote MI but no acute MI  Normal PPM function w/o recorded events at the time of death.  PEA (AS‐VP) 

Cardiac (heart failure), non‐arrhythmic 

No 

8  70♂ with sinus node dysfunction  DC PPM  Scar from remote MI. No acute MI 

or other COD  Normal PPM function with VF at the time of death.  VF  Arrhythmic  No 

9  84♂ with CHB, AF  DC PPM  No acute cause of death   No electrograms recorded (device was ERI), but intervals suggest VF.  VF  Arrhythmic  No 

10  56♂ with CHB, CHF  DC PPM  Dilated CM w/o MI or other acute COD  Normal PPM function. Device at ERI, full interrogation not possible.  Unknown  Arrhythmic  No 

11  88♀ with AF and bradycardia  DC PPM  Blunt force injuries of head/neck 

w/ CAD  Normal PPM function. AF with RVR at time of death.  AF with RVR  Occult trauma  No 

12  77♂ with CHB, AF, CAD s/p MI, CHF  DC PPM  No MI. Acute lung inflammation 

due to pneumonia  Normal PPM function. NSVT ‐‐> 

Idioventricular rhythm 

Pneumonia  No 

13  87♂ with tachy‐brady syndrome  DC PPM  No MI or other acute COD. 50% 

LAD stenosis  Normal PPM function with VF at time of death.  VF  Arrhythmic  No 

14  77♂ with CHB, CAD, idiopathic CM  CRT‐P  N/A  No device interrogation. VF recorded by paramedics.   VF  Arrhythmic  No 

15  78♂ with Dilated CM  DC ICD Massive subarachnoid hemorrhage, cardiomegaly (heart 760g) 

VF documented at time of death (likely secondary to subarachnoid hemorrhage). See eFigure 6.  VF  Subarachnoid 

hemorrhage  No 

16  76♂ with Ischemic CM, AF, CAD  DC ICD  Scar from remote MI and CM but 

no acute MI or other COD 

Episodes of VF during EMS rescue were not recorded by device and required external shocks for rescue. Delay to shock due to ATP programming in the VF zone. See Figure 2.  

VF  Arrhythmic Yes (VF episodes missed; Programming and Device 

algorithm issue) 

17  70♂ with Ischemic CM, CHF  CRT‐D  CM without acute MI or other 

COD VF undersensed with device interpreting return to sinus rhythm (no shock delivered). See Figure 3.   VF  Arrhythmic  Yes (VF undersensing; Device 

algorithm issue) 

18  74♂ with CAD s/p MI, ischemic CM, AF, VT  DC ICD  Scar from remote MI and 99% LAD 

stenosis but no acute MI 

VF with undersensing. 40 VF and 2 VT episodes identified and 17/42 shocks aborted due to undersensing. The second event showed significant undersensing with a significant delay in therapy. See eFigure 7.  

VF  Arrhythmic  Yes (VF undersensing) 

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19  54♀ with dilated CM, ESRD on HD  DC ICD  N/A 

VT that was undersensed. This was treated with ATP but wavering VT cycle length resulted in a delayed shock. VT degraded into fine VF that was undersensed. Patient left in VF/VT and device stopped recording and was unable to detect after that point. See eFigure 8.  

VF  Arrhythmic  Yes (VT undersensing) 

20  71♂ with AF, CAD, ischemic CM  SC ICD  Acute RCA thrombus. 

Cardiomegaly, cirrhosis, COPD Extended VF with undersensing leading to a delay in interval counts that delayed therapy. See eFigure 9.   VF  Arrhythmic 

Yes (VF undersensing, Programming and Device 

algorithm issue) 

21  80♂ with ischemic CM, CAD, CHF  CRT‐D  N/A 

VF storm with 4 shocks and multiple rounds of ATP. Final event shows VT but device did not rescue due to programming of tachycardia zone. See eFigure 10.  

VT  Arrhythmic  Yes (VT slower than VT zone; Programming) 

22  80♂ with Ischemic CM, AF  DC ICD  Hypertensive heart disease, COPD 

VF with successful defibrillation x 3 followed by RV lead noise and increase in lead impedance with 4th shock suggesting lead fracture. See Figure 4.  

VF  Arrhythmic  Yes (Lead fracture; Hardware failure) 

AF ‐ atrial fibrillation, CAD ‐ coronary artery disease, CHB ‐ complete heart block, CHF ‐ congestive heart failure, CM – cardiomyopathy, COD – cause of death, CRT‐P ‐ cardiac resynchronization therapy pacemaker, CRT‐D ‐ cardiac resynchronization therapy defibrillator, DC ‐ dual chamber, MI ‐ myocardial infarction, PEA ‐ pulseless electrical activity, PPM ‐ permanent pacemaker, RV ‐ right ventricle, RVR ‐ rapid ventricular response,  SC ‐ single chamber, VF ‐ ventricular fibrillation, VT ‐ ventricular tachycardia 

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eFigure1(Case5).Left:Post‐mortemdeviceinterrogationshowingnoventricularhighrateepisodes.Right:H&Esectionoflung(12.5X)demonstratingdilatedbronchialveins(arrows)andhemosiderin‐ladenmacrophages(arrowheads).ReprintedwithpermissionfromHaywardRM,UrsellPC,FosterE,TsengZH.SuddendeathduetononarrhythmiccauseinapatientwithL‐TGA.AnnNoninvasiveElectrocardiol.2014;19(3):293‐297.

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eFigure2(Case1).Top: PPM interrogation 5 weeks prior to death shows estimated battery longevity of 6 months and > 95% ventricular pacing. The patient’s PVC burden was at least 3%, which accounted for most of the non-paced ventricular beats and underlying rhythm at device check was sinus bradycardia with complete heart block and a slow junctional escape. The patient’s ventricular pacing threshold at this this time was 2.5V with a pulse width of 0.4 ms. Bottom: Pacemaker interrogation within 1 day after death demonstrates excessive voltage decrease of 0.46 V consistent with rapid battery depletion and no ventricular high rate episodes.

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eFigure3(Case2).Top:Atrialmarkerchannel.Middle:Ventricularmarkerchannel.Bottom:Intervals.VFatthetimeofdeath.ICDisaIIarecommendationin2008ACC/AHA/HRSGuidelinesforHCMpatientswithunexplainedsyncopeandseptalthickness>30mm.ThispatientdiedofVFwithaPPMinplace.

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eFigure4(Case3).Postmortem PPM interrogation demonstrating a rapid substantial increase in atrial and ventricular lead impedances that was first detected 2 days prior to death. The patient died suddenly on January 13, 2012. The intrinsic R-wave was measured at 5.5 mV on the day prior to death, suggesting intrinsic ventricular activity. However, lead fracture can be intermittent and the sensing could have been due to junctional or ventricular escape beats. Atrial lead impedance also increased, raising the possibility of changes due to acidosis or electrolyte disturbances, but atrial lead impedance normalized on the day of death. In this case, although pneumonia was found on autopsy and occult pneumonia was adjudicated as the COD, right ventricular lead fracture or a global pacemaker problem resulting in profound bradycardia or asystole could not be excluded as a contributor to sudden death.

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eFigure5(Case4).Top:Increaseinventricularleadimpedance2dayspriortodeath(thepatientdiedsuddenlyon11/3/13).Bottom:VentricularelectrogramshowsPMVT/VFatthetimeofdeath.NoacuteCODwasfoundonautopsy.TheleadmalfunctionmayhaveleddirectlytoVT/VFviapause‐dependentmechanismcausedbyinconsistentventricularcaptureorRonTphenomenonduetoundersensing.

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eFigure6(Case15).78MwithdilatedCMandVFdocumentedatthetimeofdeathwhichwasrecognizedandtreatedbytheICD(Left).VFwasduetohemorrhageintherightinsularcortex(Right)leadingtoarrhythmia(neurocardiogenicVF).

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eFigure 7 (Case 18). The patient had 40 VF and 2 VT episodes identified and 17 of 42 shocks aborted due to undersensing. Top: atrial electrogram. Middle: ventricular electrogram. Bottom: device markers. Strips are continuous. This event shows a return to sinus (*) after the previous shock due to undersensing of VF (arrowheads). This resulted in a significant delay in therapy.

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eFigure8(Case19).Top:atrialelectrogram.Middle:ventricularelectrogram.Bottom:Shockelectrogram.After3unsuccessfulATPattempts,thepatientwasinVT/VF.UndersensingresultedinawaveringVTcyclelengthanddiversionofcharging(*).ThedeviceredetectedVFanddeliveredashock,butundersensingresultedinadelaytotherapyof12.2seconds(A).Ultimately,thepatientwasleftinVFthatthedevicewasunabletodetectandstoppedrecording(B).Thepatient’sfinalrecordedrhythm,whichshowedundersensingofVF.IntervalsshowvaryingcyclelengthswaveringinandoutofVTzone(C).

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eFigure 9 (Case 20). Top and Middle Strips (continuous): Extended VF event with undersensing (arrowheads) that delays therapy. In addition, ATP delays shock therapy. Less than 1 minute later, the patient had multiple additional episodes of VT/VF requiring defibrillation. Bottom Strip: 4 minutes later, the final rhythm recorded by the device was VF with no further shocks delivered. Autopsy showed acute RCA thrombus. Cumulative delays to shock may have resulted in refractoriness of VF and further opportunity for undersensing.

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eFigure10(Case21).Top: atrial electrogram. Middle: ventricular electrogram. Bottom: device markers. After 4 shocks and multiple rounds of ATP, the patient is left in VT (mean cycle length 447 msec) but the device did not rescue due to the programming of the tachycardia zone (VT detection zone >166 bpm or <360 msec).

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