Baseline characteristics of cardiac sarcoidosis patients.

<p>Baseline characteristics of cardiac sarcoidosis patients.</p

Management of sudden cardiac death in cardiac sarcoidosis using the wearable cardioverter defibrillator

<div><p>Background</p><p>Patients with cardiac sarcoidosis are at increased risk of ventricular tachycardia/fibrillation.</p><p>Objective</p><p>We tested the hypothesis that the wearable cardioverter defibrillator can be used to mitigate the risk of sudden cardiac death among cardiac sarcoidosis patients.</p><p>Methods</p><p>A retrospective review of the commercial database identified cardiac sarcoidosis patients who wore the wearable cardioverter defibrillator. Evidence for cardiac sarcoidosis diagnosis as well as demographic, co-morbidity and left ventricular ejection fraction were provided by patient clinical records. Clinical data also included daily wearable cardioverter defibrillator wear, shock treatment and survival information.</p><p>Results</p><p>The wearable cardioverter defibrillator was worn by 46 cardiac sarcoidosis patients, 24 (52%) male. The median age was 48 years and median left ventricular ejection fraction was 30%. The wearable cardioverter defibrillator was worn a median of 23.6 hours each day. There were 11 ventricular tachycardia/fibrillation episodes occurring in 10 (22%) patients. Ventricular tachycardia/fibrillation occurred over a range of 1 to 79 days, median 24 days. First-shock success for conversion of ventricular tachycardia/fibrillation was 100%. Patient survival 24 hours after shock treatment was 100%. Follow up to determine the reason for discontinuing wearable cardioverter defibrillator use indicated that among shocked patients 7 received an implantable cardioverter defibrillator, 1 patient was admitted to the hospital ending in death 2 weeks after discontinuing wearable cardioverter defibrillator use, and 2 patients were lost to follow up. Among the not shocked patients, there were 16 who received an implantable cardioverter defibrillator while 7 achieved improved left ventricular ejection fraction.</p><p>Conclusion</p><p>Management of sudden cardiac death among cardiac sarcoidosis patients was aided by the wearable cardioverter defibrillator resulting in successful termination of ventricular tachycardia/fibrillation upon delivery of shock.</p></div

Wearable cardioverter defibrillator experience.

<p>Wearable cardioverter defibrillator experience.</p

Electrocardiogram showing 9 seconds of data recorded by the WCD side-to-side channel electrodes.

<p>(A) Heart rhythm recorded by the WCD 4 days prior to VT. (B) Shock (150J) delivered by the WCD in response to sustained VT and recovery of sinus rhythm. (C) Heart rhythm recorded 7 days after delivery of shock. Recording speed (x-axis) is 25mm/second and amplitude scale (y-axis) is 1mv/20mm. Elapsed time (seconds) following the beginning of the recording are indicated.</p

Days to appropriate shock.

<p>Days of WCD wear (x-axis) are plotted against the percentage of CS patients who had received an appropriate shock in response to VT or VF.</p

Induction of ventricular tachycardias.

<p>Representative tracings of A: TKO mice and B: WT mice. Ventricular extrastimulus (VES) pacing close to the ventricular refractory time did not lead to ventricular tachycardias (VTs) in TKO mice (S1S2: 40 ms). In WT a short VT was induced by VES pacing (S1S2: 30 ms). Surf: Surface ECG. His: Intracardiac ECG close to HIS bundle.</p

Baseline ECG parameters.

<p>Cycle lenghth, spontaneous heart rate, P wave duration and PQ time (A–D) showed a siginificant prolongation in TKO. QRS duration and QTc interval did not differ (E–F). n = 10 for TKO and n = 10 for WT.</p

Probability of induction of arrhythmias.

<p>The probability of induction of AF was significantly lower in TKO compared to WT. The probability of induction of VTs was highly significant lower in TKO as in this group not any VTs could be induced during the electrophysiological study. n = 10 for TKO and n = 10 for WT.</p

Intracardiac ECG parameters and functional testing during the electrophysiological investigation.

<p>Significant differences were found in the infra-Hisian conduction that was markedly delayed in TKO (B). The 2∶1-AV-block occurred at significantly slower fixed atrial pacing cycle lengths in TKO (D). Both the atrial and the ventricular refractory period demonstrated significant prolongation in TKO (G–H). AH: Interval from first atrial signal to His signal. HV: Interval from His to first intracardiac ventricular signal. 2∶1-block: 2∶1-AV-nodal-block. SNRT: sinus node recovery time. AVNRP: AV nodal refractory period. n = 10 for TKO and n = 10 for WT.</p

Induction of atrial fibrillation.

<p>Representative tracings of A: TKO mice and B: WT mice. Atrial burst stimulation close to the refractory period (S1S1: 30 ms) failed to induce atrial fibrillation (AF) in TKO. The same burst led to the induction of an AF episode in WT that terminated spontaneously after 8.7 seconds. Surf: Surface ECG. His: Intracardiac ECG close to His bundle.</p