The prognostic impact of shocks for clinical and induced arrhythmias on morbidity and mortality among patients with implantable cardioverter-defibrillators.
BACKGROUND
Recent investigations have demonstrated that the occurrence of implantable cardioverter-defibrillator (ICD) shocks is associated with adverse long-term outcomes. These studies have emphasized that the risk is most reasonably due to arrhythmias rather than to the shock itself. We sought to compare the impact of shock delivery for induced ventricular arrhythmias during implantation defibrillation threshold testing and noninvasive electrophysiology study (NIPS) to clinical shocks on long-term outcomes among patients with ICDs.


METHODS
This was a cohort evaluation of 1,372 patients undergoing ICD implantation at a tertiary hospital from December 1997 to January 2007. The probability of all-cause mortality and hospitalization for acute decompensated heart failure (ADHF) was evaluated based upon the type of ICD shock received using multivariable Cox proportional analyses. The four shock types analyzed were implantation shocks only (n = 694), additional NIPS shocks only (n = 319), additional appropriate shocks only (n = 128), or additional inappropriate shocks only (n = 104).


RESULTS
The risk of death (adjusted hazard ratio [AHR] 0.91 [95% confidence interval (CI) 0.69-1.20]; P = .491) or ADHF (AHR 0.71 [95% CI 0.46-1.16]; P = .277) were similar between recipients of NIPS shocks and recipients of implantation shocks. Receiving an appropriate ICD shock increased the risk of death (AHR 2.09 [95% CI 1.38-2.69]; P <.001) and ADHF (AHR 2.40 [95% CI 1.51-3.81]; P <.002) as compared with implantation shocks and also increased the risk of death (AHR 2.61 [95% CI 1.86-3.67]; P <.001) and ADHF (AHR 2.29 [95% CI 1.33-3.97]; P = .003) as compared with NIPS shocks.


CONCLUSIONS
ICD shocks delivered during induced ventricular arrhythmias at the time of NIPS testing does not increase the risk of death or ADHF as compared with recipients of appropriate ICD shocks. The occurrence of spontaneous arrhythmias in vulnerable substrates may explain the increased risk.
Bhavnani
Sanjeev P
SP
Department of Cardiology, Evidence Based Practice Center, Hartford Hospital, Hartford, Connecticut 06102-5037, USA.
Kluger
Jeffrey
J
Coleman
Craig I
CI
White
C Michael
CM
Guertin
Danette
D
Shafi
Nabil A
NA
Yarlagadda
Ravi K
RK
Clyne
Christopher A
CA
D000368:Aged; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D015331:Cohort Studies; D016001:Confidence Intervals; D003237:Connecticut; D017147:Defibrillators, Implantable; D004077:Digoxin / Q000627:therapeutic use; D004594:Electrophysiology; D005260:Female; D006333:Heart Failure / Q000401:mortality / Q000473:pathology / Q000628:therapy*; D006801:Humans; D053208:Kaplan-Meier Estimate; D008297:Male; D015999:Multivariate Analysis; D010627:Phenethylamines / Q000627:therapeutic use; D011379:Prognosis; D016016:Proportional Hazards Models; D012189:Retrospective Studies; D012307:Risk Factors; D013449:Sulfonamides / Q000627:therapeutic use; D017180:Tachycardia, Ventricular / Q000209:etiology / Q000401:mortality* / Q000473:pathology / Q000628:therapy; D016896:Treatment Outcome; D014693:Ventricular Fibrillation / Q000209:etiology / Q000401:mortality* / Q000473:pathology / Q000628:therapy
D000889:Anti-Arrhythmia Agents; D010627:Phenethylamines; D013449:Sulfonamides; D004077:Digoxin; C063533:dofetilide