Etiology and Programming Effects on Shock Efficacy in ICD Recipients (original) (raw)

The association between defibrillation shock energy and acute cardiac damage in patients with implantable cardioverter defibrillators

Journal of Arrhythmia, 2016

Background: The aim of this study was to establish a minimally invasive defibrillation testing (DT) protocol for patients with implantable cardioverter defibrillators (ICDs). Methods: Two different energy DTs were performed, immediately after (15 J-DT) and 7 days after (r10 J-DT) device implantation, in 20 consecutive ICD implantation patients. Cardiac-troponin T (c-TNT) and heart-type fatty acid binding protein (H-FABP) levels were measured before implantation, 2 h after implantation, and 1 day after each DT. For an additional 122 patients with ICD, we retrospectively analyzed 203 DTs immediately and 7 days after device implantation. Results: Serum c-TNT levels were significantly elevated 2 h after 15 J-DT [0.008 (0.004-0.019) vs. 0.053 (0.037-0.068) ng/mL, p o0.001], but not r10 J-DT [0.007 (0.004-0.018) ng/mL]. Similarly, serum H-FABP levels were significantly elevated 2 h after 15 J-DT (2.9 71.5 vs. 6.4 73.4 ng/mL, po 0.001), but not r10 J-DT (2.7 71.5 ng/mL). The changes in c-TNT and H-FABP levels between baseline and 2 h after DT were significantly greater for 15 J-DT compared with r10 J-DT [c-TnT: 0.039 (0.029-0.060) vs. 0 (0-0.003) ng/mL, p o0.001; H-FABP: 3.67 2.8 vs. À 0.16 7 1.1 ng/mL, po0.001]. The success rates of the initial shocks delivered for ventricular fibrillation were no different between r 10 J-DT (85% [78/92]) and Z15 J-DT (92% [103/111]). Conclusions: Elevated levels of myocardial damage markers such as c-TNT and H-FABP were not found after r10 J-DT. In addition, an acceptable success rate was confirmed in r 10 J-DT.

Effect of Ventricular Shock Strength on Cardiac Hemodynamics

Journal of Cardiovascular Electrophysiology, 1998

Ventricular Defibrillation and Cardiac Function. Introduction: The effect of implantable defibrillator shocks on cardiac hemodynamics is poorly understood. The purpose of this study was to test the hypothesis that ventricular defibrillator shocks adversely effect cardiac hemodynamics.Methods and Results: The cardiac index was determined by calculating the mitral valve inflow with transesophogeal Doppler during nonthoracotomy defibrillator implantation in 17 patients. The cardiac index was determined before, and immediately, 1 minute, 2 minutes, and 4 minutes after shocks were delivered during defibrillation energy requirement testing with 27- to 34-, 15-, 10-, 5-, 3-, or 1-J shocks. The cardiac Index was also measured at the same time points after 27- to 34-, and 1-J shocks delivered during the baseline rhythm. The cardiac index decreased from 2.30 ± 0.40 L/min per m2 before a 27- to 34-J shock during defibrillation energy requirement testing to 2.14 ± 0.45 L/min per m2 immediately afterwards (P= 0.001). This effect persisted for >4 minutes. An adverse hemodynamic effect of similar magnitude occurred after 15 J (P= 0.003) and 10-J shocks (P= 0.01), but dissipated after 4 minutes and within 2 minutes, respectively. There was a significant correlation between shock strength and the percent change in cardiac index (r = 0.3, P= 0.03). The cardiac index decreased 14% after a 27- to 34-J shock during the baseline rhythm (P < 0.0001). This effect persisted for <4 minutes. A 1- J shock during the baseline rhythm did not effect the cardiac index.Conclusion: Defibrillator shocks >9 J delivered during the baseline rhythm or during defibrillation energy requirement testing result in a 10% to 15% reduction in cardiac index, whereas smaller energy shocks do not affect cardiac hemodynamics. The duration and extent of the adverse effect are proportional to the shock strength. Shock strength, and not ventricular fibrillation, appears to be most responsible for This effect. Therefore, the detrimental hemodynamic effects of high-energy shocks may be avoided when low-energy defibrillation is used.

Arrhythmic complications of electrical cardioversion: Relationship to shock energy

International Journal of Cardiology, 2008

Background: Existing guidelines for electrical cardioversion (ECV) of atrial arrhythmias suggest starting at a low energy setting on the grounds that shocks of high energy might damage the myocardium or trigger more serious arrhythmias. We hypothesised that more powerful shocks would exceed the upper limit of vulnerability for inducing ventricular fibrillation. The initial use of higher energy could therefore reduce arrhythmic complications. Methods: We collected data on the sequence of shocks delivered and the resulting changes in cardiac rhythm in 1896 patients who underwent transthoracic ECV. Rhythm strips derived from 200 consecutive ECV attempts were studied to verify the accuracy of the synchronisation of the shocks delivered. Results: In 2522 attempts at transthoracic ECV, 6398 shocks were delivered, 1243 in atrial flutter or atrial tachycardia, the others in AF. Ventricular fibrillation was significantly more common after shocks of < 200 J (5 of 2959 vs. 0 of 3439 shocks, p < 0.05, Fischer's exact test). Conversion of atrial flutter or atrial tachycardia to AF was also more common at < 200 J (20 of 930 shocks vs. 1 of 313 shocks at ≥ 200 J, p < 0.05, χ 2 test). Sinus bradycardia or sinus arrest complicated 0.95% of cardioversion attempts, but none required emergency pacing. The incidence of bradycardia was not related to the energy used. Conclusions: Shocks of > 200 J are associated with fewer tachyarrhythmic complications, and do not increase the risk of other serious complications. Bradycardia after cardioversion is very rarely of clinical importance.

Evaluation and Management of Patients After Implantable Cardioverter-Defibrillator Shock

JAMA, 2006

Context There has been a tremendous increase in the use of implantable cardioverterdefibrillators (ICDs) after several large clinical trials demonstrated their ability to effectively reduce mortality in selected populations of patients with cardiac disease. Thus, the nonelectrophysiologist will often encounter patients who have received an ICD shock. Objective To assess options for the evaluation and management of patients who have received an ICD shock. Evidence Acquisition Literature search using the PubMed and MEDLINE databases to identify articles published from January 1990 to September 2006, using the Medical Subject Headings defibrillators, implantable; defibrillators, implantable/ adverse effects; anti-arrhythmic agents; electric countershock; quality of life; tachycardia therapy; algorithm; ventricular tachycardia/diagnosis; and supraventricular tachycardia/diagnosis. Case reports were excluded and articles were limited to those published in English. Scientific statements and guidelines from the American College of Cardiology, the American Heart Association, and the Heart Rhythm Society were also reviewed, as were the reference lists of retrieved articles, to identify any additional articles for inclusion. Evidence Synthesis There are multiple causes of both appropriate and inappropriate ICD shocks. Irrespective of appropriateness, receiving ICD shocks substantially impairs a patient's quality of life. A variety of techniques are available using ICD programming to reliably limit the occurrence of appropriate or inappropriate ICD shocks. Antiarrhythmic medications can also effectively reduce the occurrence of shocks. Conclusions Through the use of effective ICD programming and antiarrhythmic medications, the occurrence of ICD shocks can be reduced while maintaining the lifesaving ability of the ICD. A basic understanding of the range of available options is fundamental for evaluation and management of the patient who has received an ICD shock.

The Significance of Shocks in Implantable Cardioverter Defibrillator Recipients

Arrhythmia & electrophysiology review, 2016

Large-scale implantable cardioverter defibrillator (ICD) trials have unequivocally shown a reduction in mortality in appropriately selected patients with heart failure and depressed left ventricular function. However, there is a strong association between shocks and increased mortality in ICD recipients. It is unclear if shocks are merely a marker of a more severe cardiovascular disease or directly contribute to the increase in mortality. The aim of this review is to examine the relationship between ICD shocks and mortality, and explore possible mechanisms. Data examining the effect of shocks in the absence of spontaneous arrhythmias as well as studies of non-shock therapy and strategies to reduce shocks are analysed to try and disentangle the shocks versus substrate debate.

The effect of an unsuccessful subthreshold shock on the energy requirement for the subsequent defibrillation

American Heart Journal, 1989

The effect of an unsuccessful subthreshold shock on the energy requirement for the subsequent defibrillation The effect of an unsuccessful subthreshold shock on the energy requirement for the subsequent defibrillation was studied in 10 anesthetized dogs. Deffbrlllatfon was achieved with a spring catheter electrode in the superior vena cava and a patch electrode on the anteroapical ventricular wall. Success rates of defibrillation 20 seconds from the onset of ventricular fibrhlation were determined at three energy levels with and without a preceding subthreshold shock. Altogether, 637 epfsodes of fibrillation-defibrillation were performed (63.7 * 6.7 per dog). Predicted energy levels for defibrillation success rates of 50% and 80% (E50 and E80) acquired from a loglstfc reSression curve were 0.0303 ? 0.064 and 0.0367 + 0.0069 joule/gm, respectively, without subthreshold shocks. E50 and E80 with an unsuccessful subthreshold shock resulted in comparable values (E50: 0.0325 + 0.0041 joule/gm; E80: 0.0.380 f 0.0100 joule/gm). Our results suggest that an unsuccessful low-energy shock does not alter the energy requirement for subsequent defibrillation with an implantable defibrillator.

Survival After Implantable Cardioverter-Defibrillator Shocks

Journal of the American College of Cardiology, 2021

BACKGROUNDThere are conflicting data on the impact of implantable cardioverter-defibrillator (ICD) shocks on subsequent mortality.OBJECTIVESThe aim of this study was to determine whether the arrhythmic substrate leading to ICD therapy or the therapy itself increases mortality.METHODSThe study cohort included 5,516 ICD recipients who were enrolled in 5 landmark ICD trials (MADIT-II, MADIT-RISK, MADIT-CRT, MADIT-RIT, RAID). The authors evaluated the association of device therapy with subsequent mortality in 4 separate time-dependent models: model I, type of ICD therapy; model II, type of arrhythmia for which ICD therapy was delivered; model III, combined assessment of all arrhythmia and therapy types during follow-up; and model IV, incremental risk associated with repeated ICD shocks.RESULTSWhen analyzed by the type of ICD therapy (model I), a first appropriate ICD shock was associated with increased risk of subsequent mortality with or without concomitant occurrence of inappropriate shock during follow-up (hazard ratios [HRs]: 2.78 and 2.31; p < 0.001 and p = 0.12), whereas inappropriate shock alone was not associated with mortality risk (HR: 1.23; p = 0.42). Similarly, ICD therapy for ventricular tachycardia (VT) ≥200 beats/min or ventricular fibrillation (VF) (model II) was associated with increased risk of death with or without concomitant therapy for VT <200 beats/min (HRs: 2.25 and 2.62; both p < 0.001), whereas appropriate therapy for VT <200 beats/min or inappropriate therapy (regardless of etiology) did not reach statistical significance (all p > 0.10). Combined assessment of all therapy and arrhythmia types during follow-up (model III) showed that appropriate ICD shocks for VF, shocks for fast VT (≥200 beats/min) without prior antitachycardia pacing (ATP), as well as shocks for fast VT delivered after failed ATP, were associated with the highest risk of subsequent death (HRs: all >2.8; p < 0.001). Finally, 2 or more ICD appropriate shocks were not associated with incremental risk to the first appropriate ICD shock (model IV).CONCLUSIONThe combined data from 5 landmark ICD trials suggest that the underlying arrhythmic substrate rather than the ICD therapy is the more important determinant of mortality in ICD recipients.