Implantable Cardiac Defibrillator For Primary Prevention Research Articles

Circulation: Cardiovascular Imaging Editors’ Picks

<i>Circulation: Cardiovascular Imaging</i> Editors’ Picks

Primary prevention with a defibrillator: are therapies always really optimized before implantation?

Left ventricle ejection fraction (LVEF) ≤ 30-35% is widely accepted as a cut-off for primary prevention with an implantable cardiac defibrillator (ICD) in patients with both ischaemic and non-ischaemic cardiomyopathy supposedly on optimal medical therapy. This study reports evolutions of LVEF and treatments of patients implanted in our institution with an ICD for primary prevention of sudden death, after 2 years of follow-up. Among 84 patients with LVEF under 35% implanted between 2005 and 2007, 28 (33%) had improved their LVEF >35% after the 2 years of follow-up. During this period, even if Beta-blockers (98%) and renin-angiotensin system (RAS) blockers (95%) were already initially prescribed, treatments were significantly optimized with improvement of maximal doses of beta-blockers and RAS blockers at 2 year follow-up compared with initial prescription (62 vs. 37% and 68 vs. 45%, respectively). In patients with improved LVEF, a trend toward a better treatment optimization and revascularization procedures (in the sub-group of ischaemic patients) were observed compared with non-improved LVEF patients. In our study of patients with prophylactic ICD, one-third of them have improved their LVEF after a 2 year follow-up. Despite an optimal medical therapy at the time of implantation, we were able to further improve the maximal treatment doses after implantation. This study highlights the issue of what should be considered as 'optimal' therapy and the possibility of improvement of LVEF related to a real optimized treatment before implantation.

Parameter Signature of a Reel Problem

Clinics involved in follow-up of cardiac implantable electronic devices, especially implantable cardiac defibrillators (ICDs), increasing rely upon remote monitoring. This case describes the parameter signature characteristic of an uncommon but well-described syndrome. Analysis of the nature and timing of the sequence of abnormalities contained in the archived device data, all of which is available for review via remote monitoring, reveals the cause for failure of this primary prevention ICD system.

Can non-invasive parameters of sympatho-vagal modulation derived from Holter monitoring contribute to risk stratification for primary implantable cardiac-defibrillator implantation?

This editorial refers to ‘Relationship between cardiac autonomic function and sustained ventricular tachyarrhythmias in patients with implantable cardioverter defibrillators’ by I. Battipaglia et al ., Europace 2010;12:1725–31. Today, we face two major challenges in risk stratification for primary prevention of sudden cardiac death (SCD) to better select patients who really benefit from implantable cardiac-defibrillators (ICDs). First, among patients with impaired left ventricular ejection fraction (LVEF), the reduction in mortality ranged from 23 to 55%, depending on the risk group, in patients treated with ICD therapy compared with optimal medical therapy; thus about half the patients benefit from primary prevention ICD implant.1–3 Secondly, among patients with prior myocardial infarction (MI) and with preserved LVEF, although the risk of SCD is lower, the total number of SCD is large;4 thus, it is necessary to identify high-risk subgroups among post-MI patients with preserved LVEF, where primary ICD implantation could prevent sudden unexpected deaths. Current indications for ICD implantation for primary prevention of SCD are based mainly on a haemodynamic parameter, left ventricular dysfunction (LVEF <30–40%) both in post- MI and in non-ischaemic cardiomyopathies.1–3,5–7 Among electrophysiological parameters, only non-sustained ventricular tachycardia (NSVT), defined as three or more consecutive ventricular beats during Holter monitoring and induction of VT on electrophysiological testing, is recognized in current guidelines as predictors of benefit from ICD implant for primary prevention of SCD.1 Consistent evidence have shown that low heart rate variability (HRV) in combination with reduced LVEF contribute to identification of patients at high risk of SCD.8–11 However, according to current guidelines for the prevention of SCD, HRV was useful for risk stratification (Class IIb recommendation), but evidence was not robust enough to include HRV as a predictor in risk stratification for primary ICD implantation. …

Predictors of Death and Occurrence of Appropriate Implantable Defibrillator Therapies in Patients With Ischemic Cardiomyopathy

Most patients with chronic ischemia and an implantable cardiac defibrillator (ICD) for primary prevention do not experience therapies for ventricular arrhythmias on follow-up. The present study aimed to identify independent clinical, electrocardiographic, and echocardiographic predictors of death and occurrence of ICD therapy in patients with chronic ischemic cardiomyopathy and ICD for primary prevention. A total of 424 patients with chronic ischemic cardiomyopathy, ejection fraction ≤ 35%, and New York Heart Association (NYHA) class ≥ II were recruited. All patients underwent echocardiography before ICD insertion. Primary outcome was all-cause mortality; secondary outcome was occurrence of appropriate ICD therapy on follow-up. Primary and secondary outcomes occurred in 84 and 95 patients, respectively. Patients who died were more likely to have diabetes (hazard ratio [HR] 1.67, 95% confidence interval [CI] 1.00 to 2.79, p = 0.049), higher NYHA class (HR 1.96, 95% CI 1.15 to 3.33, p = 0.013), lower peri-infarct strain on echocardiogram (HR 1.25, 95% CI 1.07 to 1.46, p = 0.005), and lower glomerular filtration rate (HR 1.01, 95% CI 1.00 to 1.03, p = 0.022). Only peri-infarct strain (HR 1.22, 95% CI 1.09 to 1.36, p < 0.001) predicted the occurrence of ICD therapy on follow-up. In conclusion, in chronic ischemic patients with an ICD for primary prevention, the presence of diabetes, renal dysfunction, higher NYHA class, and impaired peri-infarct zone function were predictors of all-cause mortality. In contrast, only impaired peri-infarct zone function determined the occurrence of appropriate ICD therapy on follow-up.

Abstract 1740: Risk of Proarrhythmia Following Alcohol Septal Ablation in Patients with Hypertrophic Obstructive Cardiomyopathy

Background: Alcohol septal ablation (ASA) is a promising treatment option for patients with hypertrophic obstructive cardiomyopathy (HOCM), but the creation of myocardial infarct during the procedure has raised concern about the proarrhythmic risk of ASA. We analyzed the incidence of clinically significant ventricular tachycardia (VT) and sudden cardiac death (SCD) following ASA at our center. Methods: A total of 97 ASAs in 88 patients were performed between 1998 and 2007 at MGH. 34 of these patients had an implantable cardiac defibrillator (ICD) or pacemaker (PPM) implanted prior to or immediately following ASA. 8 of 34 patients had prior ICD implants for either secondary (n=4) or primary (n=4) prevention for SCD. 8 patients had prior PPMs. 3 patients had implantation of ICD post-ASA and 15 patients had PPM implanted following ASA due to atrioventricular block (AVB). Clinical records as well as device data were analyzed to determine incidence of VT or SCD following ASA. Results: There were no deaths attributable to SCD in our cohort of 88 patients (mean follow-up 35 +/− 21 months, range 4 to 70 months). 1 patient with a previous ICD for primary prevention had VT storm 6 days following ASA. 1 patient who had a cardiac arrest 11 days following the ASA (thought to be a bradycardic arrest, since he had intermittent high grade AVB post-ASA) received an ICD. Neither of these patients had subsequent detections or therapies for VT. 1 patient was upgraded to an ICD following ASA due to NSVT, and 2 patients had ICD implants for NSVT or high risk of SCD. The former had subsequent detection of NSVT 24 months after implant, and therapy for VT 3 years later. 2 patients had upgrades of their PPM to an ICD &gt; 12 months after ASA (for positive electrophysiology studies at other centers), but had no detection or therapies during the follow-up period. No other patients had therapies for tachyrrhythmias. Conclusion: In our experience of 97 procedures, we observed 1 episode of VT storm in the first week following ASA, 1 cardiac arrest, likely bradycardic, in the first 2 weeks after ASA, and only 1 patient with clinically significant VT years after ASA. Our data suggest that close follow-up is warranted in the 2 weeks after ASA, but that ASA does not seem to have a long-term proarrhythmic effect in patients with HOCM.