Jeroen Venlet

Implantable cardioverter-defibrillator longevity under clinical circumstances: An analysis according to device type, generation, and manufacturer

BACKGROUND One of the major drawbacks of implantable cardioverter-defibrillator (ICD) treatment is the limited device service life. Thus far, data concerning ICD longevity under clinical circumstances are scarce. In this study, the ICD service life was assessed in a large cohort of ICD recipients. OBJECTIVE To assess the battery longevity of ICDs under clinical circumstances. METHODS All patients receiving an ICD in the Leiden University Medical Center were included in the analysis. During prospectively recorded follow-up visits, reasons for ICD replacement were assessed and categorized as battery depletion and non-battery depletion. Device longevity and battery longevity were calculated. The impact of device type, generation, manufacturer, the percentage of pacing, the pacing output, and the number of shocks on the battery longevity was assessed. RESULTS Since 1996, 4673 ICDs were implanted, of which 1479 ICDs (33%) were replaced. Mean device longevity was 5.0 ± 0.1 years. A total of 1072 (72%) ICDs were replaced because of battery depletion. Mean battery longevity of an ICD was 5.5 ± 0.1 years. When divided into different types, mean battery longevity was 5.5 ± 0.2 years for single-chamber ICDs, 5.8 ± 0.1 for dual-chamber ICDs, and 4.7 ± 0.1 years for cardiac resynchronization therapy-defibrillators (P <.001). Devices implanted after 2002 had a significantly better battery longevity as compared with devices implanted before 2002 (5.6 ± 0.1 years vs 4.9 ± 0.2 years; P <.001). In addition, large differences in battery longevity between manufacturers were noted (overall log-rank test, P <.001). CONCLUSIONS The majority of ICDs were replaced because of battery depletion. Large differences in longevity exist between different ICD types and manufacturers. Modern ICD generations demonstrated improved longevity.

The mode of death in implantable cardioverter-defibrillator and cardiac resynchronization therapy with defibrillator patients: results from routine clinical practice.

BACKGROUND Although data on the mode of death of implantable cardioverter-defibrillator (ICD) and cardiac resynchronization therapy with defibrillator (CRT-D) patients have been examined in randomized clinical trials, in routine clinical practice data are scarce. To provide reasonable expectations and prognosis for patients and physicians, this study assessed the mode of death in routine clinical practice. OBJECTIVE To assess the mode of death in ICD/CRT-D recipients in routine clinical practice. METHODS All patients who underwent an ICD or CRT-D implantation at the Leiden University Medical Center, the Netherlands, between 1996 and 2010 were included. Patients were divided into primary prevention ICD, secondary prevention ICD, and CRT-D patients. For patients who died during follow-up, the mode of death was retrieved from hospital and general practitioner records and categorized according to a predetermined classification: heart failure death, other cardiac death, sudden death, noncardiac death, and unknown death. RESULTS A total of 2859 patients were included in the analysis. During a median follow-up of 3.4 years (interquartile range 1.7-5.7 years), 107 (14%) primary prevention ICD, 253 (28%) secondary prevention ICD, and 302 (25%) CRT-D recipients died. The 8-year cumulative incidence of all-cause mortality was 39.9% (95% confidence interval 37.0%-42.9%). Heart failure death and noncardiac death were the most common modes of death for all groups. Sudden death accounted for approximately 7%-8% of all deaths. CONCLUSION For all patients, heart failure and noncardiac death are the most common modes of death. The proportion of patients who died suddenly was low and comparable for primary and secondary ICD and CRT-D patients.

Reassessing noninducibility as ablation endpoint of post-infarction ventricular tachycardia: the impact of left ventricular function.

Background—Noninducibility is frequently used as procedural end point of ventricular tachycardia (VT) ablation after myocardial infarction. We investigated the influence of left ventricular (LV) function on the predictive value of noninducibility for VT recurrence and cardiac mortality. Methods and Results—Ninety-one patients (82 men, 67±10 years) with post–myocardial infarction VT underwent ablation between 2009 and 2012. Fifty-nine (65%) had an LV ejection fraction (EF) >30% (mean 41±7) and 32 (35%) an LVEF⩽30% (mean 20±5). Thirty patients (51%) with EF>30% and 13 (41%) with EF⩽30% were noninducible after ablation (P=0.386). During a median follow-up of 23 (Q1–Q3 16–36) months, 35 patients (38%) experienced VT recurrences and 17 (18%) cardiac death. At 1 year follow-up, survival free from VT recurrence and cardiac death for patients with LVEF>30% was 80% (95% confidence interval [CI], 70–90) compared with 42% (95% CI, 33–51) for those with LVEF⩽30% (P=0.001). Noninducible patients with LVEF>30% had a recurrence-free survival from cardiac death of 90% (95% CI, 71–100) compared with 65% (95% CI, 47–83) for inducible patients (P=0.015). In the subgroup of patients with LVEF⩽30%, the survival free from VT recurrence and cardiac death was 31% (95% CI, 0%–60%) for noninducible compared with 39% (95% CI, 27–52) for those who remained inducible (P=0.842). Conclusions—Noninducible patients with moderately depressed LV function have a favorable outcome compared with patients who remained inducible after ablation. On the contrary, patients with severely depressed LV function have a poor prognosis independent of the acute procedural outcome.

Fast nonclinical ventricular tachycardia inducible after ablation in patients with structural heart disease: Definition and clinical implications

BACKGROUND Noninducibility of ventricular tachycardia (VT) with an equal or longer cycle length (CL) than that of the clinical VT is considered the minimum ablation endpoint in patients with structural heart disease. Because their clinical relevance remains unclear, fast nonclinical VTs are often not targeted. However, an accepted definition for fast VT is lacking. The shortest possible CL of a monomorphic reentrant VT is determined by the ventricular refractory period (VRP). OBJECTIVE The purpose of this study was to propose a patient-specific definition for fast VT based on the individual VRP (fVTVRP) and assess the prognostic significance of persistent inducibility after ablation of fVTVRP for VT recurrence. METHODS Of 191 patients with previous myocardial infarction or with nonischemic cardiomyopathy undergoing VT ablation, 70 (age 63 ± 13 years; 64% ischemic) remained inducible for a nonclinical VT and composed the study population. FVTVRP was defined as any VT with CL ≤VRP400 + 30 ms. Patients were followed for VT recurrence. RESULTS After ablation, 30 patients (43%) remained inducible exclusively for fVTVRP and 40 (57%) for any slower VT. Patients with only fVTVRP had 3-year VT-free survival of 64% (95% confidence interval [CI] 46%-82%) compared to 27% (95% CI 14%-48%) for patients with any slower remaining VT (P = .013). Inducibility of only fVTVRP was independently associated with lower VT recurrence (hazard ratio 0.38; 95% CI 0.19-0.86; P = .019). Among 36 patients inducible for any fVTVRP, only 1 had recurrence with fVTVRP. CONCLUSION In patients with structural heart disease, inducibility of exclusively fVTVRP after ablation is associated with low VT recurrence.

Unipolar Endocardial Voltage Mapping in the Right Ventricle: Optimal Cutoff Values Correcting for Computed Tomography–Derived Epicardial Fat Thickness and Their Clinical Value for Substrate Delineation

Background— Low endocardial unipolar voltage (UV) at sites with normal bipolar voltage (BV) may indicate epicardial scar. Currently applied UV cutoff values are based on studies that lacked epicardial fat information. This study aimed to define endocardial UV cutoff values using computed tomography–derived fat information and to analyze their clinical value for right ventricular substrate delineation. Methods and Results— Thirty-three patients (50±14 years; 79% men) underwent combined endocardial–epicardial right ventricular electroanatomical mapping and ablation of right ventricular scar–related ventricular tachycardia with computed tomographic image integration, including computed tomography–derived fat thickness. Of 6889 endocardial–epicardial mapping point pairs, 547 (8%) pairs with distance <10 mm and fat thickness <1.0 mm were analyzed for voltage and abnormal (fragmented/late potential) electrogram characteristics. At sites with endocardial BV >1.50 mV, the optimal endocardial UV cutoff for identification of epicardial BV <1.50 mV was 3.9 mV (area under the curve, 0.75; sensitivity, 60%; specificity, 79%) and cutoff for identification of abnormal epicardial electrogram was 3.7 mV (area under the curve, 0.88; sensitivity, 100%; specificity, 67%). The majority of abnormal electrograms (130 of 151) were associated with transmural scar. Eighty-six percent of abnormal epicardial electrograms had corresponding endocardial sites with BV <1.50 mV, and the remaining could be identified by corresponding low endocardial UV <3.7 mV. Conclusions— For identification of epicardial right ventricular scar, an endocardial UV cutoff value of 3.9 mV is more accurate than previously reported cutoff values. Although the majority of epicardial abnormal electrograms are associated with transmural scar with low endocardial BV, the additional use of endocardial UV at normal BV sites improves the diagnostic accuracy resulting in identification of all epicardial abnormal electrograms at sites with <1.0 mm fat.

QRS prolongation after premature stimulation is associated with polymorphic ventricular tachycardia in nonischemic cardiomyopathy: Results from the Leiden Nonischemic Cardiomyopathy Study

BACKGROUND Progressive activation delay after premature stimulation has been associated with ventricular fibrillation in nonischemic cardiomyopathy (NICM). OBJECTIVES The objectives of this study were (1) to investigate prolongation of the paced QRS duration (QRSd) after premature stimulation as a marker of activation delay in NICM, (2) to assess its relation to induced ventricular arrhythmias, and (3) to analyze its underlying substrate by late gadolinium enhancement cardiac magnetic resonance imaging (LGE-CMR) and endomyocardial biopsy. METHODS Patients with NICM were prospectively enrolled in the Leiden Nonischemic Cardiomyopathy Study and underwent a comprehensive evaluation including LGE-CMR, electrophysiology study, and endomyocardial biopsy. Patients without structural heart disease served as controls for electrophysiology study. RESULTS Forty patients with NICM were included (mean age 57 ± 14 years; 33 men [83%]; left ventricular ejection fraction 30% ± 13%). After the 400-ms drive train and progressively premature stimulation, the maximum increase in QRSd was larger in patients with NICM than in controls (35 ± 18 ms vs. 23 ± 12 ms; P = .005) and the coupling interval window with QRSd prolongation was wider (47 ± 23 ms vs. 31 ± 14 ms; P = .005). The maximum paced QRSd exceeded the ventricular effective refractory period, allowing for pacing before the offset of the QRS complex in 20 of 39 patients with NICM vs. 1 of 20 controls (P < .001). In patients with NICM, QRSd prolongation was associated with the inducibility of polymorphic ventricular tachycardia (16 of 39 patients) and was related to long, thick strands of fibrosis in biopsies, but not to focal enhancement on LGE-CMR. CONCLUSION QRSd is a simple parameter used to quantify activation delay after premature stimulation, and its prolongation is associated with the inducibility of polymorphic ventricular tachycardia and with the pattern of myocardial fibrosis in biopsies.