Perioperative Sensor and Algorithm Programming in Patients with Implanted ICDs and Pacemakers for Cardiac Resynchronization Therapy.
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ABSTRACT: Background
ICDs and pacemakers for cardiac resynchronization therapy (CRT) are complex devices with different sensors and automatic algorithms implanted in patients with advanced cardiac diseases. Data on the perioperative management and outcome of CRT carriers undergoing surgery unrelated to the device are scarce.Methods
Data from 198 CRT device carriers (100 with active rate responsive sensor) were evaluated regarding perioperative adverse (device-related) events (A(D)E) and lead parameter changes.Results
Thirty-nine adverse observations were documented in 180 patients during preoperative interrogation, which were most often related to the left-ventricular lead and requiring intervention/reprogramming in 22 cases (12%). Anesthesia-related events occurred in 69 patients. There was no ADE for non-cardiac surgery and in pacemaker-dependent patients not programmed to an asynchronous pacing mode. Post-operative device interrogation showed significant lead parameter changes in 64/179 patients (36%) requiring reprogramming in 29 cases (16%).Conclusion
The left-ventricular pacing lead represents the most vulnerable system component. Comprehensive pre and post-interventional device interrogation is mandatory to ensure proper system function. The type of ICD function suspension has no impact on each patient's outcome. Precautionary activity sensor deactivation is not required for non-cardiac interventions. Routine prophylactic device reprogramming to asynchronous pacing appears inessential. Most of the CRT pacemakers do not require surgery-related reprogramming.
SUBMITTER: Niedermeier A
PROVIDER: S-EPMC8705781 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Cardiac resynchronization therapy (CRT) improves outcomes in patients with heart failure, yet response rates are variable. We sought to determine whether physician-specified CRT programming was associated with improved outcomes.Using data from the ALTITUDE remote follow-up cohort, we examined sensed atrioventricular (AV) and ventricular-to-ventricular (VV) programming and their associated outcomes in patients with de novo CRT from 2009-2010. Outcomes included arrhythmia burden, left ventricular (LV) pacing, and all-cause mortality at 4 years.We identified 5709 patients with de novo CRT devices; at the time of implant, 34% (n?=?1959) had entirely nominal settings programmed, 40% (n?=?2294) had only AV timing adjusted, 11% (n?=?604) had only VV timing adjusted, and 15% (n?=?852) had both AV and VV adjusted from nominal programming. Suboptimal LV pacing (<95%) during follow-up was similar across groups; however, the proportion with atrial fibrillation (AF) burden >5% was lowest in the AV-only adjusted group (17.9%) and highest in the nominal (27.7%) and VV-only adjusted (28.3%) groups. Adjusted all-cause mortality was significantly higher among patients with non-nominal AV delay >120 vs. <120 ms (adjusted heart rate (HR) 1.28, p?=?0.008) but similar when using the 180-ms cutoff (adjusted HR 1.13 for >180 vs. ?180 ms, p?=?0.4).Nominal settings for de novo CRT implants are frequently altered, most commonly the AV delay. There is wide variability in reprogramming. Patients with nominal or AV-only adjustments appear to have favorable pacing and arrhythmia outcomes. Sensed AV delays less than 120 ms are associated with improved survival.
| S-EPMC4795184 | biostudies-literature
Project description:Systolic heart failure is a major problem for Americans today, with 550,000 new cases diagnosed per year, and ultimately contributes to 287,000 deaths annually. While pharmacologic therapy has drastically improved outcomes in patients with systolic heart failure, hospitalizations from systolic heart failure continue to increase and remain a major cost burden. In response to this unmet need, recent years have seen dramatic improvements in device-based therapy targeting one cause of systolic dysfunction: dyssynchronous ventricular contraction. Cardiac resynchronization therapy aims to restore mechanical synchrony by electrically activating the heart in a synchronized manner. This review summarizes the rationale for cardiac resynchronization therapy, evidence for its use, current guidelines, and ongoing and future directions for research.
| S-EPMC3096278 | biostudies-other
Project description:Objectives: To test whether (1) electromechanical dyssynchrony induces region-specific alterations in the myocardial transcriptome and (2) dyssynchrony-induced gene expression changes can be corrected by cardiac resynchronization (CRT). Background: To date, CRT is the only heart failure treatment that can both acutely and chronically increase systolic function and prolong survival, something not yet achieved by a drug therapy. However, the mechanisms underlying the benefits of CRT remain elusive. Methods: Adult dogs underwent left bundle branch ablation (LBBB) and right atrial pacing at 200 bpm for either 6 weeks (dyssynchronous heart failure, DHF, n=12) or 3 weeks followed by 3 weeks of resynchronization by bi-ventricular pacing at the same pacing rate (CRT, n=10). Control animals without LBBB were not paced (NF, n=14). Echocardiography and invasive hemodynamic measurements were performed at 3 and 6 weeks. At 6 weeks, RNA was isolated from the anterior and lateral LV walls and hybridized onto canine-specific 44K microarrays. Results: In DHF, transcriptional changes consistent with re-expression of a fetal gene program were primarily observed in the anterior LV, resulting in increased regional heterogeneity of gene expression within the left ventricle. Dyssynchrony-induced region-specific expression changes in 1050 transcripts were reversed by CRT to levels of NF hearts (false discovery rate <5%). CRT remodeled transcripts with metabolic and cell signaling function and greatly reduced regional heterogeneity of gene expression compared with DHF. Conclusions: Our results demonstrate a profound effect of electromechanical dyssynchrony on the regional cardiac transcriptome, causing gene expression changes primarily in the anterior LV wall. CRT corrected the alterations in gene expression in the anterior wall by reversing the fetal gene expression pattern, supporting a global effect of biventricular pacing on the ventricular transcriptome that extends beyond the pacing site in the lateral wall.
2010-01-05 | GSE14338 | GEO
Project description:Objectives: To test whether (1) electromechanical dyssynchrony induces region-specific alterations in the myocardial transcriptome and (2) dyssynchrony-induced gene expression changes can be corrected by cardiac resynchronization (CRT). Background: To date, CRT is the only heart failure treatment that can both acutely and chronically increase systolic function and prolong survival, something not yet achieved by a drug therapy. However, the mechanisms underlying the benefits of CRT remain elusive. Methods: Adult dogs underwent left bundle branch ablation (LBBB) and right atrial pacing at 200 bpm for either 6 weeks (dyssynchronous heart failure, DHF, n=12) or 3 weeks followed by 3 weeks of resynchronization by bi-ventricular pacing at the same pacing rate (CRT, n=10). Control animals without LBBB were not paced (NF, n=14). Echocardiography and invasive hemodynamic measurements were performed at 3 and 6 weeks. At 6 weeks, RNA was isolated from the anterior and lateral LV walls and hybridized onto canine-specific 44K microarrays. Results: In DHF, transcriptional changes consistent with re-expression of a fetal gene program were primarily observed in the anterior LV, resulting in increased regional heterogeneity of gene expression within the left ventricle. Dyssynchrony-induced region-specific expression changes in 1050 transcripts were reversed by CRT to levels of NF hearts (false discovery rate <5%). CRT remodeled transcripts with metabolic and cell signaling function and greatly reduced regional heterogeneity of gene expression compared with DHF. Conclusions: Our results demonstrate a profound effect of electromechanical dyssynchrony on the regional cardiac transcriptome, causing gene expression changes primarily in the anterior LV wall. CRT corrected the alterations in gene expression in the anterior wall by reversing the fetal gene expression pattern, supporting a global effect of biventricular pacing on the ventricular transcriptome that extends beyond the pacing site in the lateral wall.
2010-01-05 | GSE14327 | GEO
Project description:Objectives: To test whether (1) electromechanical dyssynchrony induces region-specific alterations in the myocardial transcriptome and (2) dyssynchrony-induced gene expression changes can be corrected by cardiac resynchronization (CRT). Background: To date, CRT is the only heart failure treatment that can both acutely and chronically increase systolic function and prolong survival, something not yet achieved by a drug therapy. However, the mechanisms underlying the benefits of CRT remain elusive. Methods: Adult dogs underwent left bundle branch ablation (LBBB) and right atrial pacing at 200 bpm for either 6 weeks (dyssynchronous heart failure, DHF, n=12) or 3 weeks followed by 3 weeks of resynchronization by bi-ventricular pacing at the same pacing rate (CRT, n=10). Control animals without LBBB were not paced (NF, n=14). Echocardiography and invasive hemodynamic measurements were performed at 3 and 6 weeks. At 6 weeks, RNA was isolated from the anterior and lateral LV walls and hybridized onto canine-specific 44K microarrays. Results: In DHF, transcriptional changes consistent with re-expression of a fetal gene program were primarily observed in the anterior LV, resulting in increased regional heterogeneity of gene expression within the left ventricle. Dyssynchrony-induced region-specific expression changes in 1050 transcripts were reversed by CRT to levels of NF hearts (false discovery rate <5%). CRT remodeled transcripts with metabolic and cell signaling function and greatly reduced regional heterogeneity of gene expression compared with DHF. Conclusions: Our results demonstrate a profound effect of electromechanical dyssynchrony on the regional cardiac transcriptome, causing gene expression changes primarily in the anterior LV wall. CRT corrected the alterations in gene expression in the anterior wall by reversing the fetal gene expression pattern, supporting a global effect of biventricular pacing on the ventricular transcriptome that extends beyond the pacing site in the lateral wall. Complementary study to GSE14327. While GSE14327 was designed as a 1-color microarray experiment, this series was carried out following a 2-color design (anterior and lateral LV wall labeled with Cy3 and Cy5, respectively, including dye swaps).
2010-05-16 | E-GEOD-14338 | biostudies-arrayexpress
Project description:Objectives: To test whether (1) electromechanical dyssynchrony induces region-specific alterations in the myocardial transcriptome and (2) dyssynchrony-induced gene expression changes can be corrected by cardiac resynchronization (CRT). Background: To date, CRT is the only heart failure treatment that can both acutely and chronically increase systolic function and prolong survival, something not yet achieved by a drug therapy. However, the mechanisms underlying the benefits of CRT remain elusive. Methods: Adult dogs underwent left bundle branch ablation (LBBB) and right atrial pacing at 200 bpm for either 6 weeks (dyssynchronous heart failure, DHF, n=12) or 3 weeks followed by 3 weeks of resynchronization by bi-ventricular pacing at the same pacing rate (CRT, n=10). Control animals without LBBB were not paced (NF, n=14). Echocardiography and invasive hemodynamic measurements were performed at 3 and 6 weeks. At 6 weeks, RNA was isolated from the anterior and lateral LV walls and hybridized onto canine-specific 44K microarrays. Results: In DHF, transcriptional changes consistent with re-expression of a fetal gene program were primarily observed in the anterior LV, resulting in increased regional heterogeneity of gene expression within the left ventricle. Dyssynchrony-induced region-specific expression changes in 1050 transcripts were reversed by CRT to levels of NF hearts (false discovery rate <5%). CRT remodeled transcripts with metabolic and cell signaling function and greatly reduced regional heterogeneity of gene expression compared with DHF. Conclusions: Our results demonstrate a profound effect of electromechanical dyssynchrony on the regional cardiac transcriptome, causing gene expression changes primarily in the anterior LV wall. CRT corrected the alterations in gene expression in the anterior wall by reversing the fetal gene expression pattern, supporting a global effect of biventricular pacing on the ventricular transcriptome that extends beyond the pacing site in the lateral wall. Designed as a 1-color experiments, samples from anterior and lateral left ventricular myocardium from non-failing, DHF and CRT animals were labeled with Cy3 and hybridized onto Agilent 44K long oligonucleotide arrays.
2010-05-16 | E-GEOD-14327 | biostudies-arrayexpress
Project description:Diagnosing cardiac sarcoidosis (CS), especially in isolated cases, is challenging, particularly due to the limitations of endomyocardial biopsy, leading to potential undiagnosed cases in pacemaker-implanted patients. This study aims to provide real world findings to support new guideline for CS using 18F-fluoro-deoxyglucose positron-emission tomography computed tomography (FDG-PET/CT) which give a definite diagnosis of isolated CS (iCS) without histological findings. We examined consecutive patients with cardiac pacemakers for atrioventricular block (AV-b) attending our outpatient pacemaker clinic. The patients underwent periodical follow-up echocardiography and were divided into two groups according to echocardiographic findings: those with suspected CS and those without suspected CS. Patients suspected of having nonischemic cardiomyopathy underwent FDG-PET/CT for CS diagnosis. We investigated the utility of the new guideline for CS using FDG-PET/CT. Among the 272 patients enrolled, 97 patients were implanted with cardiac pacemakers for AV-b. Twenty-two patients were suspected of having CS during a median observation period of 5.4 years after pacemaker implantation. Of these, one did not consent, and nine of 21 cases (43%) were diagnosed with definite CS according to the new guidelines. Five of these nine patients were diagnosed with iCS using FDG-PET/CT. The number of patients diagnosed with definite CS using the new guidelines tended to be approximately 2.3 times that of the conventional criteria (p = 0.074). Three of the nine patients underwent steroid treatment. The composite outcome, comprising all-cause death, heart failure hospitalization, and a substantial reduction in left ventricular ejection fraction, were significantly lower in patients receiving steroid treatment compared to those without steroid treatment (p = 0.048). The utilization of FDG-PET/CT in accordance with the new guidelines facilitates the diagnosis of CS, including iCS, resulting in approximately 2.3 times as many diagnoses of CS compared to the conventional criteria. This guideline has the potential to support the early identification of iCS and may contribute to enhancing patient clinical outcomes.
| S-EPMC10991404 | biostudies-literature
Project description:BackgroundWhether reprogramming of cardiac resynchronization therapy (CRT) to increase electrical synchrony translates into echocardiographic improvement remains unclear. SyncAV is an algorithm that allows fusion of intrinsic conduction with biventricular pacing. We aimed to assess whether reprogramming chronically implanted CRT devices with SyncAV is associated with improved echocardiographic parameters.MethodsPatients at a quaternary center with previously implanted CRT devices with a programmable SyncAV algorithm underwent routine electrocardiography-based SyncAV optimization during regular device clinic visits. This analysis included only patients who could be programmed to the SyncAV algorithm (i.e., in sinus rhythm with intrinsic atrioventricular conduction). Echocardiography was performed before and 6 months after CRT optimization.ResultsOf 64 consecutive, potentially eligible patients who underwent assessment, 34 who were able to undergo SyncAV programming were included. Their mean age was 74 ± 9 years, 41% were female, and 59% had ischemic cardiomyopathy. The mean time from CRT implant to SyncAV optimization was 17.8 ± 8.5 months. At 6-month follow-up, SyncAV optimization was associated with a significant increase in left ventricular ejection fraction (LVEF) (mean LVEF 36.5% ± 13.3% vs 30.9% ± 13.3%; P < 0.001) and a reduction in left ventricular end-systolic volume (LVESV) (mean LVESV 110.5 ± 57.5 mL vs 89.6 ± 52.4 mL; P < 0.001) compared with baseline existing CRT programming.ConclusionCRT reprogramming to maximize biventricular fusion pacing significantly increased LVEF and reduced LVESV in patients with chronic CRT devices. Further studies are needed to assess if a continuous fusion pacing algorithm improves long-term clinical outcomes and to identify which patients are most likely to derive benefit.
| S-EPMC7067690 | biostudies-literature
Project description:BackgroundWhether reprogramming of cardiac resynchronization therapy (CRT) to increase electrical synchrony translates into echocardiographic improvement remains unclear. SyncAV is an algorithm that allows fusion of intrinsic conduction with biventricular pacing. We aimed to assess whether reprogramming chronically implanted CRT devices with SyncAV is associated with improved echocardiographic parameters.MethodsPatients at a quaternary center with previously implanted CRT devices with a programmable SyncAV algorithm underwent routine electrocardiography-based SyncAV optimization during regular device clinic visits. This analysis included only patients who could be programmed to the SyncAV algorithm (i.e., in sinus rhythm with intrinsic atrioventricular conduction). Echocardiography was performed before and 6 months after CRT optimization.ResultsOf 64 consecutive, potentially eligible patients who underwent assessment, 34 who were able to undergo SyncAV programming were included. Their mean age was 74 ± 9 years, 41% were female, and 59% had ischemic cardiomyopathy. The mean time from CRT implant to SyncAV optimization was 17.8 ± 8.5 months. At 6-month follow-up, SyncAV optimization was associated with a significant increase in left ventricular ejection fraction (LVEF) (mean LVEF 36.5% ± 13.3% vs 30.9% ± 13.3%; P < 0.001) and a reduction in left ventricular end-systolic volume (LVESV) (mean LVESV 110.5 ± 57.5 mL vs 89.6 ± 52.4 mL; P < 0.001) compared with baseline existing CRT programming.ConclusionCRT reprogramming to maximize biventricular fusion pacing significantly increased LVEF and reduced LVESV in patients with chronic CRT devices. Further studies are needed to assess if a continuous fusion pacing algorithm improves long-term clinical outcomes and to identify which patients are most likely to derive benefit.
| S-EPMC7067690 | biostudies-literature
Project description:BackgroundWhether reprogramming of cardiac resynchronization therapy (CRT) to increase electrical synchrony translates into echocardiographic improvement remains unclear. SyncAV is an algorithm that allows fusion of intrinsic conduction with biventricular pacing. We aimed to assess whether reprogramming chronically implanted CRT devices with SyncAV is associated with improved echocardiographic parameters.MethodsPatients at a quaternary center with previously implanted CRT devices with a programmable SyncAV algorithm underwent routine electrocardiography-based SyncAV optimization during regular device clinic visits. This analysis included only patients who could be programmed to the SyncAV algorithm (i.e., in sinus rhythm with intrinsic atrioventricular conduction). Echocardiography was performed before and 6 months after CRT optimization.ResultsOf 64 consecutive, potentially eligible patients who underwent assessment, 34 who were able to undergo SyncAV programming were included. Their mean age was 74 ± 9 years, 41% were female, and 59% had ischemic cardiomyopathy. The mean time from CRT implant to SyncAV optimization was 17.8 ± 8.5 months. At 6-month follow-up, SyncAV optimization was associated with a significant increase in left ventricular ejection fraction (LVEF) (mean LVEF 36.5% ± 13.3% vs 30.9% ± 13.3%; P < 0.001) and a reduction in left ventricular end-systolic volume (LVESV) (mean LVESV 110.5 ± 57.5 mL vs 89.6 ± 52.4 mL; P < 0.001) compared with baseline existing CRT programming.ConclusionCRT reprogramming to maximize biventricular fusion pacing significantly increased LVEF and reduced LVESV in patients with chronic CRT devices. Further studies are needed to assess if a continuous fusion pacing algorithm improves long-term clinical outcomes and to identify which patients are most likely to derive benefit.
| S-EPMC7067690 | biostudies-literature