Loss Of Left Ventricular Capture Research Articles

PO-04-102 LOSS OF LEFT VENTRICULAR CAPTURE DURING ACUTE HEMOPERICARDIUM

Loss of left ventricular capture from a chronic quadripolar coronary sinus lead was observed during development of an iatrogenic cardiac pericardial effusion. Subsequently, during pericardiocentesis left ventricular capture was reobtained. Reaccumulation of hemopericardium again resulted in repeated observable loss of LV capture. No previous documentation in literature review is noted. This phenomenon may have critical clinical value in predicting significant pericardial effusion or affect the clinical value of cardiac resynchronization therapy in patients with chronic pericardial effusions. To demonstrate a previously undocumented clinical phenomenon that significantly affect patient care and outcomes. N/A We present a case of an 83 YO male patient with iatrogenic pericardial effusion during transseptal puncture resulting in cardiac tamponade and observed loss of left ventricular capture. Our patient presented for Watchman implantation however after transseptal puncture prior to Watchman implantation hemopericardium developed with cardiac tamponade. Loss of LV capture resulted in RV only pacing until pericardiocentesis with placement of a pericardial drain was placed. After evacuation of 80cc volume and gross reduction in pericardial effusion size on transesophageal echocardiography with resolution of cardiac tamponade, LV capture was again noted. Device interrogation revealed stable lead thresholds. During clinical followup, reaccumulation of hemopericardium again resulted in loss of LV capture prior to clinical tamponade and again resolution of pericardial effusion resulted in regaining biventricular capture. Figure 1: Progressive loss of biventricular capture is noted during pericardial effusion accumulation leading to cardiac tamponade. Hemopericardium may result in loss of left ventricular capture from a chronic coronary sinus lead with stable thresholds. The observed loss of capture occurred prior to clinical cardiac tamponade and may offer an early qualitative measure of significant pericardial effusions.

Using a smartwatch for the detection of loss of left ventricular capture in patients receiving cardiac resynchronization therapy

Pilot studies showed promising applications for smartwatches (SWs) beyond the detection of atrial fibrillation. 1 Cobos Gil M.Á. Standard and precordial leads obtained with an Apple watch. Ann Intern Med. 2020; 172: 436 Crossref PubMed Scopus (23) Google Scholar Ammann et al 2 Ammann P. Sticherling C. Kalusche D. et al. An electrocardiogram-based algorithm to detect loss of left ventricular capture during cardiac resynchronization therapy. Ann Intern Med. 2005; 142: 968-973 Crossref PubMed Google Scholar developed a readily applicable algorithmClick or tap here to enter text. for detecting loss of left ventricular (LV) capture in patients with heart failure receiving cardiac resynchronization therapy (CRT) using leads I and V1 of the standard 12-lead electrocardiogram (ECG) (Figure 1). 3 Cao Y.-Y. Su Y.-G. Bai J. et al. The roles of the Q (q) wave in lead I and QRS frontal axis for diagnosing loss of left ventricular capture during cardiac resynchronization therapy. J Cardiovasc Electrophysiol. 2015; 26: 64-69 Crossref PubMed Scopus (4) Google Scholar We hypothesized that recording lead I and modified lead V1 ECGs with a SW allows the validation of the Ammann algorithm for detecting loss of LV capture.

Automated detection of effective left-ventricular pacing: going beyond percentage pacing counters.

AimsCardiac resynchronization therapy (CRT) devices report percentage pacing as a diagnostic but cannot determine the effectiveness of each paced beat in capturing left-ventricular (LV) myocardium. Reasons for ineffective LV pacing include improper timing (i.e. pseudofusion) or inadequate pacing output. Device-based determination of effective LV pacing may facilitate optimization of CRT response.Methods and resultsEffective capture at the LV cathode results in a negative deflection (QS or QS-r morphology) on a unipolar electrogram (EGM). Morphological features of LV cathode–RV coil EGMs were analysed to develop a device-based automatic algorithm, which classified each paced beat as effective or ineffective LV pacing. The algorithm was validated using acute data from 28 CRT-defibrillator patients. Effective LV pacing and pseudofusion was simulated by pacing at various AV delays. Loss of LV capture was simulated by RV-only pacing. The algorithm always classified LV or biventricular (BV) pacing with AV delays ≤60% of patient's intrinsic AV delay as effective pacing. As AV delays increased, the percentage of beats classified as effective LV pacing decreased. Algorithm results were compared against a classification truth based on correlation coefficients between paced QRS complexes and intrinsic rhythm QRS templates from three surface ECG leads. An average correlation >0.9 defined a classification truth of ineffective pacing. Compared against the classification truth, the algorithm correctly classified 98.2% (3240/3300) effective LV pacing beats, 75.8% (561/740) of pseudofusion beats, and 100% (540/540) of beats with loss of LV capture.ConclusionA device-based algorithm for beat-by-beat monitoring of effective LV pacing is feasible.

The roles of the Q (q) wave in lead I and QRS frontal axis for diagnosing loss of left ventricular capture during cardiac resynchronization therapy.

Loss of left ventricular (LV) capture may lead to deterioration of heart failure in patients with cardiac resynchronization therapy (CRT). Recognition of loss of LV capture in time is important in clinical practice. A total of 422 electrocardiograms were acquired and analyzed from 53 CRT patients at 8 different pacing settings (LV only, right ventricle [RV] only, biventricular [BV] pacing with LV preactivation of 60, 40, 20, and 0 milliseconds and RV preactivation of 20 and 40 milliseconds). A modified Ammann algorithm by adding a third step-presence of Q (q, or QS) wave-to the original 2-step Ammann algorithm and a QRS axis shift method were devised to identify the loss of LV capture. The accuracy of modified Ammann algorithm was significantly higher than that of Ammann algorithm (78.9% vs. 69.1%, P < 0.001). The accuracy of the axis shift method was 66.4%, which was significantly lower than the modified Ammann algorithm (P < 0.001) and similar to the original one (P = 0.412). However, in the ECGs with QRS axis shift, 96.8% were correctly classified. LV preactivation or simultaneous BV activation and LV lead positioned in nonposterior or noninferior wall could elevate the accuracies of the modified Ammann algorithm and the QRS axis shift method. The accuracy of the modified Ammann algorithm is greatly improved. The QRS axis shift method can help diagnose LV capture. The LV preactivation, or simultaneous BV activation and LV lead positioned in nonposterior or noninferior wall can increase the diagnostic power of the modified Ammann algorithm and QRS axis shift method.

The Influence of Atrial Fibrillation on Cardiac Resynchronization Therapy

More successful recognition and treatment of cardiovascular risk factors and diseases continues to decrease mortality and increase the proportion of elderly population. Therefore, there are more people with increased risk of developing heart failure and atrial fibrillation (AF) in the course of their lives. The prevalence of AF, in patients with heart failure, increases with the severity of the disease, reaching up to 40% in advanced cases. In these patients with heart failure, AF is an independent predictor of morbidity and mortality increasing the risk of death and hospitalization. Despite the excellent results obtained with different drugs, the optimal medical treatment can fail in the intention to improve symptoms and quality of life of patients with severe heart failure. Thus, the necessity to use cardiac devices emerges facing the failure of optimal medical treatment in order to achieve hemodynamic improvement. The simultaneous electric stimulation of both ventricles with Cardiac Resynchronization Therapy (CRT) results in a significant hemodynamic improvement restoring a more homogeneous contraction pattern. However, CRT is interrupted in over 30% of patients after successful implantation of a CRT device, and the most common reasons for interruption of CRT are the development of AF (18%) and loss of left ventricular capture (10%). Therefore, there should be a strong effort with different maneuvers to prevent AF, since it would significantly improve the ability to deliver CRT in patients with heart failure. The search for better pharmacological maneuvers should continue to provide the help needed to cardiac devices. The incorporation of the AF suppression algorhythm to CRT devices may be very useful in eliminating AF, allowing a better performance of the CRT device without interruption. Sinus rhythm is associated with a long-term improvement in left ventricular systolic function after AF ablation. Therefore, AF ablation may have a primary role as a rhythm control strategy in the definite treatment of AF in patients with HF.

Pérdida de estimulación biventricular continua en pacientes con terapia de resincronización cardiaca: incidencia, causas y resultados

Introduction and objectivesIn recent years, implantation of cardiac resynchronization therapy devices has significantly increased. The benefits of this therapy are directly related to the maintenance of continuous biventricular pacing. This study analyzed the incidence, causes, and outcomes of loss of continuous biventricular pacing, and the approach adopted. MethodsWe analyzed the clinical and follow-up data of a series of consecutive patients from a single center who underwent implantation of a cardiac resynchronization therapy device. ResultsThe study included 136 patients. During a mean follow-up of 33.4 months, loss of continuous biventricular pacing occurred in 45 patients (33%). The most common causes included atrial tachyarrhythmias (21.3%), lead macrodislodgement (18%), and loss of left ventricular capture (13.1%). In most patients (88.5%), loss of continuous biventricular pacing was transient and correctable, and occurred earlier in the follow-up when the cause was lead macrodislodgement, oversensing, or extracardiac stimulation. There were no significant differences in mortality between patients with and without loss of continuous biventricular pacing (P=.88). ConclusionsDespite technical advances in cardiac resynchronization therapy, loss of continuous biventricular pacing is common; however, this loss can usually be corrected. In most patients, continuous biventricular pacing can be ensured by close monitoring and follow-up and a proactive approach.Full English text available from:www.revespcardiol.org/en

Loss of Continuous Biventricular Pacing in Cardiac Resynchronization Therapy Patients: Incidence, Causes, and Outcomes

Introduction and objectivesIn recent years, implantation of cardiac resynchronization therapy devices has significantly increased. The benefits of this therapy are directly related to the maintenance of continuous biventricular pacing. This study analyzed the incidence, causes, and outcomes of loss of continuous biventricular pacing, and the approach adopted. MethodsWe analyzed the clinical and follow-up data of a series of consecutive patients from a single center who underwent implantation of a cardiac resynchronization therapy device. ResultsThe study included 136 patients. During a mean follow-up of 33.4 months, loss of continuous biventricular pacing occurred in 45 patients (33%). The most common causes included atrial tachyarrhythmias (21.3%), lead macrodislodgement (18%), and loss of left ventricular capture (13.1%). In most patients (88.5%), loss of continuous biventricular pacing was transient and correctable, and occurred earlier in the follow-up when the cause was lead macrodislodgement, oversensing, or extracardiac stimulation. There were no significant differences in mortality between patients with and without loss of continuous biventricular pacing (P=.88). ConclusionsDespite technical advances in cardiac resynchronization therapy, loss of continuous biventricular pacing is common; however, this loss can usually be corrected. In most patients, continuous biventricular pacing can be ensured by close monitoring and follow-up and a proactive approach.

Worsening heart failure following cardiac resynchronization therapy: An electrocardiographic diagnosis

The advent of biventricular devices has added new complexity to the evaluation of pacemaker function and follow-up. Consequently one must acknowledge the various circumstances that can disrupt ventricular resynchronization and provoke haemodynamic deterioration1. In this paper we report upon haemodynamic deterioration following resynchronization therapy because of an erroneous connection of an epicardial right ventricular (RV) outflow tract lead to the left ventricular (LV) channel of the device. How ECG and echocardiography can guide the diagnosis and help in prematurely detecting abnormal pacing or loss of LV capture is discussed in detail below.

Preservation of Ventricular Capture by Anodal Stimulation After Dislodgment of an Epicardial Electrode

A 58-year-old man had a bipolar epicardial left ventricular (LV) implanted for cardiac resynchronization therapy after a failed transvenous approach. The system was programmed in an LV tip-right ventricular coil configuration, but during follow-up loss of LV capture with recurrence of symptoms occurred. Changing to an LV tip-LV ring configuration restored LV pacing through anodal capture. Loss of cathodal capture was caused by dislodgment of the cathodal electrode due to a broken fixation suture. Anodal capture was used to reinstall resynchronization therapy, which resulted in clinical improvement. There were no adverse effects from anodal stimulation in a follow-up period of 6 months.

An Electrocardiogram-Based Algorithm to Detect Loss of Left Ventricular Capture During Cardiac Resynchronization Therapy

An Electrocardiogram-Based Algorithm to Detect Loss of Left Ventricular Capture During Cardiac Resynchronization Therapy

An Electrocardiogram-Based Algorithm To Detect Loss of Left Ventricular Capture during Cardiac Resynchronization Therapy

Loss of left ventricular capture in patients with cardiac resynchronization devices may account for worsening heart failure and can be difficult to diagnose without a programmer. To determine whether distinct morphologic changes on the surface electrocardiogram indicate loss of left ventricular capture. After analysis of the R-S spike ratio in the 12-lead electrocardiogram during right ventricular and biventricular pacing in 10 patients, an algorithm to detect loss of left ventricular capture was developed. University hospital. 54 patients with a cardiac resynchronization device and underlying left bundle-branch block. Leads V1 and I of a 12-lead electrocardiogram were assessed after biventricular pacing was confirmed and after the device was programmed to right ventricular pacing only (simulating loss of left ventricular capture). The sensitivity of the algorithm to correctly identify loss of left ventricular capture was 94% (95% CI, 88.2% to 97.7%), and the specificity was 93% (CI, 86.3% to 95.8%). The likelihood ratio of a positive test result was 12.8 (CI, 6.443 to 23.310), and the likelihood ratio of a negative test result was 0.06 (CI, 0.024 to 0.137). The algorithm was tested in patients in whom the right ventricular electrode was placed in the apex of the right ventricle only. Presence of biventricular capture--the prerequisite for successful cardiac resynchronization therapy--and loss of left ventricular capture can be accurately detected by an algorithm based on analysis of the R-S ratio on leads V1 and I of the surface electrocardiogram.

A novel ECG-algorithm to detect loss of left ventricular capture in patients with cardiac resynchronization therapy

A novel ECG-algorithm to detect loss of left ventricular capture in patients with cardiac resynchronization therapy

Long-term retention of cardiac resynchronization therapy

ObjectivesThe purpose of this study was to determine the frequency and causes of intermittent and permanent loss of cardiac resynchronization therapy (CRT) in patients who have undergone the successful implantation of a transvenous defibrillator that delivers CRT (CRT-D). BackgroundThe causes of loss of CRT have not been described. MethodsThe records of 512 patients who underwent an attempt at implantation of a transvenous CRT-D device as part of the VENTAK CHF/CONTAK CD Biventricular Pacing study were analyzed. ResultsDevice implantation was successful in 443 of 512 (87%) of patients. Among these 443 patients, CRT was interrupted in 161 (36%) patients during a mean follow-up of 2.5 ± 1.1 years. Reasons included the development of an atrial tachyarrhythmia (18%), loss of left ventricular capture (10%), diaphragmatic stimulation (2%), loss of right ventricular capture (2%), infection (1%), intentional discontinuation of CRT (1%), loss of right atrial sensing (1%), and ventricular oversensing (0.2%). Most patients underwent an intervention that permitted the reinstitution of CRT, such that only 20 of the 443 patients (5%) experienced the permanent loss of CRT. Using an intention-to-treat analysis, the long-term retention of CRT was 83% during the course of 2.5 years. ConclusionsCardiac resynchronization therapy is interrupted in more than one-third of patients after the successful implantation of a CRT-D device. However, CRT can be reinstituted in most patients and has a high long-term retention rate. Because patients with slower heart rates were more likely to develop atrial tachyarrhythmias, a dual-chamber rate-modulated pacing mode (DDDR) may reduce interruptions of CRT.