Can you pace a junctional rhythm

However, impulses are occasionally discharged in the atrioventricular node or by cells near the node. The following must be noted:.

In both cases listed above the impulse will originate in the junction between the atria and the ventricles, which is why ectopic beats and ectopic rhythms originating there are referred to as junctional beats and junctional rhythms.

The atria will be activated in the opposite direction, which is why the P-wave will be retrograde. In most cases, the P-wave is not visible because when impulses are discharged from the junctional area, atria and ventricles are depolarized simultaneously and ventricular depolarization QRS dominates the ECG.

ECG criteria for junctional rhythm. Symptomatic junctional rhythm is treated with atropine. Doses and alternatives are similar to management of bradycardia in general.

Junctional tachycardia is caused by abnormal automaticity in the atrioventricular node, cells near the atrioventricular node or cells in the bundle of His. It is very rare among adults and elderly, but is relatively common in children.

When occurring in adults and elderly it is referred to as nonparoxysmal junctional tachycardia NPJT whereas it is referred to as junctional ectopic tachycardia JET in children.

NPJT is caused by ischemia, digoxin overdose, theophylline, overdose cathecholamines, electrolyte disorders and perimyocarditis. As true for the other junctional beats and rhythms, the P-wave is retrograde or invisible. However, if the junctional impulse is not conducted retrogradely the atria may run an independent rhythm; this is called atrioventricular dissociation AV dissociation because the atrial and ventricular rhythms are dissociated from each other.

This type of AV dissociation is easy to differentiate from AV dissociation due to third-degree AV-block , because in third-degree AV-block the atrial rhythm is higher than the ventricular; the opposite is true in this scenario. Electrical cardioversion is ineffective and should be avoided electrical cardioversion may be pro-arrhythmogenic in patients on digoxin.

If the genesis of the arrhythmia is unknown or if the arrhythmia persists after removing medications, it is recommended that amiodarone, beta-blockers or calcium channel blockers are tried, in that order. Atrial Fibrillation. Management and diagnosis of tachycardias narrow complex tachycardia and wide complex tachycardia. Mechanisms of cardiac arrhythmias. View all chapters in Cardiac Arrhythmias. No products in the cart.

Sign in Sign up. Search for:. The mechanism is similar to junctional rhythm, but the principal pacemaker of the heart is now within the ventricles. Therefore, the depolarization of ventricles does not happen in a normal fashion and the QRS complexes are usually wide more than msec. The heart rate is also lower, between 20 to 40 bpm. Due to this low heart rate, idioventricular rhythm may cause hemodynamic instability.

Sinoatrial exit block. In sinoatrial SA block, the sinus node generates the impulse, but there is a conduction abnormality between the sinus node and the surrounding atrial tissue. In first-degree SA exit block , the time for the sinus node impulse to exit the SA node and depolarize the atrial tissue increases. Generation of an impulse in the SA node produces no deflection on surface ECG; therefore, the increased time between impulse generation and its propagation through the atria cannot be measured on surface ECG.

Second-degree SA block has two types. In type 1, it takes progressively longer for each SA node impulse to exit the node until an impulse fails to exit the node and depolarize the atria. Shortening of the PP interval is helpful to distinguish this condition from a sinus pause. Since the SA node generates the impulses at a regular rate, the PP interval surrounding the dropped complexes is two times or a multiple of the baseline PP interval.

In third-degree SA exit block , none of the generated impulses exits the SA node. Therefore, on surface ECG there will be a pause or junctional rhythm. However, diagnosis of SA exit block on surface ECG is difficult, so it often requires invasive electrophysiology studies. As a general principle, any arrhythmia that causes hemodynamic instability requires further investigation and treatment. Except for the use of atropine in selected patients with bradycardia, the mainstay of treatment is pacemaker implantation.

In making the clinical decision as to whether pacemaker placement is required, the single most important factor is correlation of the symptoms with the episodes of bradyarrhythmia. The most common symptoms include lightheadedness, dizziness, near-syncope, syncope, and fatigue. Since syncope can have serious consequences, patients who present with syncope and are found to have sinus node dysfunction may be candidates for pacemaker placement, even if a correlation between the syncope and the sinus node dysfunction has not been documented.

There is an association between sinus node dysfunction and atrial fibrillation i. In the presence of reversible causes e. Pacemaker mode. The DDDR mode, which has sensing and pacing capabilities in both the atrium and ventricle, is the most commonly used mode of pacing in patients with sinus node dysfunction. The AAIR mode, in which the atrium is paced and sensed and the pacemaker is inhibited in response to sensed atrial beats, can be used too. Its disadvantage is its lack of protection against an AV conduction abnormality.

Although it is appropriate for patients with sinus node dysfunction who have intact AV nodal function, some clinicians believe that the chance of developing an AV conduction problem is significant enough to consider implanting a dual-chamber pacemaker even for sinus node dysfunction.

In VVI mode the right ventricle is paced and sensed, and the pacemaker is inhibited in response to a sensed beat. Its advantages include that it requires only one lead and it gives protection against bradycardia of any etiology by pacing the ventricle. The disadvantage of the VVI mode is the lack of AV synchrony, which can result in pacemaker syndrome in the short term and, potentially, heart failure and atrial fibrillation in the long term.

Conduction of the impulse through the atrioventricular junction. In a normal subject, the electrical impulse passes only through the AV node to depolarize the ventricles. The AV node, about 5 mm in size, consists of specialized cells and connects to the AV bundles and His-Purkinje system. It is located beneath the right atrial endocardium at the apex of the triangle of Koch.

The triangle of Koch is limited by the base of the septal leaflet of the tricuspid valve inferiorly, tendon of Todaro anterosuperiorly, and anterior margin of the coronary sinus orifice. The speed of conduction within the AV node is slower than the His-Purkinje system 0. The His bundle arises from the AV node and divides into left and right bundle branches. The left bundle itself divides into the left anterior fascicle and the left posterior fascicle, and then supplies the left ventricle via Purkinje fibers.

The right bundle divides to a network of branches and supplies the right ventricle. The AV node has rich innervations, and its blood supply usually derives from the right coronary artery. The blood supply of the bundle of His arises from the left anterior descending artery. A wide range of pathologies may cause AV block, including cardiac ischemia, cardiomyopathy, connective tissue diseases, congenital AV block, drugs, Lev s disease idiopathic fibrosis , Lenegre s disease, infiltrative diseases, infections endocarditis, myocarditis , metabolic and endocrine disorders hyperkalemia, hypermagnesemia, hypothyroidism, Addison s disease , neurocardiogenic syncope, trauma e.

It is important to differentiate reversible from permanent causes of AV block. Some of the listed etiologies such as acute MI, trauma, and endocarditis may cause either temporary or permanent AV block. In general, the site at which the block occurs determines the type of delay in conduction, ranging from delayed transmission to the ventricles first-degree AV block , to intermittent failure of impulse transmission second-degree AV block , to complete conduction failure third-degree AV block.

Each of these abnormalities has characteristics on the surface ECG; however, the most precise way to identify the site of the block is by EPS. First-degree AV block. Delay in conduction of the atrial impulse to the ventricles may be due to abnormal conduction in the atrial tissue or a conduction disturbance at the level of the AV node, the latter being the most common cause of first-degree AV block.

The AV nodal conduction disturbance in this case is usually due to an autonomic imbalance e. Since the level of the block may change the management of the patient, it is important to pay attention to the width of the QRS complex. Second-degree AV block. The pathogenesis of second-degree AV block Mobitz type 1 is similar to that of first-degree AV block and the conduction disturbance is usually at the level of the AV node.

Mobitz type 1 usually shows the following characteristics on ECG as well: PR interval prolongation at progressively decreasing increments, the pause after the blocked P wave being less than the sum of the two beats prior to the block, and progressive shortening of RR intervals.

Similar to first-degree AV block, wide QRS complexes may indicate that the level of the block is infra-nodal. EPS would show an H electrogram that is not followed by ventricular activity. Mobitz type 2 second-degree AV block appears as an abrupt blocking of a P wave with a fixed PR interval. Mobitz type 2 is frequently associated with significant underlying disorders such as bundle branch block and usually progresses to complete heart block.

The level of conduction disturbance is at the His-Purkinje system. In EPS, the H electrogram is recorded, but there is no subsequent ventricular activity in the blocked cycle. Since the main electrocardiographic characteristic used to differentiate Mobitz 1 from Mobitz 2 is the variability of PR interval in Mobitz 1, it is impossible to categorize a second-degree AV block as either Mobitz 1 or Mobitz 2 when the conduction ratio is Determination of the site of the block in this case is by EPS.

However, features that suggest an AV nodal level for conduction disturbance are normal QRS duration, very long PR interval, concomitant type 1 block, and worsening of the degree of the block with vagal maneuvers. The opposite characteristics are seen in infra-nodal block. In high-grade AV block , two or more P waves are not conducted. It may be associated with a junctional or ventricular escape rhythm.

Third-degree complete AV block. The second potential deleterious effect is the risk of functional atrial under-sensing due to the shift of the P wave in the post-ventricular atrial refractory period, especially with fast heart rate; an exercise test would be helpful to ensure an adequate programming of the PM when the patient is exercising.

The rationale for the use of specific pacing algorithms is to avoid bradycardia and large atrial cycle length variations, which are thought to trigger atrial tachyarrhythmias AT. Specific algorithms have included rate-adaptive pacing, which periodically assesses the underlying intrinsic rate to pace just above it, elevation of the pacing rate after spontaneous atrial ectopy, transient high-rate pacing after mode switch episodes and increased post-exercise pacing to prevent an abrupt drop in heart rate.

In addition, some devices have incorporated atrial anti-tachycardia pacing ATP algorithms high rate ramp and burst pacing for termination of atrial tachycardia or atrial flutter that might degenerate into AF. After the pivotal multi-centre study of Israel et al. Finally, no consistent data from large randomized trials support the use of alternative single-site atrial pacing, w,w dual-site right atrial pacing, w or bi-atrial pacing, w alone or in association with algorithms for prevention and termination of AT.

There is strong evidence that algorithms designed to prevent AF have no incremental benefits for the prevention of AF; further trials are unlikely to change the confidence in the estimate of effect. The majority of the information in this field has come from retrospective studies based on implantations performed more than 20 years ago. In a nationwide registry of 28 patients, lead complications occurred in 3. Complications occurred in 4. The majority of the complications with pacemakers occur in-hospital or during the first 6 months.

Complications were highest in patients who had an upgrade to- or a revised CRT device These data support careful decision-making before device replacement and when considering upgrades to more complex systems. A meta-analysis of patients in 25 CRT trials showed that the implantation success rate was Haematomas are very frequent 2.

Evacuation is required in 0. Many haematomas can be avoided by careful haemostasis and preparation of the patient, allowing correct management of antiplatelet and anticoagulant drugs.

Compared with untreated patients, aspirin carries a two-fold risk of bleeding and dual antiplatelet therapy aspirin plus thienopyridine carries a four-fold risk of bleeding during the peri-operative period.

In most cases, antiplatelet medications can safely be discontinued, for a period of 5—7 days, specifically when prescribed for primary prevention of cardiovascular events Web Table Given the rapid onset and cessation of its action, no bridging therapy with low molecular weight heparin should be required and, following surgery, they should be restarted as soon as effective haemostasis has been achieved.

Infection is one of the most worrying post-operative complications. In a population-based cohort study of 46 consecutive patients, the incidence of PM infection was 1. In case of PM replacement these figures increased to 12 per PM-years and 3. The incidence of pocket infection without bloodstream infection was 1.

Infections occurred more frequently with use of temporary pacing or other procedures before implantation OR 2. A meta-analysis of antibiotic prophylaxis using a regimen of pre-procedure and post-procedure administration suggested a significant reduction in the incidence of infection. The haemodynamic and clinical effect of pacing from alternative RV sites in the His region, mid- or high ventricular septum and outflow tract has been evaluated in the last two decades Web Table Results were inconclusive with respect to exercise capacity, functional class, quality of life and survival.

Results seem to be influenced by the pacing site, with septal pacing being less effective than the outflow tract and para-Hisian region. The complication rate of non-RV apical pacing is similar to that of RV apical pacing. This Task Force is unable to give definite recommendations until the results of larger trials become available.

Although the recent ESC Guidelines on the prevention, diagnosis and treatment of infective endocarditis give some recommendations, w these were based on expert consensus documents, w,w lacking data derived from randomized trials or large observational registries.

Thus, the decision to re-implant a device should be weighed carefully. A new epicardial pacing system can be inserted, particularly if the infected lead is extracted at cardiotomy, or if venous access is impossible. The optimal timing for re-implantation is not known. However, in patients with no evidence of valvular endocarditis or lead vegetations, a new transvenous device can be implanted at a new location after control of local infection, if blood cultures obtained within 24 hours after device removal remain negative for 72 hours.

Indeed, it has recently been shown in a large, single centre, retrospective study that the infection relapse rate was higher in patients implanted during the same hospitalization for hardware removal. Patients who are not PM-dependent can be followed without a temporary PM until a new system is implanted. In patients who are PM-dependent, temporary transvenous pacing is continued until re-implantation. The ESC Guidelines on infective endocarditis recommend avoidance of temporary pacing as much as possible.

There is general consensus among experts that the indication should be re-assessed before re-implanting a PM after device explantation; if there is an established indication, re-implantation has to be performed at another site. For patients who are PM-dependent, the optimal management strategy— i. Initial experience at 0. During power-on-reset, the device is susceptible to inhibition of pacing output and activation of anti-tachycardia therapies.

A recent prospective, randomized, controlled, worldwide clinical trial, which included patients randomized to undergo an MRI over a period of 1. Suggestions for device programming when magnetic resonance imaging is required. Conventional cardiac devices Figure 2 and Recommendation 1. Because changes in device variables and programming may occur, monitoring by qualified personnel during MRI is essential.

Programme an asynchronous pacing mode in PM-dependent patients to avoid inappropriate inhibition of pacing due to detection of electromagnetic interference.

In contrast, use an inhibited pacing mode for patients without PM dependence, to avoid inappropriate pacing due to tracking of electromagnetic interference. Deactivate other pacing functions magnet, rate, noise, PVC, ventricular sense, AF response in order to ensure that sensing of electromagnetic interference does not lead to unwarranted pacing.

Magnetic resonance imaging-conditional devices Recommendation 2. Safety precautions for magnetic resonance imaging MRI in patients with conventional cardiac devices. Adapted from Nazarian et al. The basic elements are identical to conventional cardiac devices Figure For MRI-conditional devices, programming as described in iii , iv , v and vi is automatically performed by an external physician-activated device.

Alternative imaging techniques have to be considered. This possibility needs further evaluation. Complications are common in patients treated with temporary pacing.

Furthermore, longer use of temporary transvenous pacing may restrict the patient to being bedridden, with accompanying risks for infection and thrombo-embolic events.

Without recognition of the potential complications, adverse effects might outweigh the beneficial effects of the PM. Therefore, this Task Force believes that temporary pacing should be avoided as far as possible and, when used, the treatment time should be as brief as possible. The following issues are relevant as guidance for clinical practice: Transcutaneous temporary pacing by an external defibrillator. Temporary transvenous pacing shall not be used routinely—and only as a last resort when chronotropic drugs are insufficient.

Positive chronotropic drug infusion e. Temporary transvenous pacing should be limited to cases of i high-degree AV block without escape rhythm, ii life-threatening bradyarrhythmias, such as those that occur during interventional procedures e. If the indications for permanent pacing are established, every effort should be made to implant a permanent PM as soon as possible. This Task Force warns that external pacing provided by patches and an external defibrillator does not provide reliable ventricular stimulation and therefore should only be used, under strict haemodynamic and ECG monitoring, when no other option is available.

As soon as possible an alternative action should be undertaken, such as administration of chronotropic drugs or temporary or permanent pacing.

The usefulness of remote monitoring has been extensively addressed in the recent joint European and American expert consensus statement on CRT in heart failure to which we refer.

Diagnosing AF before the first complications occur is a recognized priority for an early starting of anticoagulation therapy and prevention of stroke. Google Scholar. Google Preview. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Abbreviations and acronyms. Indications for pacing. Indications for cardiac resynchronization therapy. Indications for pacing in specific conditions. Management considerations.

Editor's Choice Guidelines. Oxford Academic. Angelo Auricchio. Gonzalo Baron-Esquivias. Pierre Bordachar. Giuseppe Boriani. Ole-A Breithardt. John Cleland. Jean-Claude Deharo. Victoria Delgado. Perry M. Elliott , Perry M. Bulent Gorenek. Carsten W. Christophe Leclercq. Cecilia Linde. Luigi Padeletti. Richard Sutton. Panos E. Jose Luis Zamorano. Stephan Achenbach. Helmut Baumgartner. Jeroen J. Veronica Dean. Christi Deaton.

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Permissions Icon Permissions. Cardiac pacing , Cardiac resynchronization therapy , Pacemaker , Heart failure , Syncope , Atrial fibrillation. First-degree atrioventricular block. Committee for Practice Guidelines. Emery-Dreifuss muscular dystrophy.

Atrial Dynamic Overdrive Pacing Trial. Ablate and Pace in Atrial Fibrillation. Bradycardia detection in Bundle Branch Block. Biventricular versus right ventricular pacing in patients with AV block. CLinical Evaluation on Advanced Resynchronization. COnventional vs. Biventricular Pacing in Heart Failure and Bradyarrhythmia.

Italian Network on Congestive Heart Failure. International Study on Syncope of Unexplained Etiology. Multicenter Automatic Defibrillator Trial. Pacing to Avoid Cardiac Enlargement. Prevention of Immediate Reinitiation of Atrial Tachyarrhythmias.

Study of Atrial Fibrillation Reduction. Vasodilator in HEart Failure Trial. Table 1 Classes of recommendations. Open in new tab. Table 2 Levels of evidence. Figure 2. Open in new tab Download slide. Table 7 Suggested ECG monitoring techniques depending on symptom frequency. Indication for pacing in patients with persistent bradycardia.

Table 8 Outcome of randomized controlled trials of dual-chamber versus ventricular pacing. Figure 3. Figure 4. Indication for pacing in intermittent documented bradycardia.

Choice of pacing mode. Indication for cardiac pacing in patients with BBB. Figure 5. Indication for cardiac pacing in patients with undocumented reflex syncope. Indication for cardiac pacing in patients with unexplained syncope.

Table 10 Inclusion criteria, design, endpoints, and main findings of the randomized clinical trials evaluating cardiac resynchronization therapy in heart failure patients and sinus rhythm.

Figure 8. Clinical factors influencing the likelihood to respond to CRT. Table 13 Summary of current evidence for CRT optimization. Choice of pacing mode and cardiac resynchronization therapy optimization. Figure Table 14 Summary of evidence for upgrading from conventional pacemaker or implantable cardioverter defibrillator to cardiac resynchronization therapy devices. Table 16 Probability of best treatment for patients with left ventricular dysfunction from a meta-analysis of 12 RCTs CRT-P in primary prevention.

Indications for permanent pacing. Indication for cardiac pacing in patients with hypertrophic cardiomyopathy. Pacing in pregnancy. Indication for pacing for first-degree atrioventricular block. Indication for prevention and termination of atrial tachyarrhythmias. Magnetic resonance in patients with implanted cardiac devices.

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Early application of an implantable loop recorder allows effective specific therapy in patients with recurrent suspected neurally mediated syncope. Sick sinus syndrome treated with permanent pacemaker in patients. A follow-up study. Treatment of sinoatrial syndrome with permanent cardiac pacing in 90 patients. Long-term follow-up of patients with sick sinus syndrome: a comparison of clinical aspects among unpaced, ventricular inhibited paced, and physiologically paced groups.

Prospective randomised trial of atrial versus ventricular pacing in sick-sinus syndrome. Effects of physiologic pacing versus ventricular pacing on the risk of stroke and death due to cardiovascular causes. Canadian Trial of Physiologic Pacing Investigators. Quality of life and clinical outcomes in elderly patients treated with ventricular pacing as compared with dual-chamber pacing.

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Minimizing ventricular pacing to reduce atrial fibrillation in sinus-node disease. Implications of mechanism of bradycardia on response to pacing in patients with unexplained syncope. Permanent cardiac pacing versus medical treatment for the prevention of recurrent vasovagal syncope: a multicenter, randomized, controlled trial.

A randomized trial of permanent cardiac pacing for the prevention of vasovagal syncope. A randomized, double-blind, placebo-controlled study of permanent cardiac pacing for the treatment of recurrent tilt-induced vasovagal syncope. Dual-chamber pacing in the treatment of neurally mediated tilt-positive cardio-inhibitory syncope : pacemaker versus no therapy: a multicenter randomized study.

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Cardio-inhibitory carotid sinus hypersensitivity predicts an asystolic mechanism of spontaneous neurally mediated syncope. Carotid sinus hypersensitivity: beneficial effects of dual-chamber pacing. An acute and medium-term study. Treatment of unexplained syncope: a multicenter, randomized trial of cardiac pacing guided by adenosine 5'-triphosphate testing. Pacing in elderly recurrent fallers with carotid sinus hypersensitivity: a randomised, double-blind, placebo controlled crossover trial.

The European Cardiac Resynchronization Therapy Survey: comparison of outcomes between de novo cardiac resynchronization therapy implantations and upgrades.

Cardiac-resynchronization therapy for the prevention of heart-failure events. Clinical efficacy of cardiac resynchronization therapy using left ventricular pacing in heart failure patients stratified by severity of ventricular conduction delay. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay.

Cardiac resynchronization therapy for the treatment of heart failure in patients with intraventricular conduction delay and malignant ventricular tachyarrhythmias. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. The effect of cardiac resynchronization on morbidity and mortality in heart failure.

Meta-analysis: cardiac resynchronization therapy for patients with less symptomatic heart failure. Impact of QRS duration on clinical event reduction with cardiac resynchronization therapy: meta-analysis of randomized controlled trials.

Surface electrocardiogram to predict outcome in candidates for cardiac resynchronization therapy: a sub-analysis of the CARE-HF trial. Effects of cardiac resynchronization on disease progression in patients with left ventricular systolic dysfunction, an indication for an implantable cardioverter-defibrillator, and mildly symptomatic chronic heart failure. Randomized trial of cardiac resynchronization in mildly symptomatic heart failure patients and in asymptomatic patients with left ventricular dysfunction and previous heart failure symptoms.

Effect of QRS morphology on clinical event reduction with cardiac resynchronization therapy: meta-analysis of randomized controlled trials. Cardiac-resynchronization therapy in heart failure with narrow QRS complexes. Cardiac resynchronization therapy and the relationship of percent biventricular pacing to symptoms and survival. Reasons for loss of cardiac resynchronization therapy pacing: insights from 32 patients.

Sites of left and right ventricular lead implantation and response to cardiac resynchronization therapy observations from the REVERSE trial. Left ventricular lead position and clinical outcome in the multicenter automatic defibrillator implantation trial-cardiac resynchronization therapy MADIT-CRT trial. Targeted left ventricular lead placement to guide cardiac resynchronization therapy: the TARGET study: a randomized, controlled trial.

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Cardiac resynchronization with sequential biventricular pacing for the treatment of moderate-to-severe heart failure. Investigation of a novel algorithm for synchronized left-ventricular pacing and ambulatory optimization of cardiac resynchronization therapy: results of the adaptive CRT trial. Reduced ventricular volumes and improved systolic function with cardiac resynchronization therapy: a randomized trial comparing simultaneous biventricular pacing, sequential biventricular pacing, and left ventricular pacing.

A randomized pilot study of optimization of cardiac resynchronization therapy in sinus rhythm patients using a peak endocardial acceleration sensor vs. Comparison of 1-year effects of left ventricular and biventricular pacing in patients with heart failure who have ventricular arrhythmias and left bundle-branch block: the Bi vs.

Meta-analysis of randomized controlled trials comparing isolated left ventricular and biventricular pacing in patients with chronic heart failure.