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| {{SI}} | | __NOTOC__ |
| | {| class="infobox" style="float:right;" |
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| | | [[File:Siren.gif|30px|link= Congestive heart failure resident survival guide]]|| <br> || <br> |
| | | [[Acute decompensated heart failure resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] |
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| | {| class="infobox" style="float:right;" |
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| | | [[File:Critical_Pathways.gif|88px|link= Congestive heart failure critical pathways]]|| <br> || <br> |
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| | {{Cardiac resynchronization therapy}} |
| | {{CMG}}; {{AOEIC}}: Bhaskar Purushottam, M.D. [mailto:bpurushottam@gmail.com] |
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| {{CMG}} | | {{SK}} CRT |
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| ==Overview== | | ==[[Cardiac resynchronization therapy overview|Overview]]== |
| Introduction
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| | ==[[Cardiac resynchronization therapy indications|Indications]]== |
| | : [[Cardiac resynchronization therapy landmark trials|Landmark Trials]] |
| | :'''[[Cardiac resynchronization therapy special populations|Special Populations]]''': [[Cardiac resynchronization therapy special populations#Atrial Fibrillation and CRT|Atrial Fibrillation Patients]] | [[Cardiac resynchronization therapy special populations#Cardiac Resynchronization Therapy in Minimal Heart Failure|Minimal Heart Failure Patients]] |
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| Cardiac resynchronization therapy is an evidence based device treatment for [[congestive heart failure]] that remains symptomatic despite optimal medical therapy. It involves timed atrioventricular and biventricular pacing, which can improve left ventricular function, heart failure symptoms and may be associated with a reduction in mortality. | | ==[[Cardiac resynchronization therapy contraindications|Contraindications]]== |
| ==Indications==
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| The ACC / AHA guidelines indicate that CRT is recommended for those patients with all of the following: <ref name="pmid18483207">{{cite journal |author=Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO, Smith SC, Jacobs AK, Adams CD, Anderson JL, Buller CE, Creager MA, Ettinger SM, Faxon DP, Halperin JL, Hiratzka LF, Hunt SA, Krumholz HM, Kushner FG, Lytle BW, Nishimura RA, Ornato JP, Page RL, Riegel B, Tarkington LG, Yancy CW |title=ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons |journal=[[Circulation]] |volume=117 |issue=21 |pages=e350–408 |year=2008 |month=May |pmid=18483207 |doi=10.1161/CIRCUALTIONAHA.108.189742 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=18483207 |issn= |accessdate=2011-01-15}}</ref>
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| * An [[LVEF]] ≤35 percent
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| * A [[QRS]] duration ≥120 msec
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| * NYHA functional class III or ambulatory class IV symptoms with optimal medical therapy
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| ==Contraindications== | | ==[[Cardiac resynchronization therapy pathophysiology|Pathophysiologic Basis For CRT]]== |
| The ACC / AHA guidelines indicate that CRT is not indicated in the following patients: <ref name="pmid18483207">{{cite journal |author=Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO, Smith SC, Jacobs AK, Adams CD, Anderson JL, Buller CE, Creager MA, Ettinger SM, Faxon DP, Halperin JL, Hiratzka LF, Hunt SA, Krumholz HM, Kushner FG, Lytle BW, Nishimura RA, Ornato JP, Page RL, Riegel B, Tarkington LG, Yancy CW |title=ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons |journal=[[Circulation]] |volume=117 |issue=21 |pages=e350–408 |year=2008 |month=May |pmid=18483207 |doi=10.1161/CIRCUALTIONAHA.108.189742 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=18483207 |issn= |accessdate=2011-01-15}}</ref>
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| * Patients who are asymptomatic with a reduced [[LVEF]] who have no other indications for pacing.
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| * Patients who have a limited life expectancy due to a non-cardiac condition.
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| * Patients who have a limited [[functional capacity]] due to a chronic non-cardiac condition.
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| | ==[[Cardiac resynchronization therapy procedure|Procedure]]== |
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| 1024x768 Normal 0 false false false EN-US X-NONE X-NONE
| | ==[[Cardiac resynchronization therapy prognosis|Outcomes and Prognosis]]== |
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| | ==[[Cardiac resynchronization therapy complications|Complications]]== |
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| Indications
| | ==Related Chapters== |
| | * [[Congestive heart failure]] |
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| | [[Category:Cardiology]] |
| | | [[Category:Disease]] |
| Indications based on ACC/AHA/HRS 2008 guidelines for device based therapy of cardiac rhythm abnormalities (1).
| | [[Category:Emergency medicine]] |
| | | [[Category:Intensive care medicine]] |
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| | [[Category:Medicine]] |
| | | [[Category:Up-To-Date]] |
| 1. Patients with an left ventricular ejection fraction less than or equal to 35%, QRS duration greater than or equal to 0.12 seconds, sinus rhythm and NYHA class 3 or 4 heart failure symptoms on optimal medical therapy (considered a class 1 indication with level A evidence)
| | [[Category:Up-To-Date cardiology]] |
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| 2. Patients with an left ventricular ejection fraction less than or equal to 35%, QRS duration greater than or equal to 0.12 seconds, atrial fibrillation and NYHA class 3 or 4 heart failure symptoms on optimal medical therapy (considered a class 2a indication with level B evidence)
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| 3. Patients with an left ventricular ejection fraction less than or equal to 35%, NYHA class 3 or 4 heart failure symptoms on optimal medical therapy and who have frequent dependence on ventricular pacing (considered a class 2a indication with level B evidence)
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| 4. Patients with an left ventricular ejection fraction less than or equal to 35%, NYHA class 1 or 2 heart failure symptoms on optimal medical therapy and who are undergoing implantation of a permanent pacemaker and or ICD with anticipated frequent ventricular pacing (considered a class 2b indication with level C evidence)
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| CRT is not indicated for asymptomatic patients with reduced left ventricular ejection fraction in the absence of other indications for pacing and also for patients whose functional status and life expectancy are limited predominantly by chronic noncardiac conditions.
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| Pathophysiologic basis for CRT
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| Left ventricular systolic dysfunction is often accompanied by impaired electromechanical coupling, which may further diminish the left ventricular systolic function. The types of electromechanical dyssynchrony are atrioventricular, interventricular, intraventricular and intramural delay (3). Atrioventricular dyssynchrony results in a late diastolic ventriculoatrial gradient and so called "pre-systolic" mitral regurgitation. Interventricular dyssynchrony is the time delay between the contraction of the left and right ventricles and this is calculated by measuring the difference in the time of onset of systolic flow in the aortic and pulmonic valve. A time difference greater than or equal to 40 milliseconds is indicative of interventricular dyssynchrony. There are several echocardiographic techniques to measure intraventricular dyssynchrony, which include M mode echocardiography, tissue Doppler imaging, tissue strain, strain rate analysis and speckle tracking echocardiography. Intramural dyssynchrony is the dyssynchrony within the myocardial wall and it has been measured using speckle tracking echocardiography (6). However, the most common abnormalities are prolonged atrio-ventricular and ventricular conduction, which causes regional mechanical delay within the left ventricle.
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| This mechanical delay is responsible for ventricular dyssynchrony, which can result in the following hemodynamic abnormalities (2):
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| 1. Reduced left ventricular systolic function, decreased dP/dT and cardiac output
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| 2. Delayed contraction of lateral and posterior left ventriclular wall with abnormal septal motion
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| 3. Increased myocardial energy expenditure
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| 4. Adverse remodeling with increased left ventricular dilatation left ventricular end systolic volume
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| 5. Functional mitral regurgitation
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| 6. Delayed mitral valve opening
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| 7. Reduced left ventricular filling time with increased left atrial pressures
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| 8. Distorted mitral valve annulus
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| 9. Delayed aortic valve opening and closure with reduced systolic ejection time
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| The several landmark trials which led to the acceptance of CRT as a non-pharmacological treatment approach for heart failure almost exclusively enrolled patients with sinus rhythm and a left bundle branch block (especially, with a QRS duration greater than or equal to 0.15 seconds). However, QRS duration greater than or equal to 0.12 seconds has been used a measure for dyssynchrony and a criterion for selection of patients for CRT. It is thought that when the QRS duration is prolonged there is delayed activation of the ventricular myocardium with dyssynchronous contraction between the left and right ventricle (interventricular dyssynchrony) and within the left ventricle itself (intraventricular dyssynchrony). However, left ventricular mechanical dyssynchrony is shown to occur independent of QRS duration by echocardiographic parameters (predominantly tissue Doppler and speckle tracking imaging), which measure inter and intra left ventricular conduction delay. By such parameters, nearly half of the heart failure patients with normal QRS duration have evidence of mechanical dyssynchrony and one fifth of heart failure patients with QRS duration greater than or equal to 0.15 seconds reveal no evidence of mechanical dyssynchrony (4,5). It has also been shown that mechanical dyssynchrony measured by echocardiographic techniques is predictive of cardiac events in heart failure patients independent of their QRS duration (5). Therefore, using QRS duration, which is an electrical measure of conduction delay may not be the most reliable marker of ventricular dyssynchrony. The RethinQ trial failed to show any benefit from CRT in heart failure patients with a NYHA class 3, left ventricular ejection fraction less than or equal to 35%, narrow QRS duration(less than or equal to 0.13 seconds) with mechanical dyssynchrony as measured by tissue Doppler imaging and M-mode echocardiography. One of the major limitations of this study was the selection criteria for mechanical dyssynchrony. Currently, there are several studies underway which are looking at different echocardiographic techniques to predict intra left ventricular mechanical dyssynchrony accurately. Till we have a feasible, convenient, reproducible and accurate technique to measure mechanical intra left ventricular dyssynchrony, QRS duration will be used as a measure of dyssynchrony in selecting patients for CRT.
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| CRT in responders can reverse the above mentioned hemodynamic abnormalities to a certain extent with associated clinical and functional benefit.
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| Clinical and functional benefits of CRT
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| The following clinical benefits were demonstrated in clinical trials:
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| 1. Reduced mortality (24% to 36% benefit)
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| 2. Reduced hospitalizations (30% decrease)
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| 3. Improved 6 minute walk test (50 to 70 meter increase)
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| 4. Improved 105 -point Minnesota scale (greater than or equal to 10 point reduction of heart
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| 5. failure symptoms)
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| 6. Improved NYHA class
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| 7. Increase in peak oxygen consumption
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| PATH-CHF, MUSTIC SR, MUSTIC AF, MIRACLE, COMPANION, CARE-HF, MIRACLE-ICD, CONTAK-CD, RHYTHM-ICD and HOBIPACE landmark trials have demonstrated the above mentioned beneficial effects of CRT
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| Atrial Fibrillation and CRT
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| Atrial fibrillation poses several challenges to effective biventricular pacing. First of all, the intrinsic, intermediate-to-high irregular atrial fibrillation rhythm reduced the amount of biventricular paced captures beats. Secondly, even in patients with a normal rate atrial fibrillation there is the occurrence of spontaneous, fusion and pseudofusion beats, which once again minimize the biventricular pacing. It is well known that fast heart rates reduce diastolic filling time and hence reduce stroke volume. Also, irregular rhythm is known to negatively impact left ventricular function. The adversities posed by atrial fibrillation can be tackled by rate control with negative chronotropic agents, atrioventricular junction ablation and device mediated treatment, such as ‘Ventricular Rate Regularization. The OPISTE and PAVE trial confirmed the clinical benefits of atrio ventricular ablation with adequate rate control and the latter study a greater benefit of biventricular pacing. On the basis of these trials and recent observational data, atrioventricular junction ablation may represent a fundamental tool in improving cardiac resynchronization response.
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| Procedure
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| CRT involves a procedure similar to that of a pacemaker placement. In addition to that of the routine implantation of the atrial and right ventricular lead, a third lead is introduced into the coronary sinus and the lateral or posterior branch is accessed for stimulation of the left ventricle. Previously, an epicardial left ventricular lead was implanted after a limited lateral throacotomy. Such epicardial lead implantation is associated with high capture thresholds, suboptimal position for resynchronization, a far more invasive procedure, risk of general anaesthesia and standard complications associated with thoracotomy. However, this approach may be used if the coronary sinus or the appropriate branch cannot be accessed due to anatomical variations, vein stenosis, coronary sinus injury, tortuosity of the coronary sinus and distortion of the ostium.
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| Complications
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| The procedure itself can be associated with several complications, such as bleeding, infection, pneumothorax, lead dislodgement, myocardial injury, coronary sinus dissection or perforation (0.4 to 4%) and pericardial tamponade. Pocket erosion, hematomas, lead fracture, lead dislodgements and device infection are common post procedural complications. Given the proximity of the posterior wall of the left ventricle to the phrenic nerve, there remains the risk of inappropriate phrenic nerve stimulation.
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| Non-responders
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| 30% of the CRT recipients are considered non-responders. A patient is considered a non-responder if there are no significant clinical or functional improvement after CRT as measured in the landmark trials (as mentioned above under clinical benefits). There are several plausible causes to explain a non-responder. As mentioned earlier, not all patients with QRS duration greater than or equal to 0.12 seconds have mechanical dyssynchrony. Unfortunately, the PROSPECT trial which set out to examine the various echocardiographic parameters to predict CRT response was not successful. Some of the major limitations in the study were the technical difficulties in obtaining the dyssynchrony parameters and the discrepancies among the different centers. The other reasons could be lead placement in regions of the left ventricle which is not dyssynchronous or fibrosis with no live myocardium. In fact, anterior left ventricular lead placement has been associated with worsening hemodynamics. Also, lack of sufficient biventricular pacing could result in a non-responder secondary to high left ventricular capture thresholds, lead dislodgement, a long atrioventricular delay, atrial tachyarrhythmias with rapid ventricular response and frequent premature ventricular contractions. Lack of optimal atrioventricular and ventricular to ventricular (i.e., right ventricle to left ventricle) timing can result in a non-responder.
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| Future
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| Identifying patients who would definitely benefit from CRT would be of prime importance. There are several studies looking at different imaging modalities and dyssynchrony parameters which would accurately reveal mechanical dyssynchrony and therefore predict a CRT responder, especially in patients with a narrow QRS. Also, we need further confirmatory evidence regarding the benefit of atrioventricular ablation versus pharmacological rate control in optimizing the clinical benefits. In addition to atrioventricular and Ventricular-Ventricular optimization, other device based changes need to be explored so as to reap the complete benefits of CRT.
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| References
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| 1. Epstein et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) Developed in Collaboration With the American Association for Thoracic Surgery and Society of Thoracic Surgeons. J Am Coll Cardiol 2008;51:e1–62
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| 2. Ho et al. Cardiac resynchronization therapy for the treatment of heart failure. Anesth Analg 2010;111:1353-61
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| 3. Auricchio A et al. Cardiac resynchronization therapy: Current state of the art. Cost versus benefit. Circulation, 2004; 109: 300–307.
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| 4. Bader et al. Intra-left ventricular electromechanical asynchrony: a new independent predictor of severe cardiac events in heart failure patients. J Am Coll Cardiol. 2004;43:248-256
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| 5. Cho et al. Mechanical dyssynchrony assessed by tissue Doppler imaging is a powerful predictor of mortality in congestive heart failure with normal QRS duration. J Am Coll Cardiol. 2005;46:2237-2243.
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| 6. Bank et al. Intramural dyssynchrony and response to cardiac resynchronization therapy in patients with and without previous right ventricular pacing. Eur J Heart Fail. 2010 Dec;12(12):1317-24
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| 7. Auricchio et al. The Pacing Therapies for Congestive Heart Failure (PATH-CHF) study: rationale, design, and end points of a prospective randomized multicenter study. Am J Cardiol. 1999;83:130D-135D.
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| 8. Cazeau et al. Multisite Stimulation in Cardiomyopathies (MUSTIC) study investigators. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med. 2001;344:873-880.
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| 9. Abraham et al. Multisite Insync Randomized Clinical Evaluation (MIRACLE) investigators and coordinators. Double-blind, randomized controlled trial of cardiac resynchronization in chronic heart failure. N Engl J Med. 2002
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| 10. Linde et al. Multisite Stimulation in Cardiomyopathies (MUSTIC) study group. Long-term benefits of biventricular pacing in congestive heart failure: results form the Multisite Stimulation in Cardiomyopathy (MUSTIC) study. J Am Coll Cardiol. 2002;40:1111-1118.
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| 11. Bristow et al. COMPANION steering committee and COMPANION clinical investigators. Heart failure management using implantable devices for ventricular resynchronization: Comparison of Medical Therapy, Pacing, and Defibrillation in Chronic Heart Failure (COMPANION) trial. J Card Fail. 2000;6:276-285
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| 12. Cleland et al. The CARE-HF study (Cardiac Resynchronization in Heart Failure study): rationale, design, and end-points. Eur J Heart Fail. 2001;3:481-489
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| 13. Young et al. Safety and efficacy of combined cardiac resynchronization therapy and implantable cardioversion defibrillation in patients with advanced chronic heart failure. The Multicenter Insync ICD Randomized Clinical Evaluation (MIRACLE-ICD) trial. JAMA. 2003;289:2685-2694.
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| 14. Beshai et al. Cardiac-resynchronization therapy in heart failure with narrow QRS complexes. New Engl J Med. 2007;357:2461-2471
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| 15. Chung et al. Results of the Predictors of Response to CRT (PROSPECT) trial. Circulation. 2008;117:2608-2616
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| 16. Doshi et al. Left ventricular-based cardiac stimulation post AV nodal ablation evaluation (The PAVE study). J Cardiovasc Electrophysiol 2005;16:1160–5
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| 17. Brignole et al. Comparative assessment of right, left, and biventricular pacing in patients with permanent atrial fibrillation. Eur Heart J 2005;26:712–22 (OPSITE trial)
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| 18. William T. Abraham, Ayesha Hasan; Hurst’s The Heart (13th Edition; 2011)
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| 19. Gasparini et al. Cardiac resynchronization therapy in heart failure patients with atrial fibrillation
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| Europace (2009) 11, v82–v86
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| ==References==
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| {{reflist|2}}
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