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CRT – SUITABILITY,TIPS AND TRICKS, INDICATIONS, POST PROCEDURE ASSESMENT Dr.DURAGA PAVAN, NIMS, HYDERABAD.
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CRT – SUITABILITY,TIPS AND TRICKS,

INDICATIONS, POST PROCEDURE

ASSESMENT

Dr.DURAGA PAVAN,

NIMS,

HYDERABAD.

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OUTLINE

• INTRODUCTION

• HF-VENTRICULAR DYSSYNCHRONY

• ASSESMENT OF DYSSYNCHRONY

• RATIONALE/MECHANISM OF CRT

• TRAILS

• INDICATIONS

• PROCEDURE

• PROGRAMING

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Introduction

• The prevalence and economic burden of CHF has been increasing

• Consequence of ↑ survival from ACS and life-prolonging medications.

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Heart Failure Morbidity and Mortality

• Re-hospitalization rates

▫ 2% at 2 days

▫ 20% at 1 month

▫ 50% at 6 months

• 5-year mortality ranges from 15% to 50%

▫ Asymptomatic LVD 15%

▫ Mild-moderate HF 35%

▫ Advanced HF >50%

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Heart failure mortality reduction from

Pharmacological treatment

THERAPY Trial(s) Mortality reduction

DIGOXIN - No

DIURETICS - No

ACEI SOLVED,

CONCENSUS,

MERIT-HF

16-31%

BETA BLOCKERS CIBIS II,

COPERNICUS

35%

SPIRONOLACTONE RALES 22%

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• Normal heart electrical activation occurs with in 40ms

• With myocardial diseases electrical activation is delayed from one part to other part of heart –Dyssynchrony.

• Three types of cardiac dyssynchrony may occur: intraventricular, interventricular, and atrioventricular(AV).

DYSYSNCHRONY

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• The typical pattern seen with left bundle branch block is early activation of the IVS and late activation of the posterior and lateral LV walls.

• Dyssynchrony results in

1. Inefficient LV systolic performance

2. Increased wall stress

3. Increased end systolic volume

4. Delayed relaxation- IMPAIRED FILLING

5. Mitral regurgitation

DYSYSNCHRONYIntraventricular Dyssynchrony,

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• Interventricular dyssynchronyrefers to the time delay between contraction of the right and left ventricles

• Interventricular dyssynchronyresults in

DYSYSNCHRONYInterventricular Dyssynchrony,

Normally LV systole occurs earlier than RV

With LBBB RV systole will be earlier than RV

RV pressure high when LV in late diastole – IVS

displaced in to LV

Incomplete LV filling

Early septal activation

Incomplete LV emptying

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DYSYSNCHRONY

AV Dyssynchrony, Long AV Interval

A wave fuses with E

A wave abuts

Limited net diastolic stroke volume

Decreased LV filling

A delay between atrial and

ventricular contraction

AV dyssynchrony results in

1. Reduced LV filling

2. Diastolic MR

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DYSYSNCHRONY

Intraventricular Dys. Interventricular Dyss. AV Dyssynchrony,

Incomplete LV emptying

Incomplete LV filling

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Rationale for CRT

• CRT may confer benefits by

▫ coordinating right ventricular and LV contraction,

▫ synchronizing the LV segments,

▫ prolonging the diastolic filling period with improvements of both coronary and LV filling,

▫ restoring atrioventricular synchrony.

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Rationale for CRT

• Improved contractile function- IMPROVEMENT IN EF

▫ This improvement is associated with greater coordination of global contraction

• Reverse ventricular remodeling• Decrease secondary MR • The ability to tolerate more aggressive

medical therapy and neurohormonalblockade, particularly with improved tolerance of beta blockers

• Improved diastolic function • Improvement in heart rate variability (HRV)

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The Cardiac Resynchronization–Heart Failure trial

• in the CRT compared to no CRT group• CRT can provide up to a 30% improvement in SV

and a significant reduction in MR within 3 months of initiating therapy

• LVEF - increased by 3.7 percent at three months and 6.9 percent at 18 months .

• The increase in contractile function was associated with a rise in systolic pressure of about 6 mmHg

• a reduction in plasma N-T-pro-BNP of 225 pg/mL at 3 months and 1122pg/mL at 18 months (median baseline 1800 to 1900 pg/mL).

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• The molecular basis for these mechanical changes has not been established.

• Preliminary data from an experimental model suggest that

▫ CRT reduces regional and global molecular remodeling, generating more homogeneous activation of stress kinases and reducing apoptosis. Chakir K, Daya SK, Tunin RS, et al. Reversal of global apoptosis and regional

stress kinase activation by cardiac resynchronization. Circulation 2008; 117:1369

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CRT Induces Reverse Ventricular Remodeling

• Decrease in ESV/EDV/Lvmass

• By avg of 10% decrease in vol over a 6 month period.

▫ Yu et al

▫ CARE-HF

▫ MIRACLE trials,

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Improvement in heart rate variability

(HRV)

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Assesment of dyssynchrony

• ECG

• ECHO

• OTHERS

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QRS DURATION

• QRS duration, a marker of electrical dyssynchrony,

• Cannot be used alone to reflect mechanical dyssynchrony

• QRS interval <150 ms is a major risk factor for lack of response to CRT,

• But is easy to assess, and remains an important element for patient selection in current practice.

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LBBB

• Changed pattern of LV contraction

• Suboptimal LV FILLING

• Increased duration of MR

• Paradoxical septal motion

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Limitations

• The threshold criteria of a QRS duration of120 ms was not derived from prospective evaluation but rather from inclusion criteria of landmark clinical trials

• Although remarkable symptomatic improvement is seen in many patients, up to 30% of subjects who participated in CRT trials failed to respond to therapy or may have worsened

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• 20 % with an EF <35% and QRS 150 ms do not exhibit dyssynchrony.

Electrical evidence of conduction delay with QRS duration may not be the most reliable marker of ventricular

dyssynchrony

Cho GY,, et al. Mechanical dyssynchrony by TD imaging is a powerful predictor of mortality in CHF with normal QRS duration. JACC. 2005

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Role OF ECHO

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DYSYSNCHRONY by ECHO

Intraventricular Radial Dyssynchrony,

John Gorcsan III et al ASE recommendation of echo for CRT 2008

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DYSYSNCHRONY by ECHO

Intraventricular Dyssynchrony – Septal To Posterior Wall Delay (SPWMD)

John Gorcsan III et al ASE recommendation of echo for CRT 2008

SPWMD ≥ 130MS sensitivity of 100% and a specificity of 63% to

predict the response to CRT

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Note that time to peak strain in a normal subject occur synchronously over a very narrow time range.

Dyssynchrony is shown as the difference in timing of peak strain from earliest to latest segment

DYSYSNCHRONY by ECHO

Intraventricular Dyssynchrony – Septal To Posterior Wall Delay (SPWD)

John Gorcsan III et al ASE recommendation of echo for CRT 2008

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• In the PROSPECT study, SPWMD could not predict clinical response to CRT (54% sensitivity and 50% specificity), and a 72% interobservervariability was shown for this parameter.

• SPWMD could not be assessed in 50% of patients because of septal or posterior wall akinesis, or poor acoustic windows.

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DYSYSNCHRONY by ECHO

Intraventricular longituidinal Dyssynchrony

John Gorcsan III et al ASE recommendation of echo for CRT 2008

OPPOSING WALL DELAY ≥ 65MS

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DYSYSNCHRONY by ECHO

Intraventricular longituidinal Dyssynchrony

John Gorcsan III et al ASE recommendation of echo for CRT 2008

OPPOSING WALL DELAY ≥ 65MS

MAXIMUM WALL DELAY IN 12 SEGMENTS ≥ 100MS

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DYSYSNCHRONY by ECHO

Intraventricular longituidinal Dyssynchrony – Dyssynchrony (yu) index

John Gorcsan III et al ASE recommendation of echo for CRT 2008

YU INDEX ≥ 33MS

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DYSYSNCHRONY by ECHO

Intraventricular longituidinal Dyssynchrony

DELAY IN ONSET OF SYSTOLLIC VELOCITY ≥ 100MS

LV pre-ejection interval (LPEI)

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• PROSPECT trial (cut-off at 140 ms or more).

• This parameter had low intra- and interobservervariability (3.7% and 6.5%, respectively), could be performed in 95% of echos,

• predicted both clinical improvement and reverse remodelling after CRT, although with rather low sensitivity and specificity

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John Gorcsan III et al ASE recommendation of echo for CRT 2008

DYSYSNCHRONY by ECHO

Interventricular mechanical delay (IVMD)

DELAY IN ONSET OF SYSTOLLIC VELOCITY Ao-Pu ≥ 40 MS

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• Not used for assessing as requirement of CRT

• Used to optimize CRT once deployed

• An AV delay programmed too short will result in absence or interruption of the atrial component (mitral A wave) by the premature ventricular contraction and closure of the mitral valve..

• An AV delay programmed too long can result in suboptimal LV preload or diastolic MR, or may even allow native LV conduction, which defeats the purpose of CRT

DYSYSNCHRONY by ECHO

AV Dyssynchrony

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DYSYSNCHRONY by ECHO

• The LV filling time to RR interval ratio (LVFT/RR)

• index of atrioventricular (dys)synchrony.

• Using a 40% or greater LVFT/ RR cut-off, the PROSPECT investigators found a low sensitivity but good specificity for clinical and remodelling responses (36% and 76% for clinical response, and 41% and 74% for LVESV, respectively) to predict response to CRT

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SPECKLE TRAKING

• Velocities measured with TDI tend to underestimate the individual movement of each myocardial segment because of translational motion or tethering.

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• Whether echo criteria in pts with normal QRS can benefit pts with CRT?

• Whether echo criteria in pts with increased QRS can identify pts who are more likely to benefit with CRT?

DYSYSNCHRONY by ECHO

ECHO Dyssynchrony – Trial Evidence

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• Whether echo criteria in pts with normal QRS can benefit pts with CRT?

• Non RCT1. BLEEKER(JACC 2006)2. CHEUK-MAN (JACC 2006)3. YU(JACC 2006).

• RCT1. RETHINQ- The Resynchronization

Therapy in Normal QRS Study.2. ECHO-CRT

DYSYSNCHRONY by ECHOECHO Dyssynchrony – Trial Evidence

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Inclusion Criteria

• NYHA class III HF

• LVEF ≤ 35%

• Evidence of mechanical dyssynchrony

• QRS duration < 130msPrimary EndpointImprovement in Peak VO2 during CPET of at least 1.0ml/kg/min at 6 months.Secondary EndpointsImprovement in quality of life score at 6-monthsImprovement in NYHA classification at 6-months

RETHINQ

DYSYSNCHRONY by ECHO

ECHO Dyssynchrony – Trial Evidence – NARROW QRS

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Mechanical dyssynchrony considered present if either• M-Mode

- Septal posterior wall mechanical delay (SPWMD) ≥ 130 ms

OR• Tissue Doppler Imaging (TDI) of the basal

ventricular segments in apical 4/2/3 chamber views

- Septal to lateral delay ≥ 65ms OR

- Antero-septal to posterior delay ≥ 65ms

RETHINQ

DYSYSNCHRONY by ECHO

ECHO Dyssynchrony – Trial Evidence – NARROW QRS

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RETHINQ

DYSYSNCHRONY by ECHO

ECHO Dyssynchrony – Trial Evidence – NARROW QRS

Limitations1. Too short follow up study2. ECHO criteria less and coudn’t include strain3. Small no. of subjects

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DYSYSNCHRONY by ECHO

ECHO Dyssynchrony – Trial Evidence – NARROW QRS

ECHO-CRT

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• Primary composite endpoint:

▫ Hospitalization or all cause mortality occurred in 116 of 404 pt of CRT vs 102 of 405 control pt (28.7% vs 25.2)

ECHO-CRT

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• Whether echo criteria in pts with increased QRS can identify pts who are more likely to benefit with CRT?

• PROSPECT trial – Predictors of Response to CRT

DYSYSNCHRONY by ECHO

ECHO Dyssynchrony – Trial Evidence – WIDE QRS

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Purpose:▫ Prospective, multi-center study designed to evaluate the

ability of selected, pre-defined baseline echocardiographic parameters to predict clinical or echocardiographic response to CRT in a prospective, multi center study

Primary Endpoints at 6 months:▫ Clinical Composite Score

Subjective and objective measures of clinical status include: Survival, heart failure hospitalization, change in NYHA Class and change in Patient Global Assessment Score

▫ Left Ventricular End-Systolic Volume Definition of Improved: Reduction of ≥ 15%

DYSYSNCHRONY by ECHOECHO Dyssynchrony – Trial Evidence – WIDE QRSPROSPECT

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DYSYSNCHRONY by ECHO

PROSPECTECHO Dyssynchrony – Trial Evidence – WIDE QRS

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The results of the PROSPECT study indicate that no single echocardiographic measure of dyssynchrony, may be recommended to further improve patient selection among the CRT candidates.

Current clinical criteria including electrocardiogram, remain the standard for

CRT patient selection

DYSYSNCHRONY by ECHO

PROSPECT

ECHO Dyssynchrony – Trial Evidence – WIDE QRS

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• Various magnetic resonance imaging (MRI) techniques

• The circumferential uniformity ratio estimate -CURE index is based on tagged MRI and ranges from 0 (dyssynchronous) to 1 (synchronous).

• In a recent series of 43 heart failure patients treated with CRT, the CURE index showed an accuracy of 90% to predict clinical improvement at 6-month follow-up, with a negative predictive value of 87% and a positive predictive value of 100% .

DYSYSNCHRONY by MRI

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• Vector-velocity– encoded magnetic resonance permits the assessment of LV mechanical dyssynchrony by measuring differences in regional time to peak myocardial velocities, similar to echocardiography with TDI .

• The assessment of segmental radial motion or radial thickness of the LV along the cardiac cycle with MRI has provided novel indices of LV mechanical dyssynchrony

• The standard deviation of time to peak radial motion or thickness of 16 or more LV segments is used as a marker of LV mechanical dyssynchrony.

DYSYSNCHRONY by MRI

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CMR

• Can assess mechanical dyssynchrony differently from echocardiography from a technical perspective.

• CMR can also provide the location of myocardial scar and coronary venous anatomy, which influence the likelihood for success of CRT.

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• Nuclear imaging has also been used for assessment of LV mechanical dyssynchrony.

• LV contraction patterns

▫ Gated blood-pool ventriculography,

▫ Gated blood-pool SPECT,

▫ Gated myocardial perfusion SPECT.

• From the short-axis images,

▫ amplitude (which reflects systolic wall thickening)

▫ phase (reflecting onset of mechanical contraction) are calculated.

• Five different quantitative LV dyssynchrony indices can be derived (peak phase, phase standard deviation, bandwidth, phase histogram skewness, and kurtosis).

DYSYSNCHRONY by SPECT

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▫ The phase standard deviation

▫ the histogram bandwidth

• are the most commonly used parameters to assess LV mechanical dyssynchrony .

• In 40 patients with advanced heart failure treated with CRT, LV mechanical dyssynchrony was assessed with gated myocardial perfusion SPECT.

• Responders had significantly larger bandwidth histogram (94±23° versus 68±21°; P<0.01) and phase standard deviation (26±6° versus 18±5°; P< 0.01) at baseline than non responders.

DYSYSNCHRONY by SPECT

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CLINICAL TRIALS

• In NYHA class III or IV HF

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Multisite Stimulation in

Cardiomyopathy Trials (MUSTIC) • The first study involved 58 randomized patients

with NYHA class III HF, NSR, and a QRS duration of at least 150 msec.

• The mean distance walked in 6 minutes was 23% greater with CRT than without CRT (P <0.001).

• Significant improvement was seen in quality of life and NYHA functional class ranking.

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MIRACLE:2002Multi-center In Sync Randomized Clinical

Evaluation Trial

• Double blinded RCT

• First US trial

• Class 3 or 4, on OMT, QRS >130 ms, EF<35%

• Enrollment of 453 patients

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MIRACLE

NYHA class III-IV

LVEDD > 60 mm

QRS > 130 ms

Stable 3 month regimen of beta-blocker/ACE inhibitor

EF < 35%

Randomization

CRT on

CRT on

1- and 3-month follow-up

6-month follow-up

CRT off

1- and 3-month follow-up

6-month follow-up

Long-term follow-up

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Nonresponders: older, ischemic CM, no MR, QRS<150

Responders: had shorter duration on CHF and longer QRS>155

MIRACLE

39%34%

27%

67%

17% 16%

0%

20%

40%

60%

Improved No Change Worsened

Pro

po

rtio

n

Control N=225 CRT N=228

P < 0.001

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MIRACLE

• There was a decrease in hospitalizations of 50% at 6 months and a trend towards a decrease in mortality.

• All other primary and secondary endpoints were met: 6 minute walk time, peak Vo2, QOL, EF , NYHA class, LVEDD

Magnitude of improvement not influenced by degree of QRS

shortening with BiVP (average in all was –20msec)

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FDA Approval

•The first CRT device was approved by the FDA in

September 2001 .

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COMPANION Trial ( The Comparison of Medical

Therapy, Pacing, and Defibrillation in Heart

Failure )

• comparing the effects of CRT alone (CRT-P) or CRT-D with optimal medical therapy

• subjects were randomized in a 1:2:2: ratio.

• greater proportion of patients had ischemic cardiomyopathy.

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COMPANIONMichael R.Bristow et al,NEJM May 2004.

Total no of patients : 1520.• 128 US center • Inclusion criteria :

NYHA Class- III or IVQRS > 120 msec.LVED > 55 mmEF < 35%PR duration:150 msec.

Patient has no indication for ICD or Pace maker implantation.Randomly assigned in 1: 2: 2 treatment protocol.

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• The primary end point was a composite of time to death and hospitalization from any cause.

• Significant reduction in the primary end point in the CRT-P (34%) and the CRT-D group (40%).

• Significant 36% reduction in mortality was found with CRT-D, with a smaller (24%) non significant trend towards mortality reduction with CRT-P (p = 0.06).

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CLINICAL TRIALS

• In NYHA class III or IV HF

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• Role of CRT - where evidence is uncertain

1. In mild heart failure (NYHA class I , II )

2. In pts with AF

3. In pts with heart failure needing pacing

4. In pts with NO LBBB (RBBB , IVCD)

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• MADIT – CRT(15% NYHA class I and 85% NYHA class II).

• RAFT – (80% NYHA class II and 20% NYHA class III).

• REVERSE trial

In mild heart failure (NYHA class I , II )

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MADIT CRT

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RAFT

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• In NYHA class I or II HF

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• MUSTIC• RAFT

In AF

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• RAFT

• Block HF trail

• PACE trial

In pts with heart failure needing pacing

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HF WITH RBBB

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HF WITH RBBB

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• Sex — Indications for CRT do not vary by sex

• Age — Randomized trials have not specifically addressed the benefit of CRT in elderly patients. However, an individual patient meta-analysis of five randomized CRT trials found no significant interaction between age and CRT effect on all-cause mortality/heart failure (HF) hospitalization

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Cumulative Enrollment in Cardiac

Resynchronization Randomized

Trials

0

1000

2000

3000

4000

1999 2000 2001 2002 2003 2004 2005

Results Presented

Cu

mu

lati

ve P

ati

en

ts

PATH CHF

MUSTIC SR

MUSTIC AF

MIRACLE

CONTAK CD

MIRACLE ICD

PATH CHF II

COMPANION

MIRACLE ICD II

CARE HF

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Indications

2013 ACCF/AHA Heart Failure Guideline

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CRT - GUIDELINESCLASS 1 A recommendation

criteria ACC/AHA 2013 ESC 2012

NYHA class III , ambulatory IV II , III , ambulatory IV

LVEF < 35% < 30 %

Rhythm Sinus Sinus

BBB LBBB LBBB

Symptomatic even with optimal medical management

Yes Yes

Dyssynchrony ≥ 150ms ≥ 130ms

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2013 ACCF/AHA Heart Failure Guideline

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2013 ACCF/AHA Heart Failure Guideline

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2013 ACCF/AHA Heart Failure Guideline

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II , III , ambulatory IV refractory to optimal Rx

II , III , ambulatory IV refractory to optimal Rx

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Preimplant identification of

nonresponders• Response score• Data from 1761 patients enrolled in the MADIT-CRT

trial ▫ female sex (two points),▫ nonischemic origin (two points),▫ LBBB (two points), ▫ QRS ≥150 ms (two points), ▫ prior hospitalization for HF (two point), ▫ left ventricular end-diastolic volume ≥125 mL/m2 (two

points), ▫ left atrial volume <40 mL/m2 (three points)

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• The response score correlated with reduction in the risk of HF or death with CRT-D versus defibrillator only therapy with a 13 percent increase in clinical benefit per one point increment in the response score.

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PROCEDURE

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Procedural Aspects of Lead Positioning

• Step 1: Venous access, right atrial, and RV lead implantation

• Venous access:

▫ combined approach: cephalic vein cutdown (for the RA and RV leads) and an axillary or subclavianvein puncture for the LV lead.

▫ the axillary or subclavian veins can be used as the only venous conduit for the leads and lead delivery systems

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• Once access is obtained, the RV lead is placed first in order to provide backup pacing.▫ more difficult to cannulate the CS with the lead

implanted

• If there is no need for backup pacing or additional method is used to provide backup pacing (e.g. temporary RV apex pacing), the LV lead should be implanted first, because it may be easier to cannulate the CS.

• RA lead should be implanted last, in order to avoid dislodgements

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• Step 2: CS access:

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• CS ostium is 5–15 mm in diameter and is located on the posterior interatrial septum anterior to the Eustachian ridge and valve and posterior to the tricuspid annulus.

• ostium is often covered, to a variable extent, by the Thebesianvalve.

• The valve usually covers the superior and posterior surfaces of the ostium, but may be covered completely with formation of fenestrations.

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• landmarks for the location of the ostium

▫ calcified right coronary artery

▫ radiolucency from the fat pad running in the AV groove

▫ The CS is on average 3-10 mm above (superior to) the inferior border of the T10 vertebral body

▫ 10 - 16 mm above the dome of the left hemidiaphragm

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Angiographic views

• Right anterior oblique: (RAO) 48+/-7 projection,

▫ the fluoroscope beam is parallel to the CS plane ,

▫ the CS ostium is visualized ‘‘en face,’’ and the CS guiding catheter is straight.

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Angiographic views

• LAO/AP view

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• straight

• preshaped with different degrees of the curves,

• straight catheters with the ability of cyrtosis by external manipulation)

steerable electrophysiology diagnostic mapping catheter

Guide catheters

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Coronary sinus cannulation

• The CS catheter with a single curve easily enters the ostium of the coronary sinus from a superior approach.

• The left brachial vein access is thus often preferred.

• Although a right brachial or femoral venous approach is feasible using a reverse loop technique,

• the easiest approach to the coronary sinus is still through the right internal jugular vein.

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• Technique:

• After entering the right atrium, the catheter is rotated counterclockwise and advanced slightly until it just enters the right ventricle (detected by pressure waves or premature ventricular contractions).

• After slight additional counterclockwise rotation, the catheter is then withdrawn slowly until an atrialpressure tracing is restored.

• Gentle readvancement of the catheter from this position leads to cannulation of the coronary sinus.

• Should the right ventricle be re-entered, the same maneuver is repeated with accentuation of counterclockwise rotation.

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• Successful coronary sinus entry is confirmed by

▫ In the LAO projection, the catheter is smoothly advanced

crossing the spine or

across the plane of the tricuspid valve.

▫ the maintenance of a right atrial pressure waveform

▫ absence of premature ventricular contractions,

• confirmatory contrast injection.

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• Step 3: Defining the venous anatomy and selecting a target vein

• Balloon occlusive retrograde coronary venous angiography

▫ In AP, LAO 45 and RAO 30

▫ high-speed rotational angiography, over an arc from RAO 55 to LAO55 for better definition of the angle

Acute takeoff angles of the CS tributaries (angles of 900 between the first-degree CS tributary and the main CS) can impede cannulation.

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Optimal site

• Optimal site may vary considerably for an individual patient.

▫ In the majority of patients, preferred sites are

Lateral

Posterolateral,

Non-apical position

Non scar area

As far as possible from the RV pacing lead.

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Segmental venous classification

• Thus 9 LV venous segments are derived which when added with the conventional classification gives the best comprehensive information to place the epicardial LV leads for CRT purposes

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• Step 4: Advancing the LV lead delivery system in the CS

▫ Once the CS is cannulated with a guide, the pacing lead is advanced.

• Step 5: Cannulating a first-degree tributary of the CS

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Choice of LV lead

• first-degree CS tributary is large, a lead with a larger diameter is chosen.

• target vein is very large and there is a risk of dislodgement, then a lead with an S-shape or sigmoid shape may allow for better lead stability

▫ LV lead dislodgement rates are still approximately 5–10%

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Choice of LV lead

• Active fixation leads that have lobes at the distal endof the lead that can be deployed and compress gently against the vein wall, and thereby provide enhanced fixation of the LV lead

• leaving a guidewire in place for CS lead stabilization.

• placement of coronary stents besides the lead body.

▫ extracting or replacing difficulties

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Difficulties in step 5

• Acute takeoff angles of the CS tributaries.• Increased tortuosity of the CS branch

▫ Placing the guide sheath close to the target vessel▫ an internal mammary artery catheter▫ The double-wire technique▫ position the wire in other first-degree tributaries of the

CS, like the anterior interventricular vein or middle cardiac vein, which have extensive collaterals with the lateral/posterolateral vein, and then advancing the wire through the collaterals and terminating in the target area.

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Coronary sinus cannulation

• Recently, the use of magnetic navigation for the placement of a guide wire within the CS was advocated for difficult cases.

• a new technique for rapid cannulation of the CS and advancement of the LV pacing lead with minimum fluoroscopy and procedure time in cases where conventional techniques have been unsuccessful.

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LV lead implantation is not possible

• An epicardial approach via mini-thoracotomymight be considered.

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• Transseptal endocardial LV lead implantation. ▫ performed with endocardial screw-in leads, which

are passing by the interatrial septum and the mitral valve and are attached to the LV wall.

▫ Endocardial pacing is physiologic in experimental and clinical observations as compared to epicardialpacing.

▫ this technique has the advantage of positioning the LV lead within the LV cavity unrestricted by the coronary sinus branches.

▫ there are very limited data on the long-term safety and efficacy of this method.

▫ Patients require long-term anticoagulation ▫ there is limited data on any risk of worsening

mitral regurgitation (due to the transmitral lead position).

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• Bifocal right ventricular pacing .

• Bifocal right ventricular pacing consists of implantation of two right ventricular leads

▫ one placed septally at the apex,

▫ the other in the high septal outflow tract.

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Europace (2005) 7, 380e384

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Complications of CRT

• The most common complication ▫ inability to implant the LV pacing lead successfully in

the coronary vein• Additional complications include

▫ coronary sinus or coronary vein trauma, ▫ pneumothorax,▫ diaphragmatic/phrenic nerve pacing, ▫ infection . ▫ prolonged radiation exposure due to the complexity of

the transvenous implantation procedure , ▫ theoretical risk that pacing from an LV lead may be

proarrhythmic due to alterations in depolarization and repolarization sequences

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• In 54 studies (6123 patients) of CRT-alone devices,

▫ implantation was unsuccessful - 7 %

▫ patients died during implantation - 0.3 %

▫ During a median six-month follow-up,

5 % of CRT devices malfunctioned

2 % of patients were hospitalized for infections in the implant site.

▫ During a median follow-up of 11 months, lead problems occurred in 7 %of CRT devices

▫ did not reveal any excess risk of sudden death or noncardiac death in CRT device recipients.

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THINGS TO AVOID

• Right atrial pacing

• Pacing of the right atrial appendage in the DDD mode leads to delayed activation of the left atrium, which may impair left ventricular preload due a reduction in the left atrialcontribution.

• With VDD pacing, both atria are activated via the intrinsic conduction system

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Lead Position

• LV lead location is probably one of the most important contributing factors for CRT response

▫ Chest X-ray images (PA and lateral projection)

▫ fluoroscopy

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CRT PROGRAMMING

• Two main device-based approaches:

▫ Promoting CRT

▫ Optimizing CRT

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Promoting CRT

• Unlike conventional pacing (where the goal is to minimize unnecessary ventricular pacing), CRT should pace both ventricles as close to 100% of the time as possible.

• Percentage of LV pacing -- as high as 90%.▫ optimal CRT delivery

• lower pacining %▫ LV lead dislocation ▫ paroxysmal or permanent atrial fibrillation▫ frequent ventricular ectopic beats

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Promoting CRT- MTR

• The Maximum Tracking Rate sets the highest rate at which the ventricles will be paced in response to intrinsic atrial activity.

• If the patient has high intrinsic atrial rates (>MTR) with good conduction, it is possible that the ventricle will not be paced some of the time.

• Make sure the MTR is high enough so that even in the presence of high intrinsic atrial rates, the patient is paced in the ventricle as much as possible

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Promoting CRT- RRAVD

• Rate-responsive Av delay (RRAVD) is the automatic shortening of the AV delay as the patient’s heart rate increases.

• This keeps the AV delay short even during periods of rapid activity.

• Programmed ON in CRT patients.

• The algorithm is automatic.

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• Conventional hysteresis encourages intrinsic activity and is incompatible with CRT.

• However, negative AV hysteresis automatically shortens the AV delay whenever an intrinsic ventricular event is sensed.

• This is the “opposite” of conventional hysteresis and works to discourage intrinsic ventricular activity.

• Program it ON.

Promoting CRT: Negative AV Hysteresis

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Promoting CRT: Negative AV Hysteresis

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Optimisation

• Why do we optimize CRT?

• How do we optimize CRT?

• When should we optimizeCRT?

• does optimizing CRT benefit patients?

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Why do we optimize CRT?

• The theory behind timing optimization is that proper CRT depends on precise timing of the ventricular contractions.

• Timing must allow for :

▫ Adequate time for the filling of the ventricles (i.e.diastolic optimization).

▫ Proper contraction of the right and left ventricles with respect to each other (i.e. systolic optimization).

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Atrioventricular delay

• Atrial contraction contributes 20 –30% to stroke volume at rest.

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COMPANION Method

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Aortic VTI Method

• Objective:

▫ Identify the AV Delay that yields the maximum cardiac output as determined by an aortic VTI measurement

• Procedure:

▫ Obtain continuous wave Doppler echo of aortic valve outflow to obtain VTI measurement

▫ Record VTI values over a range of programmed AV Delays

▫ Program the AV Delay value that yields the maximum aortic VTI

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Iterative Method

• Objective:

▫ Identify the AV Delay that maximizes LV filling using mitral velocity echocardiographic measurements1

• Procedure

▫ Obtain transmitral Doppler echo at a “long” programmed AV Delay during ventricular pacing

▫ Shorten the programmed AV Delay by 10-20 ms until the echo Doppler A-wave becomes truncated (A wave is atrial contraction)

▫ Lengthen the programmed AV Delay back to the value where there is no A-wave cutoff. This timing should enable ventricular contraction to occur just at the end of atrial systole

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• to maximize DFT (i.e. separation of the E- and A-waves).

• to allow complete end-diastolic filling(marked by the end of the A-wave)before the onset of LV contraction.

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Optimal AV delay is1. E and A wave separated.2. Termination of the A wave at

approximately 40 to 60 milliseconds before the onset of the QRS.

3. Stage I diastolic filling pattern i.e A > E pattern.

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Ritter’s method

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Mitral inflow velocity time integral

• VTI is calculated representing the stroke distance of mitral inflow as a surrogate of LV filling volume.

• The AV delay with the largest VTI is considered the optimal setting.

• good correlation with optimization by LV dP/dtmax (r=0.96) in a small study of 30 patients

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Diastolic mitral regurgitation (Ishikawa)

method

• Aims to minimize diastolic MR.

• optimal AV delay = long AV delay - duration of diastolic MR

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Non-echocardiographic

optimization methods• Pulse pressure

• Invasive left ventricular dP/dtmax

• Impedance cardiography

• Finger photoplethysmography

• Expert Ease for Heart Failure algorithm(EEHF)

• Intracardiac electrogram (IEGM)(QuickOpt)

• Peak endocardial acceleration(PEA)

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Impedance cardiography

▫ Transthoracic impedance measurements calculate changes in stroke volume

▫ IC testing is fast (~ 15 minutes) but requires special equipment

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Finger photoplethysmography

• non-invasively measures change in blood pressure

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Expert Ease for Heart Failure algorithm

• Calculates both sensed and paced AV delays by measuring the intrinsic sensed and paced AV intervals (from the device) and QRS duration (from surface ECG)

• When compared with Ritter’s method and AV VTI, the EEHF algorithm was superior in predicting optimal AV delay as determined by invasive LV dP/dtmax

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Peak endocardial acceleration

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V-V Timing: synchronize the RV and the LV

• The best V-V setting by measuring the RVOT and LVOT via PW Doppler

• V-V above > 40 ms is considered abnormal

• In normals, the RV will contract before the LV in the heart by -20 ms.

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How to optimize VV delay?

• Invasive left ventricular dP/dtmax

• L VOT TVI/SV

• Tissue Doppler synchrony

• Expert Ease for Heart Failure algorithm

▫ optimal VV delay=-0.333*(RV2LV electrical delay)220 ms

Unpublished acute haemodynamic data in the PATH-CHF II studies

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Timing of optimization

• best evidence-based practice is to follow the CARE-HF protocol and optimize AV delay using the iterative method at

▫ Baseline( predischarge)

▫ 3 months,

▫ every 6 months thereafter.

• Routine optimization of VV delay cannot be recommended.

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Non responders - 30%

• A standardized definition of benefit and quantification of benefit after CRT still lacks uniformity.

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CONCLUSION

CRT address systolic heart failure

Rectify mechanical dyssynchrony

improving symptoms and reducing mortality.

There are now several recognized approaches to optimize CRT.

Imaging modalities can assist with identifying the myocardium with latest mechanical activation for targeted LV lead implantation.

Device programming can be tailored to maximize biventricular pacing and thereby its benefit.

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THANK YOU