Cardiac Resynchronization Therapy Who is the best...
Transcript of Cardiac Resynchronization Therapy Who is the best...
Cardiac Resynchronization Therapy
Who is the best candidate?
Raed Abu Shama, M.DCardiologist and Electrophysiologist
CARDIAC RESYNCHRONIZATION THERAPY
1. Improve ventricular systolic function.
2. Induce favorable remodeling.
3. Reduce metabolic costs
4. Ameliorate functional mitral regurgitation
5. Improve exercise capacity
6. Reduce HF symptoms on the MLWHF Scale
7. Decrease hospitalizations
8. Decrease mortality rate
CASE HISTORY
A 68 YOMP with CHF was referred for device implant.
IHD, S/P NSTEMI 2012 and CABG X 4
COPD, CHF, NYHA III
Echo: Dilated LV, LVEF 28%, mod-sev. TR, mod. PHTN
Optimal Medical Therapy
ECG: SR, IVCD, QRS 122 ms
Referring physician: “the one with the 3 wires may
make you feel better, and if not – no harm done”.
WHO IS THE BEST CANDIDATE?
1. NYHA class II, III, or ambulatory IV
2. LVEF ≤ 35%
3. Sinus rhythm
4. LBBB
5. QRS ≥ 150 ms
6. on GDMT
7. Life expectancy is > 1 yearEpstein et al. JACC (2013); 61, 3:e6–75Parkash R. et al. CJC; 29 (2013) 1346 – 1360Brignole, M et al. Eur Heart Journal (2013) 34, 2281–2329Yancy CW et al. Circulation. (2013);128:e240-e327McMurray JJ et al. Eur Heart Journal (2012) 33, 1787–1847
KEY FINDINGS OF OBSERVATIONAL STUDIESEVALUATING SEX DIFFERENCES IN RESPONSE TO CRT Women are generally 30% or less of the study population. Compared with men, women typically:
1. Have higher rates of:
- Nonischemic HF cause
- LBBB configuration
- Procedural complications
2. Have lower rates of:
- Atrial fibrillation
- Ischemic HF cause
3. Have smaller LV volumes
Costanzo MR. Card Electrophysiol Clin 7 (2015) 721–734
Female
Male
Women with LBBB and QRS of 130
to 149 ms have a 76% reduction in
heart failure events and mortality
from CRT-D.
Zusterzeel R et al. JAMA Intern Med. 2014;174(8):1340-1348.
MADIT CRT: LBBB WAS ASSOCIATED WITH SUBSTANTIALLY GREATER IMPROVEMENT ACROSS ALL ENDPOINTS AS COMPARED
TO THE ENTIRE STUDY POPULATION.
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LBBB Non-LBBB
HAZARD RATIOS FOR PRIMARY COMPOSITEOUTCOME* BY QRS DURATION AND MORPHOLOGY
* death from any cause or HF hospitalization
Circ Heart Fail. 2013;6:1190-1198
CLINICAL IMPLICATIONS
1. In patients with LBBB, the broader QRS the greater the
benefit from CRT.
there is likely potential benefit in all patients with LBBB
regardless of QRS duration.
2. There is no benefit of CRT in patients with non-LBBB,
especially when the QRS duration is <160 ms.
KAPLAN–MEIER ESTIMATES FOR PRIMARY-OUTCOME EVENTS
the combination of death from any cause, or
first hospitalization for worsening HF
CRT IN NARROW QRS COMPLEX
1. Does not reduce HF mortality.
2. Does not reduce HF hospitalizations.
3. Associated with higher all-cause mortality.
BACK TO OUR PATIENT . . . A 68 YOMP was referred for device implant. IHD, S/P NSTEMI 2012 and CABG X 4 COPD, CHF, NYHA III Echo: Dilated LV, LVEF 28%, mod-sev. TR, mod. PHTN Optimal Medical Therapy ECG: SR, IVCD, QRS 122 ms
Family doctor: “the one with the 3 wires may make youfeel better, and if not – no harm done”.
A single chamber ICD was implanted!
POTENTIAL REASONS FOR NONRESPONSE
1. Suboptimal lead placement
2. Failure of the LV lead to capture
3. Atrial fibrillation with rapid response
4. Lack of viable myocardium
5. Suboptimal AV and/or V to V delays
6. Latency to LV stimulation
CASE HISTORY
JJ is a 43 YOMP with ICMP, severe LV dysfunction on
OMT for 2 years.
NYHA class III with frequent hospitalization.
He was referred for CRTD implant.
FOLLOW UP ECHOCARDIOGRAM
LV systolic function is severely reduced, LVEF < 20%.
Left ventricular diastolic function is suggestive of
restrictive filling pattern.
Restrictive Filling Pattern at 1 week after CRT was
independent predictor of mortality and hospitalization
for HF.
NOVEL MARKERS OF NON-RESPONSE
Abu Sham’a R. et al. Europace (2013) 15, 266–272
Tricuspid Regurgitation
P value < 0.001
adjusted for age, gender, MR grade ≥2, PHTN, RV dysfunction, and upgrading from PM
OUTCOMES IN PATIENTS WITH AND WITHOUT TR DETERIORATION
Variables TR deterioration 25 (13%)
No TR deterioration 168 (87%) P value
Clinical response 10 (42%) 112 (70%) 0.006
Echo response 13 (52%) 93 (56%) 0.73
∆ ESPAP 4.5 +13 2.7 +12 0.438
∆ RV-FAC 0.89 +10.8 0.65 +8.5 0.886
Mortality–long term 2 (8%) 13 (8%) 0.96
Abu Sham’a R. et al. Europace (2013) 15, 266–272
CASE HISTORY A 56 YOFP diagnosed as NICMP. Her ECG showed SR, LBBB at
163 ms. She was put on OMT.
Three months later, she was referred for CRTD implant due to poor
clinical response (NYHA class III).
One month post implant, she suffered from multiple ICD shocks
associated with worsening of her Heart failure.
ECG: SR, proper BiV pacing.
Echo: Improved LVEF from 25% to 35%
Device interrogation showed:
1. Normal electric parameters
2. Multiple appropriate ICD shocks
3. Complete Heart Block!
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Raed Abu Sham’a, Hiroshi Ohira, Pablo Nery, Girish Nair, Calum Redpath, Rob Beanlands, David Birnie
Response to Cardiac Resynchronization
Therapy in Patients with Cardiac Sarcoidosis
The University of Ottawa Heart Institute
Heart Rhythm Society May 8, 2014
CONCLUSIONS
1. Patients with CS have an expected remodeling
response rate (66.7%).
2. However only minority patients had a clinical response
to CRT.
Abu Sham’a et al. HRS 2014
CASE HISTORY
A 58 YOFP with NICMP for 8 months.
LVEF <30%. NYHA lass III despite OMT.
Referred for CRTD. Very poor cardiac venous anatomy.
Referred for EPICARDIAL LV lead implant.ECG Post-CRT
COMPLETE LBBB CRITERIA1. QRS ≥ 120 ms
2. Broad notched or slurred R wave in leads I, aVL, V5, and V6.
3. Absent q waves in leads I, V5, and V6, but in the lead aVL, a narrowq wave may be present.
4. R peak time greater than 60 ms in leads V5 and V6 but normal inleads V1, V2, and V3.
5. ST and T waves usually opposite in direction to QRS.
6. Positive T wave concordance may be normal.
7. Depressed ST segment and/or negative T wave in leads with negativeQRS (negative concordance) are abnormal.
8. The appearance of LBBB may change the mean QRS axis in thefrontal plane to the right, to the left, or to a superior, in some cases ina rate-dependent manner.
Surawicz B et al. J Am Coll Cardiol 2009;53:976–81.