ECG interpretation postCRT
- 2. Increasing number of new cases of heart failure being diagnosed Recent studies show despite optimal medical drug treatment mortality remains > 25% at three years Hospital admissions and office visits are frequent following diagnosis 20-40% of patients with heart failure have conduction disease and QRSd > 120 msec
- 3. Cardiac resynchronization therapy (CRT) is a recommended treatment for patients with moderate to severe (drug-refractory) heart failure with left ventricular (LV) systolic dysfunction and evidence of ventricular dyssynchrony defined by a QRS duration >120 ms. It improves symptoms, exercise tolerance, quality of life , morbidity and mortality. However, the problem of non-response to CRT remains crucial with prevalence of 30% of non- responders for clinical response and 45% for echocardiographic response.
- 4. Notable Recommendation Changes in 2012 ACCF/AHA/HRS Focused Update 2012 DBT Focused Update Recommendations Comments Class I 1. CRT is indicated for patients who have LVEF less than or equal to 35%, sinus rhythm, LBBB with a QRS duration greater than or equal to 150 ms, and NYHA class II, III, or ambulatory IV symptoms on GDMT. (Level of Evidence: A for NYHA class III/IV; Level of Evidence: B for NYHA class II) Modified recommendation (specifying CRT in patients with LBBB of 150 ms; expanded to include those with NYHA class II symptoms). Class IIa 1. CRT can be useful for patients who have LVEF less than or equal to 35%, sinus rhythm, LBBB with a QRS duration 120 to 149 ms, and NYHA class II, III, or ambulatory IV symptoms on GDMT. (Level of Evidence: B) New recommendation 2. CRT can be useful for patients who have LVEF less than or equal to 35%, sinus rhythm, a non-LBBB pattern with a QRS duration greater than or equal to 150 ms, and NYHA class III/ambulatory class IV symptoms on GDMT. (Level of Evidence: A) New recommendation 3. CRT can be useful in patients with atrial fibrillation and LVEF less than or equal to 35% on GDMT if a) the patient requires ventricular pacing or otherwise meets CRT criteria and b) AV nodal ablation or pharmacologic rate control will allow near 100% ventricular pacing with CRT. (Level of Evidence: B) Modified recommendation (wording changed to indicate benefit based on ejection fraction rather than NYHA class; level of evidence changed from C to B). 4. CRT can be useful for patients on GDMT who have LVEF less than or equal to 35% and are undergoing new or replacement device placement with anticipated requirement for significant (40%) ventricular pacing. (Level of Evidence: C) Modified recommendation (wording changed to indicate benefit based on ejection fraction and need for pacing rather than NYHA class; class changed from IIb to IIa).
- 5. Notable Recommendation Changes in 2012 ACCF/AHA/HRS Focused Update 2012 DBT Focused Update Recommendations Comments Class IIb 1. CRT may be considered for patients who have LVEF less than or equal to 30%, ischemic etiology of heart failure, sinus rhythm, LBBB with a QRS duration of greater than or equal to 150 ms, and NYHA class I symptoms on GDMT. (Level of Evidence: C) New recommendation 2. CRT may be considered for patients who have LVEF less than or equal to 35%, sinus rhythm, a non-LBBB pattern with QRS duration 120 to 149 ms, and NYHA class III/ambulatory class IV on GDMT. (Level of Evidence: B) New recommendation 3. CRT may be considered for patients who have LVEF less than or equal to 35%, sinus rhythm, a non-LBBB pattern with a QRS duration greater than or equal to 150 ms, and NYHA class II symptoms on GDMT. (Level of Evidence: B) New recommendation Class III: No Benefit 1. CRT is not recommended for patients with NYHA class I or II symptoms and non-LBBB pattern with QRS duration less than 150 ms. (Level of Evidence: B) New recommendation 2. CRT is not indicated for patients whose comorbidities and/or frailty limit survival with good functional capacity to less than 1 year. (Level of Evidence: C) Modified recommendation (wording changed to include cardiac as well as noncardiac comorbidities).
- 6. Ventricular Dysynchrony1 Electrical: Inter- or Intraventricular conduction delays typically manifested as left bundle branch block Structural: disruption of myocardial collagen matrix impairing electrical conduction and mechanical efficiency Mechanical: Regional wall motion abnormalities with increased workload and stress—compromising ventricular mechanics Cardiac Resynchronization Therapeutic intent of atrial synchronized biventricular pacing Modification of interventricular, intraventricular, and atrial-ventricular activation sequences in patients with ventricular dysynchrony Complement to optimal medical therapy 1 Tavazzi L. Eur Heart J 2000;21:1211-1214
- 7. Abnormal interventricular septal wall motion Reduced dP/dt Reduced pulse pressure Reduced EF and CO Reduced diastolic filling time Prolonged MR duration
- 8. Intraventricular Synchrony Atrioventricular Synchrony Interventricular Synchrony LA Pressure LV Diastolic Filling RV Stroke Volume LVESV LVEDV Reverse Remodeling Cardiac Resynchronization MR dP/dt, EF, CO ( Pulse Pressure)
- 9. Transvenous Approach Standard pacing lead in RA Standard pacing or defibrillation lead in RV Specially designed left heart lead placed in a left ventricular cardiac vein via the coronary sinus Right Atrial Lead Right Ventricular Lead Left Ventricular Lead
- 10. • Use extreme care when passing the guide catheter through vessels • Due to the relative stiffness of the catheter, damage to the walls of the vessels may include dissections or perforations
- 11. Varying Patient Anatomy 1,2,3
- 12. CS Os Middle Posterior Postero-lateral Great Lateral Antero- lateral Anterior Step 2: Perform Venograms
- 13. Step 2: Perform Venograms
- 48. Response more likely Response less likely QRS duration >150ms <150ms Heart disease Non-ischemic Ischemic Dyssynchrony Present Absent Bundle branch block Left Right Scar burden(MRI) Low burden High burden Non-transmural Transmural Posterolateral segments spared Posterolateral segments involved Severity of mitral regurgitation Mild-moderate Severe Lead position Posterior-lateral Anterior or inferior
- 49. CRT Responders: functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2 ml/kg/min) during exercise Reduction in LV diameter/ LVEDV(10%)/LVESV(15%) Main reasons for non-response to CRT: Improper patient selection Suboptimal lead placement Inappropriate device programming
- 50. RV and LV capture AV and VV optimization Capture threshold test- o To assess appropriate capture in both RV and LV o Atrial capture testing is not crucial unless suspect atrial capture problems o Capture threshold varies: Normal daily variation, posture and meal times, drugs, cardiac ischemia, disease progression o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
- 51. Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually) The threshold test is initiated with a high voltage output that results in BV capture, with gradual reduction in amplitude until one of the ventricles fails to be entrained, resulting in a change in QRS morphology. The algorithm was designed to identify the ventricle which had lost capture by evaluating changes in QRS axis
- 54. The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement In some cases can cause acute or sub‐acute pulmonary edema. The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG, or it may be suspected from data from the device
- 55. Ammann et al. described loss of LV capture as R/S ratio<1 in V1 and >1 in lead I sensitivity of 94% and specificity of 93% Yong and Duby Loss of LV capture is indicated by increasing QRS positivity in lead I and loss of RV capture by increasing positivity in lead III sensitivity of 97–100% and a specificity of 92–97% In Biventricular pacing, loss of q or Q wave in lead 1 is 100% predictive of loss of LV capture.
- 56. Geneva algorithm First step- evaluates QRS width in the limb leads, whose widening points to a change from BV capture to univentricular (LV or RV) capture The second step evaluates net QRS amplitude in lead I, with greater negativity indicating increasing participation of LV capture (i.e. RV-BV or BV-LV capture).
- 57. Left ventricular lead dislodgement Increase in LV or RV pacing thresholds Right ventricular lead dislodgement Non-optimal AV delay Atrial tachyarrhythmias with rapid ventricular rate Low maximal tracking rate Frequent ventricular premature beats Atrial undersensing T Wave oversensing Far-field atrial sensing Ventricular double counting
- 58. Two major approaches are currently used to guide their adjustment: echocardiography and intracardiac electrograms (IEGMs). Echocardiography-directed adjustment can be by many different methods (e.g. the Ritter's formula, the iterative technique) but LV outflow tract velocity–time integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial, RV and LV signals.
- 59. The AV delay is the time between the atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80–120 ms A long AV delay gives the ventricle a lot of “opportunity” to beat on its own before the ventricular output pulse is delivered Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
- 60. AV delay- significant impact on systolic function Rule of thumb in AV delay optimization - program AV delay to about 75%of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing Too short AV delay- undermine CRT stimulation and increase symptoms Too long AV delay- increases MR
- 61. Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patient’s heart rate increases Program this ON Sensed AV delay is from AS to VP (the sensed AV delay starts the timer at the moment the atrial device is sensed) Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered) As a result, it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
- 63. VV optimization- harmonize activities of RV and LV Optimal VV timing delay is the one that produces the greatest VTI value using echo Echo remains the gold standard of VV timing optimization Timing optimization is that proper CRT depends on precise timing of the ventricular contractions Timing must allow for Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with respect to each other
- 64. In up to 8–10% of the patients undergoing biventricular pacemaker implantation, LV lead placement is not possible for a variety of reasons, namely inability to cannulate the CS, absence of suitable branches, lack of lead stability, phrenic nerve capture, etc. Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy, video- assisted thoracoscopy approach, and robotically enhanced systems is an option in these patients.
- 65. FAILURE RESPONSE TO CRT EUVOLEMIC? ISCHEMIC? SEVERE VALVULAR DIEASE MAXIMAL MEDICAL THERAPY? MEDICAL NON- COMPLIANCE YES CORRECT NO LOSS OF LV PACING NO OPTIMIZE AV DELAY VV DELAY NO RESPONSE DYSSYNCHRONY PRESENT POOR LEAD POSITION YES REPOSITION LV LEAD YES CORRECT ATRIAL FIBRILLATION VENTRICULAR DOUBLE COUNTING/OVERSENSING LOSS OF LV CAPTURE LOW URL LONG AV DELAY PVARP EXTENSION ATRIAL UNDERSENSING FREQUENT PVC
- 67. Typically, LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV. Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV. There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position, targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate.
- 68. The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall). However, the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection. Since CRT is a form of electrical therapy for disorderly electrical activation of the heart, it makes sense to attempt to target the region with the maximal electrical delay.