Prevención de infecciones en el implante de dispositivos
Qrs and crt final in english
1. Value of the ECG before
and after cardiac
resynchronization therapy
Sergio L. Pinski
Cleveland Clinic Florida
Weston, FL USA
2. Value of QRS in CRT
Before implant
– Patient selection
– Stimulation site selection ?
After implant
– Confirm biventricular capture
– Predict response
– Optimize programming
3.
4. Mechanisms of CRT
Reduction in mechanical dyssynchrony
of the LV
Reverse remodeling of the LV
Optimization of left heart AV interval
Reduction of mitral regurgitation
Improvement in LV diastolic function
5. Identifying Responders
In most studies, 20-30% of patients are
non responders
Poor patient selection: there is not
enough ventricular dyssynchrony
– A wide QRS (ie > 120 ms) is necessary but not
sufficient to predict a positive response
– Nonviable myocardium
Failure to resynchronize
– Electrode in non optimal position
– Inadequate A-V (o V-V) delay.
– Arrhythmias (rapid AF, frequent ventricular
ectopy)
6. Relation between intrinsic QRS with
and improvement with stimulation
Kass DA, et al. Circulation 1999;99:1567
7. Forest plot of parallel-arm randomized clinical trials
comparing outcomes by strata of baseline QRS duration
Bryant et al. J Electrocardiol 2013
8. Impact of QRS Duration on Clinical Event Reduction With Cardiac Resynchronization
Therapy: Meta-analysis of Randomized Controlled Trials
Sipahi et al. Arch Intern Med 2011; 171:1454
9. Random-effects meta-analyses of the weighted mean difference in baseline
QRS duration between responders and non-responders to CRT, using
remodeling definition of response
Bryant et al. J Electrocardiol 2013
10. QRS duration and morphology in consecutive pts
undergoing CRT at Cleveland Clinic Ohio
Dupont et al. JACC 2012; 60:592
11. Significance of QRS morphology in determining the
prevalence of mechanical dyssynchrony in heart
failure patients eligible for CRT
Haghjoo M et al. Europace 2008;10:566-571
12. Cumulative probability of heart failure (HF) event or death according to treatment (cardiac
resynchronization therapy with defibrillator [CRT-D] versus implantable cardioverter
defibrillator [ICD] only) in patients with left bundle-branch block (LBBB), non-...
Zareba W et al. Circulation 2011;123:1061-1072
13. Relative risk of primary end point (heart failure event or death) by treatment (CRT-D versus
ICD only) according to selected clinical characteristics in patients with or without LBBB
Zareba et al. Circulation 2011;123:1061
14. QRS Axis and the Benefit of CRT in Patients with Mildly
Symptomatic Heart Failure in MADIT‐ CRT
Brenyo et al. J Cardiovasc Electrophysiol 2012
16. Bundle-Branch Block Morphology as a Predictor of Outcome
After CRTD in 15,000 Medicare Patients
Bilchick et al. Circulation 2010;122:2022
17. Gold standard for LBBB
No pathology correlate
Endocardial catheter mapping
Echo doppler studies showing
delay in contraction of LV free wall
vs. septum
18. Conventional definition of LBBB
1. QRS duration ≥ 120 ms in adults
2. Broad notched or slurred R wave in leads I, aVL, V5, and V6 and an
occasional RS pattern in V5 and V6 attributed to displaced transition of QRS
complex.
3. Absent q waves in leads I, V5, and V6, but in aVL, a narrow q wave may be
present in the absence of myocardial pathology.
4. R peak time greater than 60 ms in leads V5 and V6 but normal in leads V1,
V2, and V3, when small initial r waves can be discerned in the above leads.
5. ST and T waves usually opposite in direction to QRS.
6. Positive T wave in leads with upright QRS may be normal (positive
concordance).
7. Depressed ST segment and/or negative T wave in leads with negative QRS
(negative concordance) are abnormal
8. The appearance of LBBB may change the mean QRS axis in the frontal
plane to the right, to the left, or to a superior, in some cases in a rate-
dependent manner
20. Timing of electrical activation (depolarization) wavefronts in normal conduction (A) and LBBB
(B), shown in sagittal view.
Strauss D G et al. Circ Arrhythm Electrophysiol
2008;1:327-336
23. “True” LBBB
negative terminal deflection
in V1 (QS or rS)
> 140 ms in men, >130 ms in
women
Mid QRS notching
Strauss et al. Am J Cardiol 2011;107:927
24. Combined effects of conduction defects and hypertrophy
on QRS duration.
Strauss DG. J Electrocardiol 2012;45:635
25.
26.
27. New “gold standard” for the
definition of LBBB
High probability of improvement
with CRT
30. ECG Criteria of True Left Bundle Branch Block: A Simple
Sign to Predict a Better Clinical Response to CRT
Mascioli et al. PACE 2012; 35:927
31. Patients with longer LV activation have better
outcome with CRT
Eitel et al. Europace 2012; 14:358
32. QRS morphology with
biventricular stimulation
Location of RV electrode
Location of wire in coronary wire
Presence of fusion with intrinsic
conduction
V-V timing (simultaneous versus
sequential).
Latency, exit block with epicardial
pacing from coronary vein
52. Analysis of Ventricular Activation Using Surface ECG to
Predict LV Reverse Volumetric Remodeling During Cardiac
Resynchronization Therapy.
Sweeney et al. Circulation. 121:626, 2010.
54. Analysis of Ventricular Activation Using Surface ECG to
Predict LV Reverse Volumetric Remodeling During Cardiac
Resynchronization Therapy.
Sweeney et al. Circulation. 121:626, 2010.
55. Predictors for Restoration of Normal LV Function
in Response to CRT Measured at Time of Implant
Serdoz et al. Am J Cardiol 2011;108:75
56. Resolution of Left Bundle Branch Block?Induced
Cardiomyopathy by Cardiac Resynchronization Therapy
Vaillant at al. JACC 2013
57. Optimization of the Interventricular Delay in
CRT Using the QRS Width
Tamborero et al. Am J Cardiol 2009; 2009;104:1407
Editor's Notes
Figure 4. Meta-regression analysis examining the impact of baseline QRS duration on the effect of cardiac resynchronization therapy (CRT) on composite clinical events. Each circle represents a QRS subgroup within a trial. The sizes of the circles are proportional to the sample size in each subgroup. The dashed line corresponds to a log risk ratio (RR) of 0 (ie, RR, 1.00), where there is no net benefit or harm. The further the circles are below the 0 line, the larger the clinical benefit for prevention of composite of adverse clinical events. There was a statistically significant relationship between the QRS duration at baseline and log RR (slope, -0.07 [95% confidence interval, -0.10 to -0.04]; z = -4.60) (P < .001). Accordingly, groups with QRS ranges below 150 milliseconds did not benefit from CRT (black circles, log risk ratio close to 0). Clinical benefit appeared when cases with QRS intervals of 150 milliseconds or greater were included (gray circles) and became more prominent with increasing QRS width (white circles). CARE-HF indicates Cardiac Resynchronization-Heart Failure 17; COMPANION, Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure 16; CRT, cardiac resynchronization therapy; MADIT-CRT, Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy 20; RAFT, Resynchronization-Defibrillation for Ambulatory Heart Failure Trial 22; REVERSE, Resynchronization Reverses Remodeling in Systolic Left Ventricular Dysfunction.23
Left-sided plot shows the mean value of standard deviation of time to peak myocardial systolic velocity among all 12 segments in the left bundle branch group (LBBB), right bundle branch with coexistent left fascicular hemiblocks (bifascicular RBBB) group, and pure RBBB group. Right-sided plot shows the mean value of maximal difference in time to peak myocardial systolic velocity among all 12 segments in the LBBB group, and bifascicular RBBB group, and pure RBBB group.
Cumulative probability of heart failure (HF) event or death according to treatment (cardiac resynchronization therapy with defibrillator [CRT-D] versus implantable cardioverter defibrillator [ICD] only) in patients with left bundle-branch block (LBBB), non-LBBB, right bundle-branch block (RBBB), and intraventricular conduction disturbances (IVCD) in Multicenter Automatic Defibrillator Implantation Trial–Cardiac Resynchronization Therapy (MADIT-CRT) patients.
Relative risk of primary end point (heart failure event or death) by treatment (cardiac resynchronization therapy with defibrillator [CRT-D] versus implantable cardioverter defibrillator [ICD] only) according to selected clinical characteristics in patients with left bundle-branch block (LBBB; top) and non-LBBB patients (bottom). NYHA indicates New York Heart Association; LVEF, left ventricular ejection fraction; LVEDV, left ventricular end-diastolic volume; and LVESV, left ventricular end-systolic volume.
Effect of Cardiac Resynchronization Therapy on Composite Clinical Events in patients with LBBB (total n = 3,949, I2 = 72.7%, random effects model).
Kaplan-Meier curves for BBB morphology. Kaplan-Meier plots are shown for freedom from death alone (A) and freedom from death or heart failure hospitalization (B) in patients with CRT-D. Patients with RBBB had higher rates of both outcomes than those with LBBB, and those with a nonspecific IVCD had an intermediate prognosis.
Ventricular activation sequence in narrow vs prolonged QRS duration failing hearts. A, 3D activation sequence recorded with 3D mapping system (EnSite 3000, Endocardial Solutions) in a patient with dilated cardiomyopathy, heart failure, and QRS duration of 95 ms.The activation breakthrough point waslocated in the septal region of the left ventricle. From this site, the activationimmediately propagated to the anterior and lateral walls as indicated by the arrow. The basal region of the left ventricle was the last activated. B, In contrast, in a patient with a QRS duration of 179 ms, dilated cardiomyopathy, and heart failure, the propagation wavefront was unable to cross from the anterior region to the lateral wall as a result of a functional line of block, but instead, rotated around the apex showing a U-shaped activation sequence. The lateral and posterolateral regions were the last activated area of the LV
Figure 1. Timing of electrical activation (depolarization) wavefronts in normal conduction (A) and LBBB (B), shown in sagittal view. For reference, 2 QRS-T waveforms are shown in their anatomic locations (V3 on the chest and aVF inferiorly). Electrical activation starts at the small arrows and spreads in a wavefront with each colored line representing successive 10 ms. In normal conduton, activation begins within both the LV and RV endocardium. In LBBB, activation only begins in the RV and must proceed through the septum before reaching the LV endocardium (ie, this pattern in the septum is opposite to that seen in normal conduction). By taking into account the stereotypical LBBB activation, QRS-score criteria for scar can in fact be developed in LBBB, similar to that in normal conduction. Note that although scar in the septum causes Q-waves in V1 to V3 when normal conduction is present, the same scar causes large R-waves in V1 to V3 in the presence of LBBB because of unopposed electrical forces in the RV free wall (Figure 2A). LBBB indicates left bundle branch block; LV, left ventricle; RV, right ventricle.
Electrocardiograms from a patient who developed a LV conduction delay with a QRS duration of 142 ms that can be classified as LBBB under conventional criteria but likely represents progressive LVH. The scatterplot (A) shows QRS duration measurements over time from 42 electrocardiograms from the same patient. The patient’s QRS duration increased linearly at a rate of 6.2 ms/year. Electrocardiograms are shown at baseline ( B ) and after 1.5 years ( C ), 5 years ( D ) and 6.5 years ( E ). Although later electrocardiograms (D,E) met conventional ECG criteria for LBBB (QRS duration 120 ms with a LV conduction delay), review of the serial electrocardiograms shows that QRS morphology did not change as the QRS prolonged. The onset of true complete LBBB should result in a sudden increase in QRS duration of 60 ms along with a change in QRS morphology. The electrocardiogram in (E) (QRS duration 142 ms) contains very similar QRS morphology to the previous electrocardiograms. The gradual increase in QRS duration over time strongly suggests the development of intraventricular conduction delay due to hypertrophy rather than the onset of bundle branch block. Although serial electrocardiograms are not always available, this patient did not have mid-QRS notching in front-to-back (V1, V2) or left-to-right leads (I, aVL, V5, V6), which should be present for the diagnosis of complete LBBB.
Electrocardiograms from an 82-year-old woman with a sudden increase in QRS duration from 76 ms ( A ) to 148 ms ( B ) 1 year later (a 95% increase) with the development of complete LBBB. In addition to the increase in QRS duration, notice the change in QRS morphology that includes distinctive mid-QRS notching in leads I and aVL, along with mid-QRS slurring in leads V5 and V6.
QRS morphology in complete LBBB. The LBBB activation sequence and representative QRS-T wave forms are depicted in their anatomic locations for the sagittal, transverse, and frontal planes. The key LBBB QRS morphology feature shown is the mid-QRS notching that occurs at 50 and 90 ms with slurring in between. The first notch represents the time when the electrical depolarization wave front reaches the endocardium of the LV (after proceeding through the septum). The second notch occurs when the depolarization wave front begins to reach the epicardium of the posterolateral wall. The reason there is little change in QRS amplitude between the 2 notches is that the magnitude and direction of the mean electrical vector (seen on a vectorcardiogram) remains approximately constant as depolarization does not proceed through the LV cavity. These notches are best seen in leads I, aVL, V1, V2, V5, and V6.
ECG during biventricular pacing with the right ventricular lead at the apex. There is a dominant R wave is V1 and a right superior axis in the frontal plane. The QRS complex was relatively more narrow (170 ms) than during single chamber right ventricular or left ventricular pacing
Diagram showing the usual direction of the mean frontal plane axis during apical right ventricular (RV) pacing, RV septal/outflow tract pacing, monochamber left ventricular (LV) pacing from a posterior or posterolateral coronary vein, biventricular (BIV) pacing with LV from a posterior or posterolateral coronary vein + RV from the apex or BIV pacing with LV from a posterior or posterolateral coronary vein + RV from the septal/outflow tract. (1) Monochamber RV pacing. During septal or RV outflow tract (RVOT) pacing the axis may be in the “normal” site in the left inferior quadrant and it moves to the right inferior quadrant (right axis deviation) as the site of stimulation moves more superiorly towards the pulmonary valve. (2) Monochamber LV pacing from the posterior or posterolateral coronary vein. The axis often points to the right inferior quadrant (right axis deviation) and less commonly in the right superior quadrant. (3) Biventricular pacing (LV lead in the posterior or posterolateral coronary vein) with RV apical stimulation. The axis moves superiorly from the left (starting with monochamber RV apical pacing in the left superior quadrant) to the right superior quadrant in an anticlockwise fashion during BIV pacing. This is the commonest axis direction but the axis may less commonly reside in the left superior quadrant and rarely in the other quadrants. (4) Biventricular pacing (from the posterior or posterolateral coronary vein) with RV septal/outflow tract stimulation. The axis is often directed to the right inferior quadrant (right axis deviation). The curved arrow indicates that the axis during septal/RVOT pacing can also reside in the right inferior quadrant; CRT — cardiac resynchronization therapy; RVA — RV apex. (Adapted with permission from: Barold SS, Stroobandt RX, Sinnaeve AF. Cardiac pacemakers and resynchronization step by step. An illustrated guide. Wiley-Blackwell, Hobocken NJ 2010: 324).
Impact of prolonged left ventricular (LV) latency interval on the ECG. The latency interval during LV pacing is shown in Figure 2. The figure compares QRS morphology in 12-lead ECGs during monochamber right ventricular (RV) pacing, monochamber LV pacing and biventricular (BiV) pacing in the VVI mode at 80 ppm. The patient was in atrial fibrillation with complete atrio- -ventricular (AV) block. During BiV pacing there is a left bundle branch pattern that is quite similar to that seen with RV apical pacing. The presence of complete AV block rules out fusion with the spontaneous QRS complex block and cannot be the cause of an absent dominant R wave in lead V1 during BiV pacing. RV and LV voltage outputs were at twice the threshold value. Note the typical pattern of monochamber LV pacing producing a tall R wave in lead V1
Impact of prolonged left ventricular (LV) latency interval on the ECG. The latency interval during LV pacing is shown in Figure 2. The figure compares QRS morphology in 12-lead ECGs during monochamber right ventricular (RV) pacing, monochamber LV pacing and biventricular (BiV) pacing in the VVI mode at 80 ppm. The patient was in atrial fibrillation with complete atrio- -ventricular (AV) block. During BiV pacing there is a left bundle branch pattern that is quite similar to that seen with RV apical pacing. The presence of complete AV block rules out fusion with the spontaneous QRS complex block and cannot be the cause of an absent dominant R wave in lead V1 during BiV pacing. RV and LV voltage outputs were at twice the threshold value. Note the typical pattern of monochamber LV pacing producing a tall R wave in lead V1
QRS difference (ms) between the pre-CRT QRS duration and first biventricular-paced QRS duration. CI confidence interval; CRT cardiac resynchronization therapy; LVEF left ventricular ejection fraction.
Figure 2. ECGs with QRS scoring and short-axis CMR images from 2 patients with LBBB. For the CMR images, the core regions are shown in red and the gray zone in yellow (note that the corresponding 4-chamber long axis view is also shown with the arrow denoting the septal midwall LGE). For comparison with the QRS score, total CMR scar was defined as core+½ gray (see text). The complete LBBB QRS score is shown in the online-only Data Supplement. Patient A has a nonischemic cardiomyopathy with midwall anteroseptal scar comprising 7% of the LV by CMR-LGE and received 5 QRS points (ECG-estimated scar=15%). Note the large R-waves in V1 to V2 that reflect anteroseptal scar. Patient B has an ischemic cardiomyopathy with inferior and posterolateral scar comprising 23% of the LV by CMR-LGE and received 8 QRS points (ECG-estimated scar=24%). Note the large S/S′ ratio in V1 to V2 that reflects posterolateral scar. CMR indicates cardiovascular magnetic resonance; LBBB, left bundle branch block; LGE, late-gadolinium enhancement.
Relation between baseline QRS duration (abscissa) and QRS shortening in response to cardiac resynchronization therapy (ordinate) is depicted. Combinations of baseline QRS duration and QRS shortening values that identify the 75% or 25% probability of restoration of normal left ventricular function in nonischemic patients with cardiomyopathy receiving cardiac resynchronization therapy (dashed rectangles) are displayed.
Hemodynamic response to pacing settings. Only QRS2 method improved on LV dP/dt obtained by default simultaneous biventricular pacing. *Pacing settings with paired p 0.05 compared to default programming of VV of 0 ms. IFDD interventricular fast deflection delay; VTI velocity-time integral; TDIvel peak systolic velocity with tissue Doppler imaging; TDIdisp tissue Doppler imaging displacement method.
