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
Electrocardiograms from a patient who developed a LV conduction delay with a QRS duration of 142 ms that can be classified as LBBB under conventionalcriteria but likely represents progressive LVH. The scatterplot (A) shows QRS duration measurements over time from 42 electrocardiograms from the same patient. Thepatient’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 conductiondelay), review of the serial electrocardiograms shows that QRS morphology did not change as the QRS prolonged. The onset of true complete LBBB shouldresult 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 developmentof intraventricular conduction delay due to hypertrophy rather than the onset of bundle branch block. Although serial electrocardiograms are not alwaysavailable, 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 thediagnosis 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 distinctivemid-QRS notching in leads I and aVL, along with mid-QRS slurring in leads V5 and V6.
QRS morphology in complete LBBB. The LBBB activationsequence and representative QRS-T wave forms are depicted in theiranatomic locations for the sagittal, transverse, and frontal planes. The keyLBBB QRS morphology feature shown is the mid-QRS notching thatoccurs at 50 and 90 ms with slurring in between. The first notch representsthe time when the electrical depolarization wave front reaches the endocardiumof the LV (after proceeding through the septum). The secondnotch occurs when the depolarization wave front begins to reach theepicardium of the posterolateral wall. The reason there is little change inQRS amplitude between the 2 notches is that the magnitude and directionof the mean electrical vector (seen on a vectorcardiogram) remains approximatelyconstant as depolarization does not proceed through the LVcavity. 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 V1and a right superior axis in the frontal plane. The QRS complex was relatively more narrow (170 ms) than during singlechamber 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 posterolateralcoronary vein, biventricular (BIV) pacing with LV from a posterior or posterolateral coronary vein + RV from the apexor 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 theleft inferior quadrant and it moves to the right inferior quadrant (right axis deviation) as the site of stimulation movesmore superiorly towards the pulmonary valve. (2) Monochamber LV pacing from the posterior or posterolateralcoronary vein. The axis often points to the right inferior quadrant (right axis deviation) and less commonly in the rightsuperior quadrant. (3) Biventricular pacing (LV lead in the posterior or posterolateral coronary vein) with RV apicalstimulation. The axis moves superiorly from the left (starting with monochamber RV apical pacing in the left superiorquadrant) to the right superior quadrant in an anticlockwise fashion during BIV pacing. This is the commonest axisdirection 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. Theaxis is often directed to the right inferior quadrant (right axis deviation). The curved arrow indicates that the axisduring 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 andresynchronization step by step. An illustrated guide. Wiley-Blackwell, Hobocken NJ 2010: 324).
Impact of prolonged left ventricular (LV) latencyinterval on the ECG. The latency interval during LVpacing is shown in Figure 2. The figure compares QRSmorphology in 12-lead ECGs during monochamber rightventricular (RV) pacing, monochamber LV pacing andbiventricular (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 leftbundle branch pattern that is quite similar to that seenwith RV apical pacing. The presence of complete AVblock rules out fusion with the spontaneous QRS complexblock and cannot be the cause of an absent dominantR wave in lead V1 during BiV pacing. RV and LVvoltage outputs were at twice the threshold value. Notethe typical pattern of monochamber LV pacing producinga tall R wave in lead V1
QRS difference (ms) between the pre-CRT QRS duration andfirst biventricular-paced QRS duration. CI confidence interval; CRT cardiac resynchronization therapy; LVEF left ventricular ejection fraction.
Relation between baseline QRS duration (abscissa) and QRSshortening in response to cardiac resynchronization therapy (ordinate) isdepicted. Combinations of baseline QRS duration and QRS shorteningvalues that identify the 75% or 25% probability of restoration ofnormal left ventricular function in nonischemic patients with cardiomyopathyreceiving cardiac resynchronization therapy (dashed rectangles) aredisplayed.
Hemodynamic response to pacing settings. Only QRS2 methodimproved on LV dP/dt obtained by default simultaneous biventricularpacing. *Pacing settings with paired p 0.05 compared to default programmingof VV of 0 ms. IFDD interventricular fast deflection delay; VTI velocity-time integral; TDIvel peak systolic velocity with tissue Dopplerimaging; TDIdisp tissue Doppler imaging displacement method.
Qrs and crt final
Valor del ECG pre- y post- resincronización Sergio L. Pinski Cleveland Clinic Florida Weston, FL USA
Valor del QRS en la TRC Antes del implante – Selección de pacientes – Selección del sitio de estimulación? Luego del implante – Confirmación de captura – Predicción de respuesta – Optimización de la programación
Mecanismos de la TRC Disminución de la disincronía mecánica del VI Remodelamiento reverso del VI Optimización del intervalo AV izquierdo Disminución de la insuficiencia mitral Mejoría de la función diastólica del VI
Identificación de los Pacientes conRespuestas Positivas En la mayoría de los estudios, 20-30% de los pacientes no responden clínicamente Selección imperfecta: no hay suficiente asincronía ventricular – El QRS ancho no es necesario ni suficiente para predecir una respuesta positiva – Miocardio no viable Falla de resincronización – Electrodo en posición no ideal – Retardo A-V (o V-V) inadecuado.
Relación entre el ancho del QRSintrínseco y la mejoría con estimulación Kass DA, et al. Circulation 1999;99:1567
Impact of QRS Duration on Clinical Event Reduction With Cardiac ResynchronizationTherapy: Meta-analysis of Randomized Controlled Trials Sipahi et al. Arch Intern Med 2011; 171:1454
QRS duration and morphology in consecutive pts undergoing CRT at Cleveland Clinic Ohio Dupont et al. JACC 2012; 60:592
Significance of QRS morphology in determining theprevalence of mechanical dyssynchrony in heartfailure patients eligible for CRT Haghjoo M et al. Europace 2008;10:566-571
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
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
Oct 9, 2012QRS 172 msOct 16, 2012BiVQRS 114 ms
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
Patients with long LV activation have better outcome with CRT
Morfología del QRS durante la estimulación biventricular Posición del cable del VD Posición del cable en la vena coronaria Presencia de fusión con la conducción intrínseca Retardo V-V (simultáneo versus secuencial). Latencia, bloqueo de salida en la vena coronaria