EDITORIAL
Reappraisal of ECG Lead V1 in the Assessment of Cardiac Resynchronization S. SERGE BAROLD, M.D. From the Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York
The 2012 EHRA/HRS (European Heart Rhythm Association/Heart Rhythm Society) Expert Consensus has stated that “a dominant R wave in V1 is almost invariably present in successful cardiac resynchronization therapy. It follows that a negative paced QRS complex in V1 should prompt full investigation.”1 Many workers have used an R/S > 1 with or without an equiphasic QRS complex (R/S = 1) to define a dominant R wave in lead V1.2–10 A dominant R wave in lead V1 has also been called a right bundle branch block (RBBB), though it is caused by anterior displacement of the QRS forces rather than a right-sided conduction delay.9 Lead V1 provides useful information about the timing between left ventricular (LV) and right ventricular (RV) electrical activity, and it constitutes an integral part of some algorithms for the detection of successful LV capture.3,6,10 Yet, studies focusing on the dominant R wave in V1 during cardiac resynchronization therapy (CRT) have reported an incidence of a dominant R wave in 25–100% for LV leads implanted predominantly in the posterior or posterolateral cardiac veins.2–4,5,7–9,11 Why is the incidence of a dominant R wave in lead V1 so variable? Is the preeminence of lead V1 still justified for the evaluation of CRT given that physiologic or hemodynamic evaluation is more important than electrocardiogram (ECG) manifestations? Incidence of a Dominant R Wave in Lead V1 Sweeney et al.5 analyzed the ECGs of 202 consecutive patients who received CRT devices. The position of the LV lead was not analyzed and biventricular pacing was simultaneous. A dominant R wave in lead V1 was documented in 50% of patients and in lead V2 in 24% of patients. A dominant R wave in these leads was associated with an increased probability of reverse remodeling. The study of Sweeney et al.5 was limited because the site of RV pacing Address for reprints: S. Serge Barold MD; e-mail: ssbarold@ aol.com Received October 9, 2014; revised December 2, 2014; accepted December 2, 2014. doi: 10.1111/pace.12566
was not stated (but presumed to be apical) and there were no ECGs of monochamber LV pacing and other investigations to determine the cause of negative QRS complexes in V1 (50%). Unusual pacing sites and other abnormalities including abnormal LV latency or myocardial disease with delayed conduction around the LV pacing site were not mentioned. The study did not comment on the use of a programmable V-V interval (to bring out a dominant R wave in lead V1) and the presence of ventricular fusion with the spontaneous QRS complex, a situation with triple ventricular activation, which can mask or diminish the paced contribution from the two pacing sites. Refaat et al.9 analyzed the paced ECGs of 54 consecutive patients who received a biventricular device over a period of 2 years. Fifty patients (92.6%) demonstrated an RBBB pattern (R/s > 1) in lead V1. In this group, the position of the LV lead was verified to be in the posterolateral or lateral coronary vein by coronary sinus angiography at the time of implantation and fluoroscopy. There were four patients (7.4%) with a left bundle branch block (LBBB) pattern in lead V1. The LV lead was found in all to be in the middle cardiac vein. Importantly, these four patients exhibited a QS pattern in lead V1 during biventricular pacing. No patients received a device with an interventricular offset. The very high incidence of a dominant R wave in lead V1 (100% of the cases, excluding those placed in the middle cardiac vein) is difficult to explain because some of the patients must have had ventricular fusion with the spontaneous QRS complex, especially in the setting of a short PR interval. Such fusion would have reduced the incidence of a dominant R wave in lead V1. Jastrzebski et al.3 studied a large number of patients with biventricular (BiV) pacing and found a dominant R wave in lead V1 in 33.3% (80/240) patients when all RV sites were included. With BiV and RV apical pacing, a dominant R wave in lead V1 occurred in 48.8% (39/80), which is similar to the early data of Sweeney et al.5 With BiV and RV outflow tract pacing, 22.8% (21/92) of the patients developed a tall R wave in lead V1, while BiV and RV septal pacing produced a tall R wave in lead V1 in 29.4% (20/68) of the patients. The role of fusion with the spontaneous
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rhythm and latency (and interventricular [VV] programmability), which was not considered in the study of Jastrzebski et al., might have been responsible for a relatively low incidence of a dominant R wave in the group with RV apical pacing. Indeed, this limitation was admitted by the authors. The observations confirmed previous anecdotal reports of the lower incidence of a dominant R wave in lead V1 with CRT associated with a nonapical RV pacing. Gani`ere et al.,8 who studied 54 patients to evaluate an algorithm for LV pacing, found a dominant R wave in lead V1 in only 24% of patients. A dominant R wave was observed in nine of 32 patients (28%) with RV apical pacing and in four of 22 (28%) in patients with RV septal pacing (P = 0.52). Cao et al.11 investigated 53 patients (48 with RV apical pacing) with varying degrees of LV and RV prexcitation. They found an R ࣙ 1 in 111 of 422 ECG (26% of ECGs not patients). The duration of the atrioventricular (AV) delay was not stated in the two above studies. We evaluated the ECG presentation of 40 consecutive CRT patients (RV apical pacing) who had all shown long-term improvement.7 Patients with LV leads at sites other than the posterolateral or lateral coronary veins and those with RV anodal stimulation were excluded. We found a dominant R wave in lead V1 in 71% of 40 patients during sequential biventricular pacing (V-V = 0) with the LV leads in the posterior or posterolateral cardiac veins. After V-V optimization, 87% of patients displayed a dominant R wave in lead V1. This figure increased to 93% after adding the patients with fusion with the intrinsic rhythm provided programming to the VVI mode unmasked a dominant R wave. Importance of Fusion with Spontaneous Activity Bogaard et al.2 studied 34 CRT patients using RV apical pacing. The ECGs were recorded at VV delays with LV preactivation of zero, 20 ms, 40 ms, 60 ms, and 80 ms. All the patients presented with posterior forces in leads V1 and V2 at baseline. Only 21–27% of the patients developed dominant anterior forces in leads V1 and V2. The data showed that the incidence of dominant anterior forces in V1 was more frequent during simultaneous LV and RV pacing (VV = 0) than at any value of VV delay (LV preactivation), but lead V2 showed little change with the various LV preactivated VV delays. The workers suggested that their unusual results might have resulted from using an optimal AV delay that was relatively short (approximately 60% of the intrinsic duration). In this setting, delayed delivery of RV pacing in the myocardial refractory
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period could have permitted fusion of LV pacing with spontaneous activity coming down the right bundle branch. Changes in Lead V1 When rS Wave < 1 Sweeney et al.12 recently analyzed the significance of fusion between RV and LV pacing in a larger number patients. Sweeney et al.5 had previously demonstrated in 2010 that a new R wave or an increase in amplitude in leads V1 and V2 is associated with an increased probability of reverse remodeling. In their 2014 study, Sweeney et al.12 identified three types of fusion. Group 1: From the viewpoint of leads V1 and V2: New or an increase in R wave that included a dominant R, an equiphasic complex (R = S), and an rS complex (total number of patients in Group 1 = 267). Cases with a dominant R wave in V1 were not separated. Group 2: QRS normalization with no r wave and a narrow QRS complex (n = 66), and Group 3: Persistent LBBB pattern (n = 42). The end point was ࣙ10% in the LV end-systolic volume at 6 months. One hundred and sixty-six patients (62%) reached the end point and so did 50 patients from group 2 (P = 0.034) and 40% for group 3. LV/RV fusion produced a normally narrow complex in V1 or V2 (without an R wave) in 18% of cases (type 2 fusion). This pattern was associated with the highest incidence of reverse modeling. Thus, in the 2014 study of Sweeney et al.12 reverse LV remodeling was correlated with LV and RV fusion that was associated with changes in lead V1 different from the baseline tracing, but not necessarily showing a dominant R wave. Bogaard et al.,2 who found a low incidence of a dominant R wave in lead V1, evaluated the effect of R-wave amplitude ࣙ50% compared to baseline recordings. In this evaluation, they found an increased positive voltage in lead V1 in 79–91% of cases with an increased frequency associated with a greater degree of LV prexcitation. Gani`ere et al.8 also indicated that an increasing positivity in lead V1 was observed in 89% of their cases and suggested that it represented participation of the LV in the CRT process. This is in contrast to only a 24% incidence of a dominant R in lead V1 and illustrates the importance of subtle changes in lead V1 for the evaluation of LV/RV fusion as suggested by Sweeney et al.12 Negative QRS in Lead V1 There are many causes of a negative lead V1 during CRT and this pattern is more common in association with nonapical RV pacing.3,4,13 It would be unwise to attribute a negative QRS in lead V1 automatically to the participation of nonapical RV pacing without further investigation. A negative
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LEAD V1 IN BIVENTRICULAR PACING
Table I. Causes of a Negative QRS Complex in ECG Lead V1 1. Right ventricular pacing is performed from the outflow tract or the septum 2. Incorrect placement of lead V1 (too high on the chest) 3. Lack of left ventricular capture 4. Left ventricular lead displacement 5. Marked left ventricular latency (exit block) 6. Major intraventricular conduction delay from scarring, infarction, or ischemia 7. Delayed exit from the left ventricular pacing site (without latency) 8. Ventricular fusion with the conducted QRS complex 9. Coronary venous pacing via the middle cardiac vein or the anterior cardiac vein 10. Unintended placement of two leads in the right ventricle 11. Incorrect connections with right ventricular and LV reversal. 12. Note that a QS complex is associated with an LV lead at an anterior site6 ECG = electrocardiogram; LV = left ventricular.
QRS complex in lead V1 still deserves assessment ideally with the previously described three-step protocol (Table I).14 False-Positive Dominant R Wave in Lead V1 A 12-lead ECG should be recorded during RV apical pacing soon after implantation to rule out the presence of a dominant R wave in lead V1 that might mimic successful LV capture during CRT in the presence of LV noncapture.15,16 Such a positive R wave occurs in 10–20% of cases of uncomplicated RV apical pacing.15 In contrast, a dominant R wave in lead V1 is virtually unknown during nonapical RV pacing.3,4 A tracing with a dominant R wave in lead V1 during RV apical pacing should be displayed prominently in the patient’s record and communicated to all involved in the follow-up. Lead V1 versus Leads I and aVL Only two studies have evaluated leads I and aVL together and have compared their results with lead V1 and V2.2,5 Sweeney et al.5 studied 202 patients and found ECG evidence of RV and LV fusion in lead aVL in 29.2% and lead I in 71.3% of their CRT patients compared with a 49.5% dominant R wave in lead V1. The percentage of patients with Q waves in leads I and aVL was not reported. Bogaard et al.2 studied 34 CRT patients and found evidence of RV and LV fusion (judged by a negative QRS complex) in lead I in 71% and
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in lead aVL in 59% compared to a 32% positive QRS complex in lead V1. The disparity of the results involving lead aVL may be due to varying degrees of fusion with the spontaneous rhythm. At this juncture, there is a need for further investigation to determine whether leads I and aVL in combination are superior to lead V1 in the ECG assessment of CRT. Future Directions The significance of lead V1 should be enhanced by recordings during LV and RV preexcitation, but so far there are relatively few reports about this type of manipulation.2,7,11 The usefulness of a dominant R wave in lead V1 should be further compared to the changes in leads I and aVL, which may be superior in the detection of LV capture.2,5 The ECG pattern of biventricular pacing with the LV lead at the apex should be studied because this site is hemodynamically unfavorable.17 More attention should be paid to subtle manifestations of LV/RV fusion in lead V1 as suggested by Sweeney et al.12 in the form of a nondominant R wave with a configuration and amplitude different from the usual negative (posterior) vector of underlying LBBB. An awareness of these various forms of LV/RV fusion is important to determine presence of reverse remodeling as emphasized by Sweeney et al.12 Conclusions The ECG during BiV pacing should be considered as only one of the variables involved in optimizing the hemodynamic response to CRT. In other words, hemodynamic regulation is far more important than the intricacies of the pacing ECG. The presence of a dominant V1 lead remains important in the evaluation of CRT despite a number of reports about its declining frequency, especially in association with nonapical RV pacing. The varied reported frequency of the dominant R wave in lead V1 appears to be due to various grades of fusion with the spontaneous rhythm and/or the increased use of nonapical RV pacing. It could be argued that the ECG pattern in lead V1 is inconsequential, if one has access to a programmer that permits individual programming of LV and RV pacing, thereby providing rapid evaluation of LV pacing. However, excellent performance of single-chamber LV or RV pacing does not always guarantee optimal RV/LV fusion during biventricular pacing. The declining interest of lead V1 may explain why two books published in 2014 each contains only a brief description of a single CRT ECG in terms of RBBB and atypical RBBB, but no further discussion regarding the importance of the R wave in lead
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V1 for the assessment and troubleshooting of CRT.18,19 Lead V1 configuration is a simple test of CRT function that can be particularly useful if a patient is followed away from a pacemaker center. Furthermore, lead V1 remains an integral part of some algorithms seeking failure of LV capture. Such algorithms may also supplement followup away from a pacemaker center. In addition, the QRS pattern in lead V1 is valuable for the teaching of the CRT ECG and the importance of programming optimal LV/RV fusion. All in all, analysis of the experience with lead V1 in this review strongly suggests that the R wave in lead V1
despite its limitations should and will continue to play an important role in the care of CRT patients. The ECGs in this discussion are rarely recorded at the time of implantation. Ideally, an ECG of lead V1 might be useful during biventricular pacing, especially if the RV lead is apical. If the QRS is negative, lead V1 could then be recorded during LV pacing alone to verify the integrity of the LV system. If lead V1 shows a QS pattern during biventricular pacing, the LV lead is anterior at an unsatisfactory site. Further ECG investigations would be performed postoperatively.
References 1. Daubert JC, Saxon L, Adamson PB, Auricchio A, Berger RD, Beshai JF, Breithard O, et al.; European Heart Rhythm Association; European Society of Cardiology; Heart Rhythm Society; Heart Failure Society of America; American Society of Echocardiography; American Heart Association; European Association of Echocardiography; Heart Failure Association. 2012 EHRA/HRS expert consensus statement on cardiac resynchronization therapy in heart failure: Implant and follow-up recommendations and management. Heart Rhythm 2012; 9: 1524–1576. 2. Bogaard MD, Hesselink T, Meine M, Loh P, Hauer RN, Cramer MJ, Doevendans PA, et al. The ECG in cardiac resynchronization therapy: Influence of left and right ventricular preactivation and relation to acute response. J Cardiovasc Electrophysiol 2012; 23:1237–1245. 3. Jastrzebski M, Kukla P, Fijorek K, Czarnecka D. Universal algorithm for diagnosis of biventricular capture in patients with cardiac resynchronization therapy. Pacing Clin Electrophysiol 2014; 37:986–993. 4. .Jastrzebski M, Kukla P, Fijorek K, Sondej T, Czarnecka D. Electrocardiographic diagnosis of biventricular pacing in patients with nonapical right ventricular leads. Pacing Clin Electrophysiol 2012; 35:1199–1208. 5. Sweeney MO, van Bommel RJ, Schalij MJ, Borleffs CJ, Hellkamp AS, Bax JJ. Analysis of ventricular activation using surface electrocardiography to predict left ventricular reverse volumetric remodeling during cardiac resynchronization therapy. Circulation 2010; 121:626–634. 6. Ploux S, Bordachar P, Deplagne A, Mokrani B, Reuter S, Laborderie J, Garrigue S, et al. Electrocardiogram-based algorithm to predict the left ventricular lead position in recipients of cardiac resynchronization systems. Pacing Clin Electrophysiol 2009; 32(Suppl 1):S2–S7. 7. Herweg B, Ali R, Ilercil A, Madramootoo C, Cutro R, Weston MW, Barold SS. Site-specific differences in latency intervals during biventricular pacing: Impact on paced QRS morphology and echooptimized V-V interval. Pacing Clin Electrophysiol 2010; 33: 1382–1391. 8. Gani`ere V, Domenichini G, Niculescu V, Cassagneau R, Defaye P, Burri H. A new electrocardiogram algorithm for diagnosing loss of ventricular capture during cardiac resynchronisation therapy. Europace 2013; 15:376–381.
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9. Refaat M, Mansour M, Singh JP, Ruskin J, Heist EK. Electrocardiographic characteristics in right ventricular vs biventricular pacing in patients with paced right bundle-branch block QRS pattern. J Electrocardiol 2011; 44:289–295. 10. Ammann P, Sticherling C, Kalusche D, Eckstein J, Bernheim A, Schaer B, Osswald S. An electrocardiogram-based algorithm to detect loss of left ventricular capture during cardiac resynchronization therapy. Ann Intern Med 2005; 142(Pt 1):968–973. 11. Cao YY, Su YG, Bai J, Wang W, Wang JF, Qin SM, Ge JB. The roles of the Q (q) wave in lead I and QRS frontal axis for diagnosing loss of left ventricular capture during cardiac resynchronization therapy. J Cardiovasc Electrophysiol 2014 (in press; doi: 10.1111/jce.12527. [Epub ahead of print] PMID: 25112169). 12. Sweeney MO, Hellkamp AS, van Bommel RJ, Schalij MJ, Borleffs CJ, Bax JJ. QRS fusion complex analysis using wave interference to predict reverse remodeling during cardiac resynchronization therapy. Heart Rhythm 2014; 11:806–813. 13. Barold SS, Herweg B. Usefulness of the 12-lead electrocardiogram in the follow-up of patients with cardiac resynchronization devices. Part I. Cardiol J 2011; 18:476–486. 14. Herweg B, Barold SS. Three-step electrocardiographic evaluation of cardiac resynchronization. Pacing Clin Electrophysiol 2012; 35:249–252. 15. Barold SS, Giudici MC, Herweg B. Reappraisal of the electrographic manifestations of right ventricular apical pacing. J Electrocardiol 2012; 45:373–375. 16. Cooper JM, Patel RK, Emmi A, Wang Y, Kirkpatrick JN. RV-only pacing can produce a Q wave in lead 1 and an R wave in V1: Implications for biventricular pacing. Pacing Clin Electrophysiol 2014; 37:585–590. 17. Singh JP, Klein HU, Huang DT, Reek S, Kuniss M, Quesada A, Barsheshet A. Left ventricular lead position and clinical outcome in the multicenter automatic defibrillator implantation trial-cardiac resynchronization therapy (MADIT-CRT) trial. Circulation 2011; 123:1159–1166. 18. Cha YM. Cardiac resynchronization therapy. In: Ellenbogen KA, Kaszala K (eds.): Cardiac Pacing and ICDs, 6th Ed. Hoboken, NJ, Wiley-Blackwell, 2014, pp. 374–412. 19. Gard JJ, Asirvatham SJ. Right ventricular pacing-related cardiomyopathy. In: Yu CM, Hayes DL, Auricchio A (eds.): Cases in Cardiac Resynchronization Therapy. Philadelphia, PA, Elsevier, Saunders, 2014, pp. 65–69.
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Reappraisal of ECG Lead V1 in the Assessment of Cardiac Resynchronization S. SERGE BAROLD, M.D. From the Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York
The 2012 EHRA/HRS (European Heart Rhythm Association/Heart Rhythm Society) Expert Consensus has stated that “a dominant R wave in V1 is almost invariably present in successful cardiac resynchronization therapy. It follows that a negative paced QRS complex in V1 should prompt full investigation.”1 Many workers have used an R/S > 1 with or without an equiphasic QRS complex (R/S = 1) to define a dominant R wave in lead V1.2–10 A dominant R wave in lead V1 has also been called a right bundle branch block (RBBB), though it is caused by anterior displacement of the QRS forces rather than a right-sided conduction delay.9 Lead V1 provides useful information about the timing between left ventricular (LV) and right ventricular (RV) electrical activity, and it constitutes an integral part of some algorithms for the detection of successful LV capture.3,6,10 Yet, studies focusing on the dominant R wave in V1 during cardiac resynchronization therapy (CRT) have reported an incidence of a dominant R wave in 25–100% for LV leads implanted predominantly in the posterior or posterolateral cardiac veins.2–4,5,7–9,11 Why is the incidence of a dominant R wave in lead V1 so variable? Is the preeminence of lead V1 still justified for the evaluation of CRT given that physiologic or hemodynamic evaluation is more important than electrocardiogram (ECG) manifestations? Incidence of a Dominant R Wave in Lead V1 Sweeney et al.5 analyzed the ECGs of 202 consecutive patients who received CRT devices. The position of the LV lead was not analyzed and biventricular pacing was simultaneous. A dominant R wave in lead V1 was documented in 50% of patients and in lead V2 in 24% of patients. A dominant R wave in these leads was associated with an increased probability of reverse remodeling. The study of Sweeney et al.5 was limited because the site of RV pacing Address for reprints: S. Serge Barold MD; e-mail: ssbarold@ aol.com Received October 9, 2014; revised December 2, 2014; accepted December 2, 2014. doi: 10.1111/pace.12566
was not stated (but presumed to be apical) and there were no ECGs of monochamber LV pacing and other investigations to determine the cause of negative QRS complexes in V1 (50%). Unusual pacing sites and other abnormalities including abnormal LV latency or myocardial disease with delayed conduction around the LV pacing site were not mentioned. The study did not comment on the use of a programmable V-V interval (to bring out a dominant R wave in lead V1) and the presence of ventricular fusion with the spontaneous QRS complex, a situation with triple ventricular activation, which can mask or diminish the paced contribution from the two pacing sites. Refaat et al.9 analyzed the paced ECGs of 54 consecutive patients who received a biventricular device over a period of 2 years. Fifty patients (92.6%) demonstrated an RBBB pattern (R/s > 1) in lead V1. In this group, the position of the LV lead was verified to be in the posterolateral or lateral coronary vein by coronary sinus angiography at the time of implantation and fluoroscopy. There were four patients (7.4%) with a left bundle branch block (LBBB) pattern in lead V1. The LV lead was found in all to be in the middle cardiac vein. Importantly, these four patients exhibited a QS pattern in lead V1 during biventricular pacing. No patients received a device with an interventricular offset. The very high incidence of a dominant R wave in lead V1 (100% of the cases, excluding those placed in the middle cardiac vein) is difficult to explain because some of the patients must have had ventricular fusion with the spontaneous QRS complex, especially in the setting of a short PR interval. Such fusion would have reduced the incidence of a dominant R wave in lead V1. Jastrzebski et al.3 studied a large number of patients with biventricular (BiV) pacing and found a dominant R wave in lead V1 in 33.3% (80/240) patients when all RV sites were included. With BiV and RV apical pacing, a dominant R wave in lead V1 occurred in 48.8% (39/80), which is similar to the early data of Sweeney et al.5 With BiV and RV outflow tract pacing, 22.8% (21/92) of the patients developed a tall R wave in lead V1, while BiV and RV septal pacing produced a tall R wave in lead V1 in 29.4% (20/68) of the patients. The role of fusion with the spontaneous
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rhythm and latency (and interventricular [VV] programmability), which was not considered in the study of Jastrzebski et al., might have been responsible for a relatively low incidence of a dominant R wave in the group with RV apical pacing. Indeed, this limitation was admitted by the authors. The observations confirmed previous anecdotal reports of the lower incidence of a dominant R wave in lead V1 with CRT associated with a nonapical RV pacing. Gani`ere et al.,8 who studied 54 patients to evaluate an algorithm for LV pacing, found a dominant R wave in lead V1 in only 24% of patients. A dominant R wave was observed in nine of 32 patients (28%) with RV apical pacing and in four of 22 (28%) in patients with RV septal pacing (P = 0.52). Cao et al.11 investigated 53 patients (48 with RV apical pacing) with varying degrees of LV and RV prexcitation. They found an R ࣙ 1 in 111 of 422 ECG (26% of ECGs not patients). The duration of the atrioventricular (AV) delay was not stated in the two above studies. We evaluated the ECG presentation of 40 consecutive CRT patients (RV apical pacing) who had all shown long-term improvement.7 Patients with LV leads at sites other than the posterolateral or lateral coronary veins and those with RV anodal stimulation were excluded. We found a dominant R wave in lead V1 in 71% of 40 patients during sequential biventricular pacing (V-V = 0) with the LV leads in the posterior or posterolateral cardiac veins. After V-V optimization, 87% of patients displayed a dominant R wave in lead V1. This figure increased to 93% after adding the patients with fusion with the intrinsic rhythm provided programming to the VVI mode unmasked a dominant R wave. Importance of Fusion with Spontaneous Activity Bogaard et al.2 studied 34 CRT patients using RV apical pacing. The ECGs were recorded at VV delays with LV preactivation of zero, 20 ms, 40 ms, 60 ms, and 80 ms. All the patients presented with posterior forces in leads V1 and V2 at baseline. Only 21–27% of the patients developed dominant anterior forces in leads V1 and V2. The data showed that the incidence of dominant anterior forces in V1 was more frequent during simultaneous LV and RV pacing (VV = 0) than at any value of VV delay (LV preactivation), but lead V2 showed little change with the various LV preactivated VV delays. The workers suggested that their unusual results might have resulted from using an optimal AV delay that was relatively short (approximately 60% of the intrinsic duration). In this setting, delayed delivery of RV pacing in the myocardial refractory
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period could have permitted fusion of LV pacing with spontaneous activity coming down the right bundle branch. Changes in Lead V1 When rS Wave < 1 Sweeney et al.12 recently analyzed the significance of fusion between RV and LV pacing in a larger number patients. Sweeney et al.5 had previously demonstrated in 2010 that a new R wave or an increase in amplitude in leads V1 and V2 is associated with an increased probability of reverse remodeling. In their 2014 study, Sweeney et al.12 identified three types of fusion. Group 1: From the viewpoint of leads V1 and V2: New or an increase in R wave that included a dominant R, an equiphasic complex (R = S), and an rS complex (total number of patients in Group 1 = 267). Cases with a dominant R wave in V1 were not separated. Group 2: QRS normalization with no r wave and a narrow QRS complex (n = 66), and Group 3: Persistent LBBB pattern (n = 42). The end point was ࣙ10% in the LV end-systolic volume at 6 months. One hundred and sixty-six patients (62%) reached the end point and so did 50 patients from group 2 (P = 0.034) and 40% for group 3. LV/RV fusion produced a normally narrow complex in V1 or V2 (without an R wave) in 18% of cases (type 2 fusion). This pattern was associated with the highest incidence of reverse modeling. Thus, in the 2014 study of Sweeney et al.12 reverse LV remodeling was correlated with LV and RV fusion that was associated with changes in lead V1 different from the baseline tracing, but not necessarily showing a dominant R wave. Bogaard et al.,2 who found a low incidence of a dominant R wave in lead V1, evaluated the effect of R-wave amplitude ࣙ50% compared to baseline recordings. In this evaluation, they found an increased positive voltage in lead V1 in 79–91% of cases with an increased frequency associated with a greater degree of LV prexcitation. Gani`ere et al.8 also indicated that an increasing positivity in lead V1 was observed in 89% of their cases and suggested that it represented participation of the LV in the CRT process. This is in contrast to only a 24% incidence of a dominant R in lead V1 and illustrates the importance of subtle changes in lead V1 for the evaluation of LV/RV fusion as suggested by Sweeney et al.12 Negative QRS in Lead V1 There are many causes of a negative lead V1 during CRT and this pattern is more common in association with nonapical RV pacing.3,4,13 It would be unwise to attribute a negative QRS in lead V1 automatically to the participation of nonapical RV pacing without further investigation. A negative
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LEAD V1 IN BIVENTRICULAR PACING
Table I. Causes of a Negative QRS Complex in ECG Lead V1 1. Right ventricular pacing is performed from the outflow tract or the septum 2. Incorrect placement of lead V1 (too high on the chest) 3. Lack of left ventricular capture 4. Left ventricular lead displacement 5. Marked left ventricular latency (exit block) 6. Major intraventricular conduction delay from scarring, infarction, or ischemia 7. Delayed exit from the left ventricular pacing site (without latency) 8. Ventricular fusion with the conducted QRS complex 9. Coronary venous pacing via the middle cardiac vein or the anterior cardiac vein 10. Unintended placement of two leads in the right ventricle 11. Incorrect connections with right ventricular and LV reversal. 12. Note that a QS complex is associated with an LV lead at an anterior site6 ECG = electrocardiogram; LV = left ventricular.
QRS complex in lead V1 still deserves assessment ideally with the previously described three-step protocol (Table I).14 False-Positive Dominant R Wave in Lead V1 A 12-lead ECG should be recorded during RV apical pacing soon after implantation to rule out the presence of a dominant R wave in lead V1 that might mimic successful LV capture during CRT in the presence of LV noncapture.15,16 Such a positive R wave occurs in 10–20% of cases of uncomplicated RV apical pacing.15 In contrast, a dominant R wave in lead V1 is virtually unknown during nonapical RV pacing.3,4 A tracing with a dominant R wave in lead V1 during RV apical pacing should be displayed prominently in the patient’s record and communicated to all involved in the follow-up. Lead V1 versus Leads I and aVL Only two studies have evaluated leads I and aVL together and have compared their results with lead V1 and V2.2,5 Sweeney et al.5 studied 202 patients and found ECG evidence of RV and LV fusion in lead aVL in 29.2% and lead I in 71.3% of their CRT patients compared with a 49.5% dominant R wave in lead V1. The percentage of patients with Q waves in leads I and aVL was not reported. Bogaard et al.2 studied 34 CRT patients and found evidence of RV and LV fusion (judged by a negative QRS complex) in lead I in 71% and
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in lead aVL in 59% compared to a 32% positive QRS complex in lead V1. The disparity of the results involving lead aVL may be due to varying degrees of fusion with the spontaneous rhythm. At this juncture, there is a need for further investigation to determine whether leads I and aVL in combination are superior to lead V1 in the ECG assessment of CRT. Future Directions The significance of lead V1 should be enhanced by recordings during LV and RV preexcitation, but so far there are relatively few reports about this type of manipulation.2,7,11 The usefulness of a dominant R wave in lead V1 should be further compared to the changes in leads I and aVL, which may be superior in the detection of LV capture.2,5 The ECG pattern of biventricular pacing with the LV lead at the apex should be studied because this site is hemodynamically unfavorable.17 More attention should be paid to subtle manifestations of LV/RV fusion in lead V1 as suggested by Sweeney et al.12 in the form of a nondominant R wave with a configuration and amplitude different from the usual negative (posterior) vector of underlying LBBB. An awareness of these various forms of LV/RV fusion is important to determine presence of reverse remodeling as emphasized by Sweeney et al.12 Conclusions The ECG during BiV pacing should be considered as only one of the variables involved in optimizing the hemodynamic response to CRT. In other words, hemodynamic regulation is far more important than the intricacies of the pacing ECG. The presence of a dominant V1 lead remains important in the evaluation of CRT despite a number of reports about its declining frequency, especially in association with nonapical RV pacing. The varied reported frequency of the dominant R wave in lead V1 appears to be due to various grades of fusion with the spontaneous rhythm and/or the increased use of nonapical RV pacing. It could be argued that the ECG pattern in lead V1 is inconsequential, if one has access to a programmer that permits individual programming of LV and RV pacing, thereby providing rapid evaluation of LV pacing. However, excellent performance of single-chamber LV or RV pacing does not always guarantee optimal RV/LV fusion during biventricular pacing. The declining interest of lead V1 may explain why two books published in 2014 each contains only a brief description of a single CRT ECG in terms of RBBB and atypical RBBB, but no further discussion regarding the importance of the R wave in lead
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V1 for the assessment and troubleshooting of CRT.18,19 Lead V1 configuration is a simple test of CRT function that can be particularly useful if a patient is followed away from a pacemaker center. Furthermore, lead V1 remains an integral part of some algorithms seeking failure of LV capture. Such algorithms may also supplement followup away from a pacemaker center. In addition, the QRS pattern in lead V1 is valuable for the teaching of the CRT ECG and the importance of programming optimal LV/RV fusion. All in all, analysis of the experience with lead V1 in this review strongly suggests that the R wave in lead V1
despite its limitations should and will continue to play an important role in the care of CRT patients. The ECGs in this discussion are rarely recorded at the time of implantation. Ideally, an ECG of lead V1 might be useful during biventricular pacing, especially if the RV lead is apical. If the QRS is negative, lead V1 could then be recorded during LV pacing alone to verify the integrity of the LV system. If lead V1 shows a QS pattern during biventricular pacing, the LV lead is anterior at an unsatisfactory site. Further ECG investigations would be performed postoperatively.
References 1. Daubert JC, Saxon L, Adamson PB, Auricchio A, Berger RD, Beshai JF, Breithard O, et al.; European Heart Rhythm Association; European Society of Cardiology; Heart Rhythm Society; Heart Failure Society of America; American Society of Echocardiography; American Heart Association; European Association of Echocardiography; Heart Failure Association. 2012 EHRA/HRS expert consensus statement on cardiac resynchronization therapy in heart failure: Implant and follow-up recommendations and management. Heart Rhythm 2012; 9: 1524–1576. 2. Bogaard MD, Hesselink T, Meine M, Loh P, Hauer RN, Cramer MJ, Doevendans PA, et al. The ECG in cardiac resynchronization therapy: Influence of left and right ventricular preactivation and relation to acute response. J Cardiovasc Electrophysiol 2012; 23:1237–1245. 3. Jastrzebski M, Kukla P, Fijorek K, Czarnecka D. Universal algorithm for diagnosis of biventricular capture in patients with cardiac resynchronization therapy. Pacing Clin Electrophysiol 2014; 37:986–993. 4. .Jastrzebski M, Kukla P, Fijorek K, Sondej T, Czarnecka D. Electrocardiographic diagnosis of biventricular pacing in patients with nonapical right ventricular leads. Pacing Clin Electrophysiol 2012; 35:1199–1208. 5. Sweeney MO, van Bommel RJ, Schalij MJ, Borleffs CJ, Hellkamp AS, Bax JJ. Analysis of ventricular activation using surface electrocardiography to predict left ventricular reverse volumetric remodeling during cardiac resynchronization therapy. Circulation 2010; 121:626–634. 6. Ploux S, Bordachar P, Deplagne A, Mokrani B, Reuter S, Laborderie J, Garrigue S, et al. Electrocardiogram-based algorithm to predict the left ventricular lead position in recipients of cardiac resynchronization systems. Pacing Clin Electrophysiol 2009; 32(Suppl 1):S2–S7. 7. Herweg B, Ali R, Ilercil A, Madramootoo C, Cutro R, Weston MW, Barold SS. Site-specific differences in latency intervals during biventricular pacing: Impact on paced QRS morphology and echooptimized V-V interval. Pacing Clin Electrophysiol 2010; 33: 1382–1391. 8. Gani`ere V, Domenichini G, Niculescu V, Cassagneau R, Defaye P, Burri H. A new electrocardiogram algorithm for diagnosing loss of ventricular capture during cardiac resynchronisation therapy. Europace 2013; 15:376–381.
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9. Refaat M, Mansour M, Singh JP, Ruskin J, Heist EK. Electrocardiographic characteristics in right ventricular vs biventricular pacing in patients with paced right bundle-branch block QRS pattern. J Electrocardiol 2011; 44:289–295. 10. Ammann P, Sticherling C, Kalusche D, Eckstein J, Bernheim A, Schaer B, Osswald S. An electrocardiogram-based algorithm to detect loss of left ventricular capture during cardiac resynchronization therapy. Ann Intern Med 2005; 142(Pt 1):968–973. 11. Cao YY, Su YG, Bai J, Wang W, Wang JF, Qin SM, Ge JB. The roles of the Q (q) wave in lead I and QRS frontal axis for diagnosing loss of left ventricular capture during cardiac resynchronization therapy. J Cardiovasc Electrophysiol 2014 (in press; doi: 10.1111/jce.12527. [Epub ahead of print] PMID: 25112169). 12. Sweeney MO, Hellkamp AS, van Bommel RJ, Schalij MJ, Borleffs CJ, Bax JJ. QRS fusion complex analysis using wave interference to predict reverse remodeling during cardiac resynchronization therapy. Heart Rhythm 2014; 11:806–813. 13. Barold SS, Herweg B. Usefulness of the 12-lead electrocardiogram in the follow-up of patients with cardiac resynchronization devices. Part I. Cardiol J 2011; 18:476–486. 14. Herweg B, Barold SS. Three-step electrocardiographic evaluation of cardiac resynchronization. Pacing Clin Electrophysiol 2012; 35:249–252. 15. Barold SS, Giudici MC, Herweg B. Reappraisal of the electrographic manifestations of right ventricular apical pacing. J Electrocardiol 2012; 45:373–375. 16. Cooper JM, Patel RK, Emmi A, Wang Y, Kirkpatrick JN. RV-only pacing can produce a Q wave in lead 1 and an R wave in V1: Implications for biventricular pacing. Pacing Clin Electrophysiol 2014; 37:585–590. 17. Singh JP, Klein HU, Huang DT, Reek S, Kuniss M, Quesada A, Barsheshet A. Left ventricular lead position and clinical outcome in the multicenter automatic defibrillator implantation trial-cardiac resynchronization therapy (MADIT-CRT) trial. Circulation 2011; 123:1159–1166. 18. Cha YM. Cardiac resynchronization therapy. In: Ellenbogen KA, Kaszala K (eds.): Cardiac Pacing and ICDs, 6th Ed. Hoboken, NJ, Wiley-Blackwell, 2014, pp. 374–412. 19. Gard JJ, Asirvatham SJ. Right ventricular pacing-related cardiomyopathy. In: Yu CM, Hayes DL, Auricchio A (eds.): Cases in Cardiac Resynchronization Therapy. Philadelphia, PA, Elsevier, Saunders, 2014, pp. 65–69.
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