High Incidence of Dilated Cardiomyopathy After Right Ventricular Inlet Pacing in Patients With Congenital Complete Atrioventricular Block

Abstract

Background: Some patients with congenital complete atrioventricular block (CCAVB) develop dilated cardiomyopathy (DCM) after pacemaker implantation (PMI). We evaluated the relationship between pacing site and DCM incidence.

Methods and Results: We retrospectively evaluated 38 patients with CCAVB; 8 (25%) of 32 patients who had PMI developed DCM/heart failure death (HFD) after PMI, although none of the 6 patients without PMI showed DCM/HFD. All DCM/HFD occurred within 50 months of PMI. Among the 32 patients with PMI, the DCM/HFD incidence was 55% (6/11) for right ventricular inlet (RVI), 18% (2/11) for RV apex (RVA), and 0% for left ventricle (LV) (P=0.013). At the endpoint, the LV ejection fraction and septal-to-posterior wall motion delay of patients with LV pacing were better than those for patients with other pacing sites. Among the 8 DCM/HFD patients, 2 in whom the pacing site was changed from RVI to LV apex or in whom therapy was upgraded to cardiac resynchronization remained alive with no heart failure symptoms, whereas the other 6 died of heart failure.

Conclusions: A total of 25% of the patients who underwent PMI because of CCAVB, but none in the non-PMI group, developed DCM/HFD. DCM/HFD incidence was higher in patients with RVI pacing. Ventricular dyssynchrony related to pacing site may be one cause of DCM in patients with CCAVB. (Circ J 2016; 80: 1251–1258)

Congenital complete atrioventricular block (CCAVB) without intracardiac structural abnormalities is a relatively rare disease that occurs in 1/20,000 live births.¹ It is associated with maternal autoimmune disorders, such as systemic lupus erythematosus and Sjögren’s syndrome. The SS-A/Ro and SS-B/La antibodies are considered to cause CCAVB by inducing injury, fibrosis, and scarring of the fetal cardiac conduction system.^2–4 The prognosis for children with CCAVB after pacemaker implantation (PMI) has been considered to be benign; however, some develop dilated cardiomyopathy (DCM), with a reported prevalence of 5–30%,^4–10 mostly within 1 year of PMI.^2,9

Editorial p 1110

The site of ventricular pacing has an effect on the mechanical synchrony and pump function of the left ventricle (LV) in animals and children.^11–15 Janousek et al¹¹ reported on the effect of permanent pacing on the mechanical synchrony, efficiency, and pump function of the LV in 178 children (age <18 years) with atrioventricular block and a structurally normal heart.¹¹ However, the direct relationship between ventricular pacing sites and DCM incidence in patients with CCAVB is uncertain.

In this study, we aimed to evaluate and assess (1) the DCM and/or heart failure death (HFD) incidence with or without PMI, (2) the relationship of ventricular pacing site with DCM/HFD incidence, (3) the effect on LV function of the pacemaker and pacing sites, and (4) the clinical course of patients who developed DCM/HFD.

Methods

Patients

A total of 38 patients (18 male, 20 female) with CCAVB followed up at National Cerebral and Cardiovascular Center, Osaka, Japan, from October 1978 to June 2015 were retrospectively evaluated. They had no structural anomalies of the heart, except for a small patent ductus arteriosus and mild pulmonary artery stenosis. The endpoints were determined as the onset of DCM/HFD, the day of changing the pacing lead, the day of final medical consultation owing to hospital transfer, and the last medical consultation until June 2015. We assert that all procedures contributing to this work complied with the ethical standards of the relevant national guidelines on human experimentation (Japan) and with the Helsinki Declaration of 1975 (as revised in 2008) and were approved by the institutional ethics committees.

Clinical Measurements

We first compared the clinical parameters in the DCM/HFD, non-DCM/HFD, and non-PMI groups and then compared the same clinical parameters in 3 groups divided according to pacing site and the non-PMI group.

DCM was defined as the presence of LV dilatation and LV systolic dysfunction in the absence of abnormal loading conditions, such as hypertension and valvular disease, or coronary artery disease sufficient to cause global systolic impairment.^16,17 We used the criteria of Manolio et al¹⁸ for DCM diagnosis and defined DCM as having 117% of the normal LV end-diastolic diameter (LVDd) and less than 45% of the LV ejection fraction (LVEF), as measured by transthoracic echocardiography (TTE). We did not use B-type natriuretic peptide (BNP) values for the definition of DCM because BNP levels would be elevated by inappropriate bradycardia without DCM and the normal range of BNP is higher in the neonatal period than in older ages.¹⁹

We checked the cardiothoracic ratio (CTR) on chest radiographs, BNP levels, QRS duration (QRSd) on 12-lead ECG, LVDd, LVEF, and septal-to-posterior wall motion delay (SPWMD) by TTE as parameters of cardiac function immediately before PMI, within 1 year of PMI, and at the endpoint. QRSd was measured manually as the maximum value in any lead with a sweep speed of 25 mm/s. LVDd, LVEF, and SPWMD were measured from the parasternal short-axis M-mode. We adopted the normal value of LVDd established by Kampmann et al.²⁰ SPWMD was measured as the time interval between the peak systolic septal wall motion and LV posterior wall motion and/or thickening.²¹

Pacing Sites

We assessed pacing sites from biplane chest radiographs, ventriculography, and 12-lead ECGs at the endpoint, with assessment becoming easier as the patient’s age increased. A leftward QRS axis together with left bundle branch block morphology was designated as right ventricle (RV) lateral wall. RV and LV apical pacing were characterized by superior axis and left and right bundle branch block morphology, respectively, in lead I. A rightward QRS axis together with right bundle branch block morphology was designated as the LV lateral wall or LV base.¹¹ The pacing sites were classified into 6 segments of RV and 17 segments of LV. To delineate the RV segments, a line was drawn from the membranous septum to the apex to divide the septum into anterior and inferior halves; further subdividing the base to apex length into 3 parts (basal, middle, and apical) provided 6 segments. The inferior basal and middle segments corresponded to the RV inlet (RVI), whereas the 2 apical segments plus the anterior middle segment matched the RV apex (RVA). The remaining anterobasal segment corresponded to the RV outflow tract (RVOT).^22,23 We used the 17 segments of the LV advocated by the American Heart Association.²⁴

Statistical Analysis

The values are presented as median (range). Differences between groups were compared by Wilcoxon rank-sum test. For categorical variables, the χ² test or Fisher’s exact test was applied. Multiple comparisons among different patient groups were performed by Kruskal-Wallis one-way analysis of variance. Kaplan-Meier product limit estimates were used to plot survival and freedom from DCM/HFD. Two-sided tests were used for all analyses. All statistical analyses were done with JMP^® version 10 (SAS Institute Inc, Cary, NC, USA). Significance was accepted at P<0.05.

Results

Patients Characteristics

Patient characteristics are shown in Table 1 : 32 patients (84.2%) had PMI, while 6 patients with CCAVB did not have PMI until their endpoints. There were no significant differences in patient characteristics between the PMI and non-PMI groups. In the PMI group, 8 patients (25.0%) developed DCM/HFD after PMI during the observation period of 69.6 months (0.0–272.3 months) after PMI, whereas no patient developed DCM/HFD in the non-PMI group.

Table 1. Characteristics of Patients With Congenital Complete Atrioventricular Block and Their Clinical Measurements

	n	Total	PMI				n	Non-PMI	P value
			n	DCM/HFD	n	Non-DCM
n		38		8 (25%)		24 (75%)		6
Age at the end of follow-up (years)	38	6.8 (0.0–33.9)	8	2.4 (0.0–8.0)	24	8.6 (3.5–33.9)***	6	12.0 (0.7–25.8)*	0.001
Sex (M:F)	38	18:20	8	7:1	24	10:14***	6	1:5*	0.021
Maternal autoantibodies	28	18 (64%)	7	4 (57%)	16	9 (56%)	5	5 (100%)	NS
Fetal bradycardia	37	35 (95%)	8	8 (100%)	24	22 (92%)	5	5 (100%)	NS
Gestational age at diagnosis of bradycardia (weeks)	26	28 (20–38)	6	29 (21–35)	17	29 (20–38)	3	22 (20–23)	NS
Fetal hydrops	38	2 (5.3%)	8	0 (0%)	24	2 (8.3%)	6	0 (0%)	NS
Gestational age on delivery (weeks)	37	38 (28–41)	8	37 (34–39)	24	38 (28–41)	5	38 (37–38)	NS
Own ventricular rate (beats/min)	37	49 (35–75)	8	52 (45–75)	23	50 (35–73)
Own atrial rate (beats/min)	36	130 (55–187)	8	147 (97–187)	22	131 (70–170)
Age at PMI (days)	32	10 (0–4,478)	8	3 (1–2,799)	24	39 (0–4,478)
Observation period from PMI (months)	32	69.3 (0.0–272.3)	8	17.0 (0.0–48.3)	24	81.8 (20.6–272.3)***
Pacing site (RVI:RVA:LV)	32	11:11:10	8	6:2:0	24	5:9:10***
Proportion of dual chamber pacing (DDD/VDD)	32	11 (34%)	8	3 (38%)	24	8 (33%)
Lower ventricular pacing rate	32	110 (60–130)	8	120 (80–120)	24	105 (60–130)
Ventricular lead approach (epicardial vs. endocardial)	32	30:2	8	8:0	24	22:2
Ventricular lead polarity (unipolar vs. bipolar)	32	13:19	8	3:5	24	10:14

*P<0.05 vs. DCM/HFD, **P<0.05 vs. non-DCM, ***P<0.05 vs. DCM/HFD. DCM, dilated cardiomyopathy; HFD, heart failure death; LV, left ventricle; NS, not significant; PMI, pacemaker implantation; RVA, right ventricular apex; RVI, right ventricular inlet.

In the comparisons between the DCM/HFD and non-DCM groups, there were no significant differences in patient characteristics before PMI, except for sex ratio, age at the end of follow-up, and observation period from PMI [17.0 (0.0–48.3) vs. 81.8 (20.6–272.3) months, P=0.001]. Among the variables after PMI, there were statistical differences in pacing site between the DCM/HFD and non-DCM groups, whereas there were no differences in age of PMI, ventricular pacing rate, pacing lead approach, or ventricular lead polarity. In total, 23 patients (71.9%) had their initial PMI within 1 year, and most patients required ventricular pacing during the neonatal period (Figure 1). Fetal hydrops was found only in the DCM/HFD group, and no endocardial-fibroelastosis was found in any patient.

Figure 1.

Proportion of CCAVB patients who developed DCM, based on age at the time of PMI: 23 patients (71.9%) had initial PMI at ≤1 year of age. CCAVB, congenital complete atrioventricular block; DCM, dilated cardiomyopathy; PMI, pacemaker implantation; HFD, heart failure death.

Pacing Sites and Development of DCM

Pacing sites are shown in Figure 2. The initial PMI was done using an endocardial approach (n=2), epicardial approach with lateral thoracotomy (n=1), or epicardial approach with median sternotomy (n=29); 13 unipolar and 19 bipolar leads were used for the ventricular leads. The pacing site was RVI in 11 patients (34.4%), RVA in 11 patients (34.4%), and LV in 10 patients (31.3%). There was a DCM/HFD incidence of 55% (6/11) with RVI pacing, 18% (2/11) with RVA pacing, and 0% (0/10) (P=0.013) with LV pacing. Patients characteristics stratified according to pacing site are shown in Table 2. Except for the patients’ own ventricular and atrial rates, there were no significant differences in their characteristics before PMI among the 3 groups.

Figure 2.

Pacing sites in patients with congenital complete atrioventricular bloc: RVI in 11 patients (34.4%), RVA in 11 patients (34.4%), and LV in 10 patients (31.3%). The pacing sites in the DCM/HFD group (purple dots) were at the RVI in 6 patients (75%) and at the RVA in 2 patients (25%). No patient was paced at the LV in the DCM/HFD group. The pacing sites in the non-DCM group are shown as orange dots. DCM, dilated cardiomyopathy; HFD, heart failure death; LV, left ventricle; RV, right ventricle; RVA, RV apex; RVI, RV inlet; RVOT, RV outflow tract.

Table 2. Characteristics of Patients With Congenital Complete Atrioventricular Block and Their Clinical Measurements According to Pacing Site

	n	RVI	n	RVA	n	LV	P value
n		11 (34%)		11 (34%)		10 (31%)
Age at the end of follow-up (years)	11	4.0 (0.0–16.5)	11	6.6 (2.3–33.9)	10	9.9 (3.5–26.1)**	NS
Sex (M:F)	11	9:2	11	4:7***	10	4:6**	NS
Maternal autoantibodies	8	4 (50%)	8	4 (50%)	7	5 (71%)	NS
Fetal bradycardia	11	11 (100%)	11	10 (91%)	10	9 (90%)	NS
Gestational age at diagnosis of bradycardia (weeks)	11	30 (20–35)	9	29 (21–34)	6	23 (22–38)	NS
Fetal hydrops	11	1 (9%)	11	0 (0%)	10	1 (10%)	NS
Gestational age on delivery (weeks)	11	37 (32–39)	11	38 (28–39)	10	37 (32–41)	NS
Own ventricular rate (beats/min)	11	55 (45–75)	11	45 (40–73)	9	40 (35–71)**	NS
Own atrial rate (beats/min)	10	147 (95–187)	11	115 (70–150)***	9	155 (97–170)*	0.015
Age of PMI (days)	11	4 (1–114)	11	9 (0–4,478)***	10	81 (0–2,245)**	NS
Observation period from PMI (months)	11	48.3 (0.0–198.0)	11	65.2 (3.6–272.3)	10	103.3 (42.0–249.6)	NS
Proportion of dual chamber pacing (DDD/VDD)	11	4 (36%)	11	4 (36%)	10	3 (30%)	NS
Lower ventricular pacing rate	11	120 (90–130)	11	110 (70–120)***	10	120 (90–120)	NS
Ventricular lead approach (epicardial vs. endocardial)	11	11:0	11	9:2	10	10:0	NS
Ventricular lead polarity (unipolar vs. bipolar)	11	5:6	11	3:8	10	5:5	NS

*P<0.05 vs. RVI, **P<0.05 vs. RVA, ***P<0.05 vs. RVI. Abbreviations as in Table 1.

The Kaplan-Meier survival curve against DCM/HFD after PMI is shown in Figure 3. Kaplan-Meier product limit estimates were used to plot survival and freedom from DCM/HFD, and the survival rates at 50 months were compared. No patient developed DCM or died after 50 months of PMI. The cumulative probability of avoidable DCM/HFD and survival at 50 months was 100% with LV pacing, 80.8% with RVA pacing, and 45.5% with RVI pacing (P=0.02).

Figure 3.

Kaplan-Meier survival curves against the development of DCM/HFD in CCAVB patients after PMI. The cumulative probability of avoidable DCM/HFD at 50 months is 100% with LV pacing, 80.8% with RVA pacing, and 45.5% with RVI pacing (P=0.02). No patient developed DCM or died after 50 months of PMI. CCAVB, congenital complete atrioventricular block; DCM/HFD, dilated cardiomyopathy/heart failure death; PMI, pacemaker implantation; LV, left ventricle; RV, right ventricle; RVA, RV apex; RVI, RV inlet.

Relationship of Pacing Site With Cardiac Function and Ventricular Dyssynchrony

Data obtained immediately before PMI and within 1 year of PMI are shown in Table 3. Before PMI and within 1 year of PMI, there were no significant differences among the pacing sites in terms of the parameters measured, except for LVDd.

Table 3. Characteristics of Patients With Congenital Complete Atrioventricular Block and Their Clinical Measurements Before PMI and Within 1 Year of PMI According to Pacing Site

	n	RVI	n	RVA	n	LV	P value
n		11		11		10
DCM/HFD	11	6 (55%)	11	2 (18%)	10	0 (0%)*	0.013
Observation period from PMI (months)	11	48.3 (0.0–198.0)	11	65.2 (3.6–272.3)	10	103.3 (42.0–249.6)	NS
Age at PMI (days)	11	4 (1–1,14)	11	9 (0–4,478)	10	81 (0–2,245)	NS
Atrial pacing with ventricular pacing	11	4 (36%)	11	4 (36%)	10	3 (30%)	NS
Before PMI
CTR (%)	10	62.9 (55.9–65.0)	9	59.0 (54.7–64.4)	9	58.0 (55.5–72.3)	NS
BNP (pg/ml)	1	464	4	13 (2–471)	3	330 (236–2,636)	ND
QRSd (ms)	9	80 (60–100)	11	80 (60–170)	7	80 (40–120)	NS
LVDd (% of normal)	9	121 (110–141)	10	114 (99–123)***	8	131 (105–157)**	0.013
LVEF (%)	10	66 (44–88)	10	77 (53–84)	8	73 (30–84)	NS
SPWMD (ms)	3	84 (41–121)	4	48 (20–182)	5	61 (5–81)	NS
Within 1 year of PMI
CTR (%)	11	57 (53–69)	8	59 (52–69)	9	55 (50–70)	NS
BNP (pg/ml)	1	44.1	2	25 (7–36)	4	80 (14–124)	ND
QRSd (ms)	10	130 (70–140)	11	120 (80–200)	9	120 (90–160)	NS
LVDd (% of normal)	8	100 (91–131)	9	102 (81–112)	9	117 (86–131)**	NS
LVEF (%)	9	65 (48–74)	8	70 (54–78)	8	75 (58–86)	NS
SPWMD (ms)	2	82 (80–84)	4	85 (10–229)	4	15 (10–52)*	NS

*P<0.05 vs. RVI, **P<0.05 vs. RVA, ***P<0.05 vs. RVI. BNP, B-type natriuretic peptide; CTR, cardiothoracic ratio; LVDd, left ventricular end-diastolic diameter; LVEF, left ventricular ejection fraction; ND, not detected; QRSd, QRS duration; RV, right ventricle; SPWMD, septal-to-posterior wall motion delay. Other abbreviations as in Table 1.

At the endpoint (Figure 4), we compared the parameters between the different pacing sites and the non-PMI group. The CTR after RVI pacing was larger than that for other pacing sites and in the non-PMI group. LVEF after LV pacing and without pacing was higher than that for other pacing sites; in addition, RVI pacing showed the lowest LVEF (P=0.006). SPWMD after LV pacing was shorter than that for other pacing sites; in addition, RVI pacing showed a longer SPWMD than with LV pacing and non-pacing. Although QRS duration without pacing was shorter than that for other pacing sites, BNP and QRSd did not significantly differ among the pacing sites.

Figure 4.

Comparison of clinical parameters at the endpoint between different pacing sites and the non-PMI group. At the endpoint, (A) CTR after RVI pacing was larger than for other pacing sites. (B) BNP and (C) QRS duration did not significantly differ among the pacing sites, though QRS duration without pacing was shorter than for other pacing sites. (D) LVDd after RVA pacing was significantly larger than after LV pacing. (E) LVEF after LV pacing and without pacing was higher than for other pacing sites. RVI pacing showed the lowest LVEF. (F) SPWMD after LV pacing was shorter than for other pacing sites. RVI pacing showed longer SPWMD than for LV pacing and non-pacing. *P<0.05. BNP, B-type natriuretic peptide; CTR, cardiothoracic ratio; ND, not detected; NS, not significant; LV, left ventricle; LVDd, left ventricular end-diastolic diameter; LVEF, left ventricular ejection fraction; PMI, pacemaker implantation; QRSd, QRS duration; RV, right ventricle; RVA, RV apex; RVI, RV inlet; SPWMD, septal-to-posterior wall motion delay.

Clinical Course of Patients Who Developed DCM

The clinical course of the patients in the DCM/HFD group (n=8) is shown in Figure 5. The 6 patients who developed DCM before October 2001 did not have their pacing site changed after development of DCM, but they all died of heart failure. On the other hand, after October 2001, the pacing site was changed for 1 patient from the RVI to the LV apex and another patient was upgraded to cardiac resynchronization therapy, after which they lived for 7 and 8 years, respectively, with New York Heart Association functional class I under maintenance therapy with β-blockers and angiotensin-converting enzyme inhibitors.

Figure 5.

Clinical course of 8 patients who developed DCM/HFD after PMI. All 6 patients (75%) in the DCM/HFD group who did not undergo a change of pacing site after developing DCM died of heart failure. The other 2 patients in whom the pacing site was changed from the RVI to the LV apex or in whom therapy was upgraded to cardiac resynchronization lived without any symptoms of heart failure. CRT, cardiac resynchronization therapy; DCM, dilated cardiomyopathy; HFD, heart failure death; LVA, LV apex; PMI, pacemaker implantation; RV, right ventricle; RVA, RV apex; RVI, RV inlet.

Discussion

In our institution, 25.0% of patients who underwent PMI for CCAVB developed DCM and/or HFD, the majority of which occurred after RVI pacing but none after LV pacing. On the other hand, no cases of DCM/HFD occurred in the non-PMI group. No patients developed DCM after 50 months of PMI. In addition, LVEF was higher after LV pacing and without pacing, and SPWMD was shorter after LV pacing than after the other pacing sites at the endpoint. The 2 patients in whom the pacing site was changed from the RVI to the LV apex or in whom therapy was upgraded to cardiac resynchronization remained alive, and the other 6 died of heart failure.

The prognosis for children with CCAVB after PMI has been considered benign, but some develop DCM, which is detected within 1 year in most cases.^2,9 Previous reports cite a prevalence of DCM of 5–30%,^4–9 which is consistent with our results. The etiology DCM is unknown but considered multifactorial.³ In some reports, DCM was observed to be either a sequela of in utero autoimmune myocarditis or its postnatal reactivation.^25–29 Indeed, a study reported on the relationship between the presence of antibodies and development of DCM.³⁰ In another report, pacing at high heart rates was hypothesized to cause DCM.³¹ Others have mentioned that the pacing site was related to developing detrimental ventricular remodeling.^5–8 However, a direct relationship of the prevalence of DCM with pacing sites has not yet been reported. Indeed, risk factors that were reported by previous studies as influencing DCM development in patients with CCAVB did not include the pacing site.^5,9 Our results showed that the pacing site was the only variable showing differences between the DCM/HFD and non-DCM groups, not maternal antibodies, pacing rate, or ventricular approach.

In our study, 30 patients (94%) in the PMI group had epicardial pacing, and all 8 with DCM/HFD had epicardial pacing. The high DCM/HFD incidence might be related to epicardial pacing, although there were no statistical differences in the ventricular approach between the DCM/HFD and non-DCM groups. However, Kim et al³² reported that 4 patients (6%) with evidence of cardiomyopathy among 63 patients with CCAVB after PMI in the RV had undergone endocardial pacing. Because 35 (56%) of the 63 patients underwent epicardial pacing in their study, the risk of developing DCM in CCAVB was not considered to be related to epicardial pacing, which supports our results.

We showed that the DCM/HFD incidence was higher with RVI pacing than with RVA and LV pacing (P=0.013), whereas there was no occurrence of DCM/HFD in the non-PMI group. Moreover, no patients with LV pacing developed DCM/HFD. To the best of our knowledge, this is the first report to show objective evidence of a relationship between ventricular pacing site and DCM incidence in patients with CCAVB. Some previous studies have reported the effect of the pacing site on ventricular function in patients with CCAVB. Previous reports of young patients with CCAVB showed relationships between the pacing site and LV function, pacing site and ventricular synchrony, and pacing duration and LV function.^11,14 They reported that LVEF was significantly inversely correlated with SPWMD (R²=0.454, P<0.001).¹¹ In the present study, the clinical parameters were the same among patients with RVI, RVA, and LV pacing within 1 year of PMI. These results may be explained by the retrospective study design, which included data from 30 years ago. However, LVEF and SPWMD after LV pacing and LVEF in the non-PMI group were better than those of other pacing sites at the endpoint. Based on this finding and the results of previous reports, it is highly possible that ventricular dyssynchrony related to pacing site affects the development of DCM in CCAVB patients.

Based on the present findings, we strongly suggest that patients with CCAVB who need ventricular pacing should have PMI at the LV, not the RVI. Several previously published papers have demonstrated that pacing on the RV free wall, both endocardial and epicardial, should be avoided for optimal results in children; instead, they advocate the use of single LV apex and LV free wall sites for chronic ventricular pacing.^15,33,34 Their recommendation is almost the same as ours. In addition, we suggest that close follow-up within 50 months after PMI to assess for development of DCM is prudent.

Study Limitations

There were several limitations of this study, such as the small sample size and retrospective design. Regarding the definition of the pacing site, we used biplane chest radiographs, ventriculography, and 12-lead ECGs at the endpoints, as old as possible. However, there were still some limitations in differentiating between RVI and RVA in small hearts. In addition, it was difficult to apply paired t-tests for comparison because of insufficient data. Further, it would be better to assess mechanical delay (eg, septal to lateral, apical to basal, and maximum LV) with 2D strain measurements. In this study, however, we assessed ventricular synchrony only by QRSd and SPWMD because measurement of 2D strain was not available. Nonetheless, QRSd and SPWMD were easy to detect and may be sufficient to represent ventricular synchrony because mechanical dyssynchrony usually follows electrical dyssynchrony.

Conclusions

In this study, 25% of patients with CCAVB developed DCM and/or HFD after PMI compared with none of the patients in the non-PMI group. The DCM/HFD incidence was higher in patients with RVI pacing than in those with RVA and LV pacing. No patient with LV pacing developed DCM/HFD. It is highly possible that ventricular dyssynchrony related to the pacing site is a cause of DCM in CCAVB.

Grants

None.

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