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European Journal of Heart Failure 2003 5(2):165-170; doi:10.1016/S1388-9842(02)00203-9
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© 2002 European Society of Cardiology

Distinct left bundle branch block pattern in ischemic and non-ischemic dilated cardiomyopathy

Antoni Bayes-Genisa,*, Laura Lopeza, Xavier Viñolasa, Roberto Elosuab, Vicenç Brossaa, Marta Campreciósa, Miriam Mateoa, Juan Cincaa and Antonio Bayes de Lunaa

a Servei de Cardiologia, Hospital de la Santa Creu i Sant Pau C/ San Antonio Ma Claret 167, 08025 Barcelona, Spain
b Institut Municipal d'Investigacions Mèdiques Barcelona, Spain

* Corresponding author. Tel.: +34-93-291-92-94; fax: +34-93-291-94-24 E-mail address: abayesgenis{at}hsp.santpau.es


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
Background: A high percentage of patients with dilated cardiomyopathy have the electrocardiographic (ECG) pattern of advanced left bundle branch block (LBBB). In the present study we sought to investigate whether patients with dilated cardiomyopathy of ischemic or non-ischemic etiology can be differentiated on the basis of LBBB pattern.

Methods and Results: The study population included 41 patients with dilated cardiomyopathy of non-ischemic (NIC) (n=26) or ischemic origin (IC) (n=15) and LBBB on surface ECG. ECG duration and voltage were digitally measured. The presence of notching of S wave in right precordial leads (V1–V3) was not statistically different between the groups. The voltages of precordial leads V2, V3 and the {Sigma}(V1+V2+V3 voltages) were significantly more prominent in patients with NIC (P=0.002, P<0.001 and P=0.002, respectively). The discriminative power of receiver operating characteristic analysis was best at voltages of V3 of 2100 µV (area under the curve, 0.805; standard error, 0.001). The sensitivity and specificity of V3 voltage >2100 µV on surface ECG in the presence of LBBB to identify a cardiomyopathy of non-ischemic origin were 85 and 73%, respectively.

Conclusions: A single ECG criteria, voltage of lead V3, appears to be a useful parameter to identify patients with dilated cardiomyopathy of ischemic or non-ischemic origin in the presence of advanced LBBB.

Key Words: Left bundle branch block • Electrocardiogram • Dilated cardiomyopathy

Received May 24, 2002; Revised July 18, 2002; Accepted October 4, 2002


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 References
 
Dilated cardiomyopathy is characterized by left ventricular or biventricular dilatation and impaired myocardial contractility [1]. Patients with dilated cardiomyopathy and congestive heart failure frequently have a prolonged QRS duration (>120 ms) due to intraventricular conduction delay or left bundle branch block (LBBB) [2]. Conduction abnormalities occur in over 80% of cases in non-ischemic dilated cardiomyopathy, and include first-degree atrioventricular block, LBBB, and left anterior hemiblock [3,4]. In dilated cardiomyopathy of ischemic origin, LBBB may appear during the acute phase of myocardial infarction [5,6], or at follow-up during left ventricle remodeling and dilation [7]. In chronic myocardial infarction, even if important zones of the left ventricle are necrotic, the overall direction of depolarization vectors conditioned by LBBB remains unchanged, thus hampering the inscription of Q waves [8]. Various electrocardiographic (ECG) criteria have been proposed in the past as indicators of chronic myocardial infarction in the presence of LBBB [8]. More accurate reports show that specificity and predictive accuracy of these ECG criteria are too low to be clinically useful as indicators of myocardial infarction [9,10].

In the present study, we sought to investigate whether patients with dilated cardiomyopathy and severely reduced ejection fraction of ischemic or non-ischemic origin have distinct LBBB patterns. Analysis of digitally recorded ECGs were performed to test whether QRS duration and voltage are different in ischemic and non-ischemic cardiomyopathy with LBBB.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 References
 
2.1. Study population
The study population included 41 patients with dilated cardiomyopathy of non-ischemic (n=26) or ischemic origin (n=15) and advanced LBBB on surface ECG, from our database of 133 cardiomyopathy patients being evaluated for heart transplantation from May to December 2001. Non-ischemic dilated cardiomyopathy (NIC) was defined as left ventricular dilation with global systolic dysfunction without a frank scar or aneurysm by echocardiography and absence of coronary artery disease. Ischemic cardiomyopathy (IC) was defined as one or more documented hospital admissions for myocardial infarction, and echocardiographic evidence of regional wall motion abnormalities with left ventricular dilation. Heart rates above 100 beats/min were excluded from the study because of the possibility of tachycardia-related cardiomyopathy. Patients with right bundle branch block, or pacemaker rhythm were also excluded. Patient demographics included age, sex, body mass index, and cardiovascular risk factors. Clinical and echocardiographic evaluation was also performed, including left ventricle ejection fraction, left ventricle end-diastolic diameter, wall thickness and motion, and left atrium diameter.

2.2. ECG analysis
The diagnosis of advanced LBBB was based on the following criteria [8]: QRS duration of >=120 ms, QS morphology in lead VR, QS or rS morphology in lead V1, and solitary R morphology in lead V6.

Ten second simultaneous 12-lead ECG recordings were obtained at rest. Analog to digital conversion was performed at 600 Hz sample rate (Cardioperfect CCW recorder, Cardio ControlTM, Amsterdam, The Netherlands), and digital data were stored in a Windows based PC. Visualization and measurement of the ECG recordings were done using commercial software (Cardiocontrol Medical Workstation Windows 1.1TM), which allows magnification of each individual lead and provides onscreen digital calipers for duration and voltage measurements. A template of the average 10 s recording in each lead was used for measurements. Two investigators, blinded for the etiology of the cardiomyopathy performed the measurements. Interobserver variability was <5%.

2.3. Statistical analysis
Comparison of the distribution of the variables in the two groups was performed using {chi}2, Fisher exact test, or Student's t-test when appropriate. Associations were assessed by Pearson correlation coefficient. A P-value <0.05 was considered statistically significant. Receiver operating characteristic (ROC) analysis on different ECG variables was performed to assess the sensitivity and specificity of different threshold values to distinguish between IC and NIC.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 References
 
3.1. Demographic, clinical and echocardiographic variables
As shown in Table 1, patients with ischemic dilated cardiomyopathy were older than patients with cardiomyopathy of non-ischemic origin (P=0.046). No differences in height, weight, or known confounding factors of QRS voltage, were observed. No differences were found between the two groups in the prevalence of cardiovascular risk factors (Table 1). Ischemic cardiomyopathy was secondary to an antero-lateral myocardial infarction in 13 patients (87%), an infero-posterior infarction in 6 patients (40%), and 4 patients had infarctions of the antero-lateral and infero-posterior walls (27%).


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  		Table 1 Demographic, clinical, and echocardiographic characteristics of patients with ischemic and non-ischemic dilated cardiomyopathy

 
Patients from both groups were clinically stable. The majority of patients were in NYHA class II (73% IC vs. 58% NIC, P=NS), and only 3 patients with IC (20%) and 7 patients with NIC (27%) were in NYHA class III (Table 1).

Both groups had similar left ventricle ejection fraction and septal thickness (Table 1). Only 2 patients, one in each group had a septal thickness >12 mm. Echocardiography showed a substantially larger left ventricular end diastolic cavity (LVEDD) in patients with NIC (P=0.04).

3.2. ECG analysis
Table 2 shows voltage and magnitude of digitally analyzed ECG variables. QRS duration was not statistically different between the groups. However, only 3 patients with IC (33%) compared to 18 patients with NIC (69%) had a QRS duration >170 ms (P=0.026). The presence of prominent notching of the upstroke or downstroke of S wave in right precordial leads (V1–V3) was not statistically different between the groups, (Table 2). No differences in QRS axis or the presence of left axis deviation were found between the groups.


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  		Table 2 Analysis of surface ECG with LBBB of patients with ischemic and non-ischemic dilated cardiomyopathy

 
Table 2 shows that no differences were found between the groups in the voltage of frontal plane leads (I, II and III). Conversely, voltages of precordial leads V2 and V3, and the {Sigma}(V1+V2+V3 voltages) were significantly more prominent in patients with NIC compared to IC (P=0.002, P<0.001, and P=0.002, respectively) (Table 2). The ratio of the {Sigma}(voltage of V1+V2+V3)/{Sigma}(voltage of I+II+III) was also different between the groups (P=0.009). Fig. 1 illustrates with boxplots the significant difference in voltage of V3 found between patients with ischemic and non-ischemic cardiomyopathy. Fig. 2 shows electrocardiograms of patients with NIC (left) and IC (right). Note the prominent voltages observed in right precordial leads in NIC.


Figure 1
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  		Fig. 1 Boxplot of voltages of V3 in patients with ischemic and non-ischemic dilated cardiomyopathy. IC, ischemic cardiomyopathy; NIC, non-ischemic cardiomyopathy.

 


Figure 2
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  		Fig. 2 ECGs of patients with non-ischemic (NIC) and ischemic cardiomyopathy (IC). Both ECGs have a similar QRS width, and are recordings from hearts with matched LVEF and LVEDD. Note the pronounced voltages of right precordial leads, particularly V2 and V3 (arrow), in non-ischemic cardiomyopathy compared to ischemic cardiomyopathy.

 
No association was found between voltage of V2 or V3 and QRS duration, LVEDD, and left ventricle ejection fraction. A positive association was found between voltage of V3 and voltage of II in patients with NIC (r=0.541, P=0.004), which was not present in IC patients (r=–0.317, P=0.25).

ROC analysis was assayed for voltage of V2, voltage of V3, and {Sigma}(V1+V2+V3 voltages), only voltage of V3 showed a substantial discriminative power. ROC analysis for voltage of V3 was performed ranging from 1032 to 4568 µV. The discriminative power of the ROC analysis (combined sensitivity and specificity) for diagnosing NIC from an ECG with LBBB was best at voltages of V3 of 2100 µV (area under the curve, 0.805; standard error, 0.001) (Fig. 3). The sensitivity and specificity of voltage of V3>2100 µV on surface ECG in the presence of LBBB to identify a cardiomyopathy of non-ischemic origin were 85 and 73%, respectively. Moreover, in this series voltage of V3>3872 µV identified patients with NIC with a specificity of 100%, at the expense of a reduced sensitivity of 27%. Considering the criteria: voltage of V3+notching of upstroke of S wave in V3, the diagnostic sensitivity and specificity for NIC were 80 and 77%, respectively, which was not significantly better than voltage of V3 alone.


Figure 3
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  		Fig. 3 ROC analysis for voltage of V3. Optimal voltage of V3 cutoff value was 2100 µV. Area under the curve, 0.805; standard error, 0.001.

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
References
 
In the present study, we investigated the ECG characteristics of patients with dilated cardiomyopathy of ischemic and non-ischemic origin with LBBB on surface ECG. We found that a voltage of V3>2100 µV identified patients with dilated cardiomyopathy of non-ischemic origin with a sensitivity of 85% and a specificity of 73%.

When the conduction of the electrical impulse through the left bundle branch is interrupted or severely delayed, the left ventricular excitation wave is mainly conducted through the right bundle branch. Activation begins low on the right septal surface, in the region corresponding in the left side to the base of the anterior papillary muscle. From there, the wave of activation spreads to the right ventricle and transeptally to the left ventricle. In this situation, the initial vector of ventricular activation have their origin in the right side of the septum and are directed mainly to the left, and most often anteriorly and inferiorly, to depolarize the lower part of septal mass. Only afterwards does the myocardium of the free wall of the left ventricle begin to be depolarized, either from cell to cell or reutilizing the peripheral fascicles of the subdivisions of the left bundle branch. This late activation of the left ventricular mass generates electrical forces directed towards the left and posteriorly. Therefore, in advanced LBBB the major portion of the QRS loop is especially located posteriorly and to the left, pointing slightly either inferiorly or somewhat superiorly, and so produces an increased amplitude of the S wave in leads V1–V3 [8,11]. This classical pattern of advanced LBBB activation is what we found in patients with non-ischemic dilated cardiomyopathy. In chronic myocardial infarction, even if important zones of the left ventricle are necrotic, the overall direction of the depolarization vectors continue to point posteriorly and from right to left, impeding usually the inscription of a Q wave of necrosis [8]. The reduced voltage in right precordial leads in patients with non-ischemic dilated cardiomyopathy observed in this study may be explained by a reduced magnitude of the repolarization vector due to a limited ventricular depolarized mass after a large myocardial infarction.

The various ECG criteria that have been proposed in the past as indicators of myocardial infarction in the presence of advanced LBBB lack sensitivity and predictive accuracy [9,10]. In addition, they are subjected to considerable interobserver variability. Wackers found that Cabrera's sign (notching of the upstroke of S wave in V3, V4, or V5) had a diagnostic sensitivity of prior myocardial infarction of only 27% [9]. Moreover, Kindwall et al. found that Chapman's sign (notching of upstroke of the R wave in I, VL or V6), another classical criteria for chronic myocardial infarction in the presence of advanced LBBB, is more common in patients without myocardial infarction [10]. Thus, this is the first report that provides a simple ECG criteria, voltage of V3, for the diagnosis of ischemic cardiomyopathy in the presence of LBBB. The combination of voltage of V3 and notching of the upstroke of V3 did not provide additional information to voltage of V3 alone.

Echocardiographic studies revealed that even mildly prolonged QRS duration (>=120 ms) resulting from intraventricular conduction delay is associated with left ventricular dysfunction [12]. An abnormal sequence of electrical activation has long been recognized to have detrimental effects on the mechanical efficiency of left ventricular contraction [13]. The negative hemodynamic effects of abnormal intraventricular conduction include reduction of the left ejection fraction and the rate of systolic pressure rise, and have been recognized in patients with isolated LBBB. A recent report concluded that QRS duration has a significant inverse relationship with ejection fraction, and prolongation of QRS duration (>=170 ms) in the presence of LBBB is a marker of significant left ventricular dysfunction [14]. In our study, we found that patients with NIC more often have QRS duration >170 ms, but we did not find an association between the magnitude of voltage of V3 and QRS duration or left ventricle ejection fraction.

In the 1960s, reports identified that patients with congestive heart failure had lower QRS voltages on their ECG than they had when compensated [15]. More recently, a phenomenon consisting of a reduction in ECG amplitude commensurate with weight gain in patients with anasarca was reported [16]. Another morphometric variable, height, has also been reported as being related to voltage of ECG. A signal averaged ECG report found a negative correlation between size and voltage of the last 40 ms of the QRS: the taller the subject, the smaller the value of the voltage [17]. In our study, in order to avoid the influence of biomorphometric factors on the ECG parameters measured, patients were matched for weight and height, and did not have anasarca or volume overload at the time the ECG was recorded.

The results of this study point to new avenues of research in the field of ECG patterns, and indicate that a careful interpretation of LBBB morphology in 12-lead surface ECG may be useful to identify the etiology of the underlying disease process. With the advent of resynchronization therapy in patients with congestive heart failure and LBBB [18], a better characterization of this ECG pattern may be of additional value when selecting the appropriate candidates for this emerging therapy.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 

  1. William D.G., Fuster V. Medical progress: idiopathic dilated cardiomyopathy. N Engl J Med (1994) 1564–1575.
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  9. Wackers F.J. The diagnosis of myocardial infarction in the presence of left bundle branch block. Cardiol Clin (1987) 5:393–401.[Medline]
  10. Kindwall K.E., Brown J.P., Josephson M.E. Predictive accuracy of criteria for chronic myocardial infarction in pacing-induced left bundle branch block. Am J Cardiol (1986) 57:1255–1260.[CrossRef][Web of Science][Medline]
  11. Padua F., Pereirinha A., Lopes M.G. Conduction defects. In: Comprehensive electrocardiology. Theory and practice in health and disease—MacFarlane P.W., Veitch Lawrie T.D., eds. (1989) New York: Pergamon Press, Inc. 480–483.
  12. Tabuchi H., Kawi N., Sawayama T. Estimation of left ventricular systolic function based on electrocardiograms in cases with left bundle branch block. Am J Cardiol (1998) 31:23–30.
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  16. Madias J.E., Bazaz R., Agarwal H., Win M., Medepalli L. Anasarca-mediated attenuation of the amplitude of ECG complexes: a description of a heretofore unrecognized phenomenon. J Am Coll Cardiol (2001) 38:756–764.[Abstract/Free Full Text]
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