Skip to main content
Annals of Noninvasive Electrocardiology logoLink to Annals of Noninvasive Electrocardiology
. 2006 Jul 3;11(3):230–236. doi: 10.1111/j.1542-474X.2006.00108.x

Effect of Right Bundle Branch Block on Electrocardiographic Amplitudes, Including Combined Voltage Criteria Used for the Detection of Left Ventricular Hypertrophy

Peter G Chan 1, Michael Logue 1, Paul Kligfield 1
PMCID: PMC6932690  PMID: 16846437

Abstract

Background: Although right bundle branch block (RBBB) delays right ventricular depolarization, its effect on cancellation of right and left ventricular forces within the QRS complex has not been quantified during stable temporal and physiological conditions. Systematic changes in QRS amplitude during transient RBBB bear directly on performance of standard ECG criteria for left ventricular hypertrophy (LVH), and these changes require quantification.

Methods: We examined the instantaneous effect of RBBB on QRS amplitudes and LVH voltages in 40 patients who had intermittent complete RBBB during a single 10 sec standard 12‐lead ECG recording, comprising 0.1% of approximately 400,000 consecutive ECGs in a university teaching hospital setting. Amplitudes were measured by magnifying graticule to the nearest 25 microvolts, averaged for up to 3 normal and 3 RBBB complexes, and compared by paired t test.

Results: RBBB was associated with an increase in initial QRS forces (RV1, RV2, and QV6) but significant decreases in mean mid‐QRS amplitudes that reflect left ventricular depolarization (RaVL [−75 microvolts], SV1 [−389 microvolts], SV3 [−617 microvolts], RV5 [−100 microvolts], and RV6 [−123 microvolts]). All late QRS forces were increased with RBBB (R'V1, SV5, SI). As a result, combined voltages used for LVH criteria were significantly reduced by RBBB: Sokolow‐Lyon voltage decreased from 1520 ± 739 to 1014 ± 512 microvolts (p < 0.001), and Cornell voltage decreased from 1438 ± 683 to 746 ± 399 microvolts (p < 0.001).

Conclusions: RBBB is associated with significant reduction in "left ventricular" QRS amplitudes of the standard ECG, consistent with cancellation, rather than unmasking, of left ventricular mid‐QRS forces by altered septal and delayed right ventricular depolarization. Because QRS voltages that are routinely combined for the detection of LVH are reduced in RBBB, standard LVH criteria will perform with lower sensitivity in patients with RBBB.

Keywords: right bundle branch block, QRS complex, ECG voltage

INTRODUCTION

The electrocardiogram (ECG) recorded from the surface of the body represents the net uncancelled potential difference between pairs of electrodes. With normal intraventricular conduction, the ordinarily larger amplitude posterior and leftward directed forces of the left ventricle are partially cancelled by the smaller anterior and rightward directed forces of the right ventricle. Right bundle branch block (RBBB) results in a delay in depolarization of the right ventricle with respect to the onset of electrical activation of the heart and the normal depolarization of the left ventricle. 1 , 2 In addition to the appearance of delayed anterior and rightward electrical forces from the right ventricle in the terminal portion of the widened QRS complex, the presence of RBBB should also alter the cancellation pattern of mid‐QRS forces from both ventricles. 3 , 4 Delay in right ventricular activation might be expected to unmask some early left ventricular forces and alter the net magnitude of mid‐QRS forces. 5 It is generally recognized that RBBB alters ECG amplitudes to reduce the already poor sensitivity of standard voltage criteria for the detection of left ventricular hypertrophy (LVH). 4 , 5 , 6 , 7 , 8 , 9 However, the magnitude of QRS voltage changes caused by RBBB in the standard leads of the routine ECG has not been quantified in patients and subjects who are in a temporally and physiologically constant state. The present study examined the effect of RBBB on QRS amplitudes and voltage criteria used for the detection of LVH in a consecutive series of patients with intermittent bundle branch block and normal (i.e., nonRBBB) intraventricular conduction during simultaneous lead recording of a single 10‐second ECG.

METHODS

Study Population

From a database of approximately 400,000 consecutive 10‐second standard 12‐lead ECG digital files recorded during a 6‐year period in a university teaching hospital, all tracings with a diagnosis of intermittent RBBB were selected for review. ECGs were included in the present evaluation if there was at least one normal QRS complex (with no terminal anterior forces in lead V1) and one complete RBBB complex (QRS duration >100 ms with a terminal R′ in V1 of at least 40 ms) present in the recording, with no coincident axis change suggesting intermittent hemiblock. Patients were not included in the present study if the RBBB pattern was determined on review to be incomplete (defined for this purpose as terminal R′ in V1 less than 40 ms). All tracings were classified by an experienced electrocardiographer (PK) before measurement and analysis of the data. Tracings from 40 separate patients with intermittent (complete) RBBB and normal (i.e., nonRBBB) complexes on the same tracing fulfilled entry criteria and form the basis of this report. This study was not designed to test the relationship of ECG voltages, with and without RBBB, to LVH. Measured left ventricular mass was not available in this population, and the number of subjects with LVH by nonelectrocardiographic methods in this group is unknown.

Electrocardiography

ECGs were retrieved by printing 10 seconds of original recording for each of the standard 12 leads, so that both normal (i.e., normal meaning absence of RBBB or right ventricular conduction delay, not necessarily normal amplitude or axis or absence of infarction) and RBBB complexes were available for the same complexes in each lead. This allowed us to examine the effect of RBBB on each ECG under constant temporal and physiological conditions, with no change in patient position or lead placement. For each tracing, we examined the effect of RBBB on the amplitudes of selected individual QRS components and on combined voltages used for the diagnosis of LVH. Selected amplitudes included those representing initial QRS forces (R in V1 and V2; Q in I, III, V5, and V6), middle QRS forces (S in V1, V3, and III; R in I, aVL, V5, and V6), and late QRS forces (R′ in V1 and V2, S in I, V5, and V6). Voltage criteria for LVH included Gubner‐Ungerleider voltage (R in I + S in III > 25 mm), 10 Sokolow‐Lyon voltage (S in V1+ the greater of R in V5 or R in V6 > 35 mm), 11 Cornell voltage (R in aVL + S in V3 > 28 mm for men, >20 mm for women), 12 and the R wave ratio of V5 and V6. 13 Amplitudes were measured by magnifying graticule to the nearest 25 μV (0.25 mm) by a single observer (PGC), and averaged for three QRS complexes of each type when available.

Statistical Methods and Data Presentation

Data were entered into SPSS (version 11.0) for analysis. Mean values are presented with the standard deviation (SD) as the index of dispersion. Kolmogorov‐Smirnov tests were performed on amplitude measurements to determine whether the distribution of data was normal. For parametric data, paired t‐tests were used to compare measurements from normal and RBBB QRS complexes. For nonparametric data, Wilcoxon signed rank tests were used. The same methods were applied for comparison of the various voltage criteria for the detection of LVH. For illustrative purposes, differences between waveform measurements in RBBB and in normal complexes are shown by means of boxplots, showing median, 25 and 75th percentile ranges, whiskers, and outliers. The relation of RBBB and normal complex measurements was also examined by means of linear regression, using RBBB values as the independent variable and normal complex values as the dependent variable. Selected regression findings were included in scatterplots to illustrate the predictive value of a given RBBB value for the normal complex value. Intraobserver reproducibility was examined by repeat measurement of selected amplitudes (R in V1, R in V5, and S in V3) in 10 ECGs by one observer (PGC), which were compared by paired t‐tests. This demonstrated high reproducibility, with a mean difference of −4 μV (0.04 mm amplitude) and a SD of 24 μV.

RESULTS

Demographics

Of the 40 patients, 18 were male and 22 were female, and the mean age was 74 years (range 50–91 years). All patients had intermittent complete RBBB as defined in the methods: 29 subjects had a normal axis, 8 had left axis deviation (−30° or more leftward in the frontal plane) and 3 had right axis deviation (+105° or more rightward). In no patient included in this report was there a clinically relevant axis difference between the RBBB and normal complexes used for amplitude measurement. In this group, mean Sokolow‐Lyon voltage was 15.2 ± 7.4 mm (range 4.4–36 mm), mean Cornell voltage was 14.4 ± 6.8 mm (range 3.25–40.4 mm), and mean Gubner‐Ungerleider voltage was 9.5 ± 7.2 mm (range 0.5–31.2 mm) in the normal complexes. Patients were consecutively selected according to entry criteria and not selected for high voltages; voltage criteria for LVH were present in only one patient by Sokolow‐Lyon voltage, in two patients by Gubner‐Ungerleider voltage, and in five patients by sex‐adjusted Cornell voltage.

Effect of RBBB on QRS Waveform Amplitudes in Normal Beats

Mean waveform amplitudes of QRS components and mean differences between corresponding waveform amplitudes for RBBB and normal complexes, together with the 95% confidence intervals of the mean differences and the SD of the mean difference, are shown in Table 1. Differences between RBBB and normal complex amplitude pairs are also shown as boxplots, with 25–75th percentile range, whiskers, and outliers, for initial QRS forces (Fig. 1), mid‐QRS forces (Fig. 2), and late QRS forces (Fig. 3). Regression equations relating measured QRS waveforms of RBBB complex amplitudes to normal complex amplitudes are shown in Table 2, with the slope, intercept, coefficient of linear correlation, and r2 for the data from each pair. These regressions relate narrow complex amplitudes to observed RBBB complex amplitudes. Selected scatterplots of these data, for weak and for strong correlations, are shown in Figure 4.

Table 1.

Mean Waveform Amplitudes and Mean Differences Between RBBB and Normal Complexes

Normal QRS Mean ± 1 SD RBBB QRS Mean ± 1 SD RBBB—Normal Mean Difference (95% CI) SD of Difference Sig. (two‐tailed) Test
Initial QRS amplitudes (in mm)
 R in V1 1.38 ± 1.59 2.22 ± 2.24 0.84 (0.19 to 1.48) 2.02 0.027 W
 R in V2 6.31 ± 4.52 7.26 ± 4.62 0.95 (−0.12 to 2.02) 3.34 0.080 T
 Q in V5 0.29 ± 0.51 0.38 ± 0.56 0.08 (−0.02 to 0.19) 0.33 0.079 W
 Q in V6 0.38 ± 0.53 0.49 ± 0.60   0.11 (0.01 to 0.22)    0.34 0.044 W
 Q in III 1.73 ± 3.01 1.26 ± 2.33 −0.46 (−1.00 to 0.07)  1.68 0.034 W
 Q in I 0.35 ± 0.41 0.44 ± 0.51 0.09 (−0.01 to 0.18) 0.30 0.161 W
Mid QRS amplitudes (in mm)
 S in V1 5.77 ± 5.26 1.88 ± 2.08 −3.89 (−5.43 to −2.34) 4.84 0.000 T
 S in V3 9.27 ± 6.39 3.10 ± 3.02 −6.17 (−8.04 to −4.30) 5.84 0.000 T
 R in V5 8.96 ± 4.37 7.96 ± 4.13 −1.00 (−1.60 to −0.40) 1.88 0.002 T
 R in V6 7.66 ± 4.16 6.43 ± 3.86 −1.23 (−1.81 to −0.65) 1.82 0.000 T
 S in III 3.15 ± 4.52 3.25 ± 4.68 0.10 (−0.64 to 0.84) 2.31 0.538 W
 R in I 6.32 ± 3.98 5.11 ± 3.58 −1.21 (−1.68 to −0.73) 1.48 0.000 T
 R in aVL 5.12 ± 3.91 4.37 ± 3.73 −0.75 (−1.11 to −0.39) 1.13 0.000 T
Late QRS amplitudes (in mm)
 R′ in V1 0.00 ± 0.01 6.19 ± 3.59 6.93 (5.67 to 8.18)   3.94 0.000 T
 R′ in V2 0.14 ± 0.91 3.36 ± 3.40 4.01 (2.24 to 5.78)   5.53 0.000 W
 S in V5 2.76 ± 2.72 3.93 ± 2.75 1.17 (0.52 to 1.81)   2.02 0.001 T
 S in V6 1.47 ± 1.65 3.17 ± 1.94 1.71 (1.23 to 2.18)   1.48 0.000 T
 S in I 0.65 ± 0.77 2.69 ± 0.83 2.05 (1.75 to 2.34)   0.91 0.000 T

T = paired t‐test; W = Wilcoxon signed ranks test (T vs W decided by one‐sample Kolmogorov‐Smirnov test on differences).

Figure 1.

Figure 1

Change in initial QRS forces with RBBB. Boxplots of absolute differences in normal conduction amplitudes from RBBB amplitudes (positive when normal > RBBB, negative when normal < RBBB) for initial‐QRS forces. Amplitudes are in mm (=0.1 mV). The box indicates the 25–75% range of difference values, with the line representing the median, and the whiskers include all values except indicated outliers (defined as being beyond 1.5 boxlengths from the edge of the box. These plots provide a overview of the distribution of data that complements the mean values reported in the tables. As an example, there is a small increase in the initial R wave in V1 during RBBB compared with normal conduction.

Figure 2.

Figure 2

Change in mid QRS forces with RBBB. Boxplots of absolute differences in normal from RBBB amplitudes (positive when normal > RBBB, negative when normal < RBBB) for mid‐QRS forces. See legend for Figure 1. As examples, there are decreases in the absolute amplitudes of SV1 and SV3 (i.e., smaller S waves) during RBBB compared with normal conduction.

Figure 3.

Figure 3

Change in late QRS forces with RBBB. Boxplots of differences in normal from RBBB amplitudes (positive when normal > RBBB, negative when normal < RBBB) for late‐QRS forces. See legend for Figure 1. There are increases in terminal rightward and anterior forces during RBBB, as exemplified by larger R′ in V1 (not present during normal conduction) and by larger S waves in V6.

Table 2.

Linear Regression Equations Relating RBBB to Normal Complex Amplitudes

m b r r2 SE
Initial QRS amplitudes
 R in V1 0.35 0.61 0.490 0.240 1.41
 R in V2 0.72 1.10 0.733 0.538 3.12
 Q in V5 0.75 0.01 0.815 0.665 0.30
 Q in V6 0.73 0.02 0.828 0.685 0.30
 Q in III 1.07 0.37 0.831 0.690 1.70
 Q in I 0.66 0.06 0.816 0.666 0.24
Mid QRS amplitudes
 S in V1 0.99 3.91 0.391 0.153 4.91
 S in V3 0.87 6.58 0.409 0.167 5.91
 R in V5 0.96 1.34 0.904 0.816 1.90
 R in V6 0.97 1.43 0.900 0.809 1.84
 S in III 0.84 0.41 0.874 0.764 2.22
 R in I 1.03 1.04 0.928 0.862 1.50
 R in aVL 1.00 0.74 0.957 0.916 1.15
Late QRS amplitudes
 R′ in V1 0.00 0.00 0.035 0.001 0.01
 R′ in V2 0.02 0.07 0.114 0.013 0.91
 S in V5 0.72 −0.06  0.726 0.527 1.89
 S in V6 0.57 −0.34  0.669 0.448 1.24
 S in I 0.33 −0.24  0.352 0.124 0.73

Normal QRS = m (RBBB QRS) + b, where voltages are in mm (0.1 mV) at standard ECG gain; m = the slope of linear regression; b = the intercept; r = the coefficient of linear correlation; SE = standard error of estimate.

Figure 4.

Figure 4

Selected scatterplots for weak and strong correlations of amplitude measurements during normal conduction and during RBBB. The weak correlation of SV1 in RBBB (sv1b) and SV1 in normal conduction (sv1n) is shown on the left. The strong correlation of RV6 in RBBB (rv6b) and RV6 in normal conduction (rv6n) is shown on the right.

Among the six measured amplitudes associated with mean initial rightward and anterior QRS forces during normal conduction, RBBB resulted in a small horizontal plane increase in RV1 (84 μV) and in QV6 (11 μV) (Table 1). Of the eight measured amplitudes associated with mean leftward and posterior mid‐QRS forces, all mean amplitudes were significantly decreased in RBBB complexes, except for SIII in the frontal plane; the mean decrease in amplitude was greatest in SV3 (617 μV), large in SV1 (389 μV) and 100 μV or greater in RV5 and RV6. All measured amplitudes associated with late rightward and anterior QRS forces were increased with RBBB; the mean increase was largest for R′V1 (of 693 μV) and R′V2 (401 μV), with smaller but significant increases in SV5 and SV6 (117 μV and 171 μV, respectively. The boxplots of 1, 2, 3 illustrate the range and deviation from central tendency for individual waveform differences.

Effect of RBBB on Voltage Criteria Used for the Detection of LVH

Mean combined waveform amplitudes used for the detection of LVH and mean differences between corresponding combined LVH amplitudes for RBBB and normal complexes, together with the 95% CI of the mean differences and the SD of the mean difference, are shown in Table 3. These differences are also shown as boxplots in Figure 5. Regression equations relating measured combined LV amplitudes from RBBB complexes and normal complexes are shown in Table 4.

Table 3.

Mean Combined Amplitudes for LVH Detection and Differences Between RBBB and Normal Complex Sums

Normal QR Mean ± 1 SD RBBB QRS Mean ± 1 SD RBBB—Normal Mean Difference (95% CI) SD of Difference Sig. (two‐tailed) Test
LVH voltage criteria (in mm, except for ratio)
 Gubner‐Ungerleider  9.47 ± 7.23  8.36 ± 7.14 −1.11 (−2.18 to −0.04) 3.34 0.042 T
 Sokolow‐Lyon 15.20 ± 7.39 10.14 ± 5.12 −5.06 (−6.88 to −3.23) 5.71 0.000 T
 Cornell 14.39 ± 6.83  7.46 ± 3.99 −6.93 (−8.95 to −4.91) 6.32 0.000 T
 RV5/RV6  1.23 ± 0.35  1.36 ± 0.44 0.13 (0.04 to 0.22)  0.28 0.002 W

T = paired t‐test; W = Wilcoxon signed‐rank test; (T vs W decided by one‐sample Kolmogorov‐Smirnov test on differences).

Figure 5.

Figure 5

Change in combined voltages during RBBB. Boxplots of differences in normal from RBBB amplitudes (positive when normal > RBBB, negative when normal < RBBB) for voltage combinations used for the detection of LVH. See legend for Figure 1, and methods for definitions of voltage combinations. Gubner‐Ungerleider voltage decreases less than Sokolow‐Lyon voltage and Cornell voltage during RBBB, while the RV5/RV6 ratio changes little.

Table 4.

Regression Equations Relating Combined LVH Amplitudes from RBBB to Those for Normal Complex Amplitudes

m B r r2 SE
LVH voltage criteria
 Gubner‐Ungerleider 0.90 1.92 0.892 0.795 3.31
 Sokolow‐Lyon 0.92 5.87 0.637 0.406 5.77
 Cornell 0.71 9.07 0.416 0.173 6.30
 RV5/RV6 0.61 0.40 0.771 0.595 0.22

Normal QRS = m (RBBB QRS) + b, where voltages are in mm (0.1 mV) at standard ECG gain; m = the slope of linear regression; b = the intercept; r = the coefficient of linear correlation; SE = standard error of estimate.

Combined voltages used for the ECG detection of LVH were significantly reduced by RBBB. The reduction of voltage was greatest for Cornell voltage (693 μV) and nearly as much for Sokolow‐Lyon voltage (506 μV), both of which incorporate horizontal plane measurements. Gubner‐Ungerleider voltage, based on the frontal plane limb leads I and III, was reduced proportionally less, while the RV5:RV6 ratio was least affected. The boxplots of Figure 5 illustrate the range and deviation from central tendency for individual combined LVH waveform differences.

DISCUSSION

Changes in QRS Amplitudes During Transient RBBB

Under constant temporal and physiologic conditions, RBBB causes systematic changes in QRS amplitudes in comparison with normal conduction. Our data indicate that RBBB is associated with small increases in mean rightward and anterior early‐QRS amplitudes, with none of the differences exceeding 0.1 mm (100 μV). There were larger decreases in nearly all mean leftward and posterior mid‐QRS amplitudes, as much as 6 mm (600 μV) for the S wave in precordial lead V3. These findings suggest important mid‐QRS cancellation of major left ventricular forces, rather than unmasking of mid‐QRS forces, by altered septal and delayed right ventricular depolarization in complete RBBB. By definition, mean rightward and anterior late‐QRS amplitudes were significantly increased during RBBB, reflecting the delayed depolarization of the right ventricle.

The larger changes in mid‐QRS forces than in early‐QRS forces during RBBB are evident in the boxplots of Figures 1 and 2. Reduced amplitudes for SV1, RV5, and RV6 during RBBB were qualitatively noted by Gertsch; 5 these observations are quantified by our findings. Our data also indicate that absolute changes in mid‐QRS forces during RBBB generally are larger in the precordial leads than in the limb leads. This is consistent with a previous study of the effect of RBBB on the detection of LVH by Vandenberg et al., 4 who found limb lead voltage criteria for LVH during RBBB had higher sensitivities than did criteria using precordial lead voltages, particularly those that use right precordial S waves. Our findings quantify the marked reduction in amplitude of right precordial S waves during RBBB.

Effect of RBBB on Voltage Criteria Used for the Detection of LVH

Systematic reduction of leftward and posterior QRS amplitudes on the standard 12‐lead ECG during RBBB would systematically reduce the sensitivity of voltage criteria used for the detection of LVH. These are poor even in the presence of normal conduction, 10 , 11 , 12 , 13 and it is well recognized that performance of these criteria is even further reduced in the presence of RBBB. 3 In an early study of autopsied patients with RBBB, Booth et al. 14 found that the ECG detected LVH in only 1 of 15 patients. Other small series of autopsied patients have also shown decreased sensitivity of conventional voltage criteria for LVH detection in the presence of RBBB. 15 More recent studies using echocardiography as the gold standard for LVH also have demonstrated reduced sensitivity of ECG voltage criteria in the presence of RBBB. 4 , 6 , 7 , 8 Our findings quantify the reduction in leftward and posterior mid‐QRS amplitudes during RBBB that explain these observations. In our population, both Sokolow‐Lyon and Cornell voltage combinations were greatly reduced (5–7 mm, 500–700 μV) in the presence of RBBB. The effect of RBBB on Gubner‐Ungerleider voltage, which is entirely determined in the frontal plane, was less marked. This is consistent with the observation by Vandenberg et al. 4 that in the presence of RBBB, RI + S3 voltage had relatively maintained sensitivity for the detection of LVH. The relatively similar reduction in RV5 and RV6 during RBBB might be expected to maintain the ability of the RV5/RV6 ratio to detect LVH. This provides an explanation for the finding by Nalbantgil et al. 9 that this ratio remains relatively sensitive for the detection of echocardiographic LVH in RBBB patients with essential hypertension.

Detection of LVH During RBBB

Recognition and quantification of the systematic reduction in voltages used for the detection of LVH in patients with RBBB raises possibilities for criteria enhancement. Most simply, lower voltage thresholds for LVH might be developed directly from measurements of RBBB amplitudes in comparison with a gold standard method for determination of left ventricular mass. Such a direct approach might be confounded by the different magnitudes of the RBBB effect on voltages in the limb leads and in the precordial leads, and within planes on the voltages in the individual leads. Our linear regression data suggest an alternative method for estimating normal QRS voltage combinations in patients with RBBB, with separate lead amplitude correction before combination. On the other hand, the relative poor correlations between RBBB and normal morphology components of both Sokolow‐Lyon voltage (SV1) and Cornell voltage (SV3) may well limit the use of these standard voltage combinations for the detection of LVH in RBBB. Our findings suggest that criteria based on limb lead voltages and on left precordial R wave amplitudes may have more useful correlative value for this purpose. The potential applicability and value of these approaches requires focused testing in appropriate populations.

REFERENCES

  • 1. Agarwal AK, Venugopalan P. Right bundle branch block: Varying electrocardiographic patterns. Aetiological correlation, mechanisms and electrophysiology. Int J Cardiol 1999;71:33–39. [DOI] [PubMed] [Google Scholar]
  • 2. Schamroth L. The 12 Lead Electrocardiogram. Oxford , Blackwell Scientific, 1989. [Google Scholar]
  • 3. Chou TC. Electrocardiography in Clinical Practice, 5th Edition Philadelphia , WB Saunders, 2001. [Google Scholar]
  • 4. Vandenberg B, Sagar K, Paulsen W, et al Electrocardiographic criteria for diagnosis of left ventricular hypertrophy in the presence of complete right bundle branch block. Am J Cardiol 1989;63:1080–1084. [DOI] [PubMed] [Google Scholar]
  • 5. Gertsch M. The ECG: A Two‐Step Approach to Diagnosis. Berlin, Springer, 2004, pp. 117–124. [Google Scholar]
  • 6. De Leonardis V, Goldstein SA, Lindsay J Jr. Electrocardiographic diagnosis of left ventricular hypertrophy in the presence of complete right bundle branch block. Am J Cardiol 1988;62:590–593. [DOI] [PubMed] [Google Scholar]
  • 7. Vandenberg BF, Romhilt DW. Electrocardiographic diagnosis of left ventricular hypertrophy in the presence of bundle branch block. Am Heart J 1991;122:818–822. [DOI] [PubMed] [Google Scholar]
  • 8. Fragola PV, Autore C, Magni G, et al Limitations of the electrocardiographic diagnosis of left ventricular hypertrophy: The influence of left anterior hemiblock and right bundle branch block. Int J Cardiol 1992;34:41–48. [DOI] [PubMed] [Google Scholar]
  • 9. Nalbantgil I, Onder R, Kiliccioglu B, et al Electrocardiographic diagnosis of left ventricular hypertrophy in the presence of right bundle branch block in cases with essential hypertension. Angiology 1994;45:101–105. [DOI] [PubMed] [Google Scholar]
  • 10. Gubner R, Ungerleider H. Electrocardiographic criteria of left ventricular hypertrophy. Arch Int Med 1943;72:161–186. [Google Scholar]
  • 11. Sokolow M, Lyon T. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads. Am Heart J 1943;37:161–186. [DOI] [PubMed] [Google Scholar]
  • 12. Casale PN, Devereux RB, Alonso DR, et al Improved sex‐specific criteria of left ventricular hypertrophy for clinical and computer interpretation of electrocardiograms: Validation with autopsy findings. Circulation 1987;75:565–572. [DOI] [PubMed] [Google Scholar]
  • 13. Koito H, Spodick DH. Electrocardiographic RV6:RV5 voltage ratio for diagnosis of left ventricular hypertrophy. Am J Cardiol 1989;63:252–254. [DOI] [PubMed] [Google Scholar]
  • 14. Booth RW, Chou TC, Scott RC. Electrocardiographic diagnosis of ventricular hypertrophy in the presence of right bundlebranch block. Circulation 1958;18:169–176. [DOI] [PubMed] [Google Scholar]
  • 15. Murphy ML, Thenabadu PN, De Soyza N, et al Left atrial abnormality as an electrocardiographic criterion for the diagnosis of left ventricular hypertrophy in the presence of right bundle branch block. Am J Cardiol 1983;52:381–383. [DOI] [PubMed] [Google Scholar]

Articles from Annals of Noninvasive Electrocardiology : The Official Journal of the International Society for Holter and Noninvasive Electrocardiology, Inc are provided here courtesy of International Society for Holter and Noninvasive Electrocardiology, Inc. and Wiley Periodicals, Inc.

RESOURCES