Usefulness of Left Atrial Abnormality forPredicting Left Ventricular Hypertrophy

in the Presence of Left BundleBranch Block

Anurag Mehta, MD, Abnash C. Jain, MD, Mahaveer C. Mehta, MD, and Mike Billie

The objective of this study was to identify left atrial (LA)abnormality on the electrocardiogram and other relatedvariables as predictors of left ventricular (LV) hypertro-phy in the presence of left bundle branch block (LBBB). Inthe presence of complete LBBB, the diagnosis of electro-cardiographic abnormalities is problematic and that ofLV hypertrophy remains difficult. The usual electrocar-diographic criteria applied for the diagnosis of LV hy-pertrophy may not be reliable in the presence of LBBB.Therefore, noninvasive criteria will help physicians di-agnose LV hypertrophy with electrocardiography. LAabnormality on the electrocardiogram was assessed by2 independent observers as predictor of LV hypertrophyin the presence of LBBB in 120 patients, and data werecompared with those of 100 patients without LA abnor-mality. LV mass was calculated from echocardiographicdata. Besides LA abnormality, the other variables stud-ied for prediction of LV hypertrophy were gender, age,body surface area, body mass index, frontal axis, andQrS duration. Of the 6 criteria analyzed, the P terminalforce was found to be the most common and consistentcriterion to detect LA abnormality. LV hypertrophy wasconfirmed by echocardiographic determination of LVmass in both groups. Observers reliably differentiatedbetween the hypertrophied and normal-sized left ventri-cle in the presence of LBBB by correlating LA abnormalitywith LV mass determined by echocardiography. Ob-server 1 detected LA abnormality in 89% and observer 2in 84% of patients. False-positive results were present in

11% and 16%. The observer’s recognition of LA abnor-mality in the present study was 91%. The 2 observersshowed a sensitivity of 81% and 79% and a specificity of91% and 88%, respectively, when diagnosis of LV hy-pertrophy was determined. LV mass increased signifi-cantly and was diagnostic of LV hypertrophy in 92% ofpatients with LA abnormality. In the remaining 11 pa-tients (8%), the LA abnormality was of marginal abnor-mal magnitude. Each 0.01-mV/s increase in LA abnor-mality gave an increase of 30 g of LV mass. LV mass wasincreased in 86% of patients when corrected by bodysurface area. LV hypertrophy in the presence of LBBB onelectrocardiography was found in only 13 patients(10%) when the 6 frequently used conventional criteriafor diagnosis of LV hypertrophy by electrocardiographywere used. Regression analysis revealed LA abnormalityto be a strong independent predictor of increased LVmass. Multivariate analysis also revealed age, bodymass index, body surface area, frontal axis, and QrSduration to be significant predictors of LV mass. Thisnoninvasive study correlates LA abnormality by electro-cardiogram and LV hypertrophy with echocardiographyto conclude that LA abnormality was significantly diag-nostic of LV hypertrophy in the presence of LBBB. Age,body mass index, body surface area, frontal axis, andQrS duration were also significant predictors of LV mass.Q2000 by Excerpta Medica, Inc.

(Am J Cardiol 2000;85:354–359)

In the presence of complete left bundle branch block(LBBB), the diagnosis of electrocardiographic ab-

normalities is problematic1,2 and the criteria for thediagnosis of left ventricular (LV) hypertrophy remainunreliable.3 LBBB is associated with LV hypertrophyat autopsy in.90% of hearts studied.2 Various crite-ria of left atrial (LA) abnormality described by us andothers4–6 are recognized as markers of LV hypertro-phy and LV dysfunction.5–7 Echocardiography accu-

rately quantitates LV mass and detects LV hypertro-phy8,9 earlier than electrocardiography.10 This studyevaluates LA abnormality as an independent predictorof LV hypertrophy in the presence of LBBB by cor-relating electrocardiographic and echocardiographicdata.

METHODSPatient population: Electrocardiograms from 61,000

files of patients aged 16 to 83 years (mean 656 13) wereinterpreted from 1995 to 1998. Of the 220 patients(66 women, 30%) with complete LBBB, LA abnormal-ity was diagnosed in 120 patients (group 1) and datawere compared with 100 race-, age-, and sex-matchedpatients without LA abnormality (group 2). Patients wererandomly included whose electrocardiograms and echo-cardiograms were recorded for diagnostic evaluation onthe same day. LV mass was calculated from echocardio-

From the Department of Medicine, Section of Cardiology, West Vir-ginia University School of Medicine, Robert C. Byrd Health SciencesCenter, Morgantown, West Virginia. Manuscript received June 14,1999; revised manuscript received September 3, 1999, and ac-cepted September 6.

Address for reprints: Anurag Mehta, MD, Section of Cardiology,West Virginia University, 2203 Robert C. Byrd Health Sciences Cen-ter South, P.O. Box 9157, Morgantown, West Virginia 26506-9157.

354 ©2000 by Excerpta Medica, Inc. All rights reserved. 0002-9149/00/$–see front matterThe American Journal of Cardiology Vol. 85 February 1, 2000 PII S0002-9149(99)00746-8

graphic data. The other variables studied for predictionof LV hypertrophy were gender, age, body mass index(weight [kg]/height [m2]), body surface area, frontal axis,and QrS duration. According to Haskell et al,11 LVhypertrophy should be strongly considered in the pres-ence of LBBB if the QrS duration is.155 ms.

Left atrial abnormality criteria: With a hand lens,various criteria of LA abnormalities were studied: (1)P terminal force V1 5 0.04 mV/s4–7,9; (2) depth ofnegative phase of P V1 $1 mV4,5; (3) duration ofnegative phase of P V1 $40 ms5; (4) total P-waveduration$110 ms12; (5) interpeak duration of notchedP wave$40 ms13; (6) P-wave duration/PR interval$1.6.14 Of all 6 criteria of LA abnormalities, the Pterminal force V1 (92%) was found to be the mostcommon as well as the most consistent criteria of LAabnormality,4–6 and was used to resolve conflicts aris-ing due to use of multiple criteria for the inclusion ofpatients in this study (Figure 1).

Left bundle branch block criteria: LBBB criteriawere (Figure 1) (1) QrS interval measured$120 ms;(2) a slurred wide R wave in leads I, aVL, V5, V6; (3)slurred and broad S waves in V1 and V2 with absent orsmall r wave; (4) midconduction delay defined asnotching or a plateau in the mid-QrS; (5) ventricularactivation time.50 ms; (6) M-shaped QrS variantwith an occasional wide R in V5 and V6; (7) no initialQ wave over the left precordium; (8) absence ofpreexcitation; and (9) presence of intact atrioventric-ular conduction.15

LV hypertrophy criteria: The electrocardiographiccriteria used to diagnose LV hypertrophy were: (1)Lewis index16; (2) Sokolow Lyon index17; (3) frontalaxis; (4) R wave in aVL.13 mm18; (5) R wave in V5

or V6 .25 mm3; and (6) QrS duration.11 Romhilt’sscoring system19 was applied only to resolve anyconflicts due to use of multiple singular criteria.

Interobserver variability: To assess interobservervariability, 2 experienced electrocardiographers diag-nosed LA abnormality, LBBB, and LV hypertrophy.They were blinded to echocardiographic results andtheir diagnosis of LA abnormality and LV hypertro-phy were correlated and compared with LV massdetermined with echocardiography.

Echocardiographic studies: Echocardiography (M-mode and 2-dimensional) measured LV internal di-mension at end-diastole (LVID), posterior wall thick-ness (PW), and interventricular septum (IVS). Echo-cardiograms showing unambiguous high-qualityimages recorded at the peak of the R wave weredeemed technically adequate. Calculation of LV masswas done according to the Penn8 and American Soci-ety of Echocardiography conventions.20 A standardnomogram provided body surface area.21 The Pennconvention modified D3 formula8,20 estimated LVmass: LV mass5 1.04 [(LVID 1 IVS 1 PW)3 2(LVID) 3] 2 13.6.

As defined in the various echocardiographic stud-ies,22,23patients with LV mass.215 g (for women) or.225 g (for men) were classified as predicitve of LVhypertrophy. Using the same D3 formula, normal lim-its corrected for body surface area23 were 134 g/m2 inmen and 110 g/m2 in woman.10

Statistical analysis: Statistical analysis was per-formed using an analysis of variance and Student’sttest. Values are expressed as mean6 SD. The sensi-tivity and specificity of various electrocardiographic

FIGURE 1. An electrocardiogram of LBBB depicting LA abnormality as evaluated by various criteria: (1) P terminal force V1 5 0.04mV/s; (2) depth of negative phase of P V1 >1 mV; (3) duration of negative phase of P V1 >40 ms; (4) total P-wave duration >110ms; (5) interpeak duration of notched P wave >40 ms; (6) P-wave duration/PR interval >1.6. Of all the 6 criteria of LA abnormalityin this and other studies by us5,9 and others, P terminal force V1 (92%) was the most common and consistent criteria of LA abnormal-ity. Echocardiographic estimation of LV mass (mean 320 g) diagnosed LV hypertrophy.

ARRHYTHMIAS AND CONDUCTION DISTURBANCES/LA ABNORMALITY PREDICTS LV HYPERTROPHY BY ECG 355

criteria for LV hypertrophy were calculated using thestandard formulas;

Sensitivity 5true positives correctly diagnosed

total true positives3 100

Specificity 5true negatives correctly diagnosed

total true negatives3 100

Predictive Accuracy5true positives1 true negatives

total number of cases3 100

Univariable results were compared with controlsby pairedt test. Multivariable analysis was performedusing logistic regression and multiple regression anal-yses. Univariate, bivariate, and multivariate analysesand coefficient of correlation were done by Pearson’smoment/Spearman‘s correlation method using Statis-tica software (version 6.0, 1996, Tulsa, Oklahoma). Ap value,0.05 was considered significant.

RESULTSClinical diagnosis: There were 66 (55%) versus 50

(50%) patients with coronary artery disease in groups1 and 2. Coronary artery disease was diagnosed bycardiac catheterization, angiography, and or increasedcreatine kinase-MB levels. Of these patients 28 (23%)in group 1 versus 16 (16%) in group 2 had associatedmyocardial infarction, 18 (15%) versus 13 (13%) hadangina pectoris, 29 (24%) versus 16 (16%) had hy-pertensive heart disease (well-documented history ofchronically elevated blood pressure.145/95 mmHg), and 6 (5%) versus 4 (4%) had chronic obstructivepulmonary heart disease. Of the remaining 54 patientsin group 1 and 50 in group 2, 24 (20%) versus 18(18%) had hypertensive heart disease, 6 (5%) versus14 (14%) had chronic obstructive pulmonary heartdisease; 12 ([10%] aortic stenosis, 5; aortic regurgita-tion, 3; mitral regurgitation, 2; and mitral stenosis withmitral regurgitation, 2) versus 9 ([9%] aortic stenosis,3; aortic regurgitation, 2; mitral stenosis, 2; mitralstenosis with mitral regurgitation, 1; and mitral valveprolapse, 1) had valvular heart disease; 8 (7%) versus6 (6%) had cardiomyopathy and 4 (ventricular septaldefect, 2; patent ductus arteriosus, 1; atrial septaldefect with hypertension, 1) versus 3 (ventricular sep-tal defect, 2; and atrial septal defect, 1) had congenitalheart disease (Figure 2).

LV hypertrophy by electrocardiographic parameters:Six conventional criteria of LV hypertrophy accu-rately diagnosed LV hypertrophy in 13 patients (10%)in the presence LBBB.

Left atrial abnormality: In group 1, LA abnormalityranged from 0.04 to 0.12 mV/s (mean 0.076 0.024).In group 2 it ranged from 0.022 to 0.039 (mean0.0326 0.03). LA abnormality strongly predicts LVmass as shown by correlation coefficients (Table I)and bivariate as well as multivariate analyses (TablesI, II, and III).

Interobserver variability: Two expert electrocardio-graphers independently analyzed electrocardiogramsfor the presence or absence of LA abnormality in all220 patients included in this study. An evaluation ofthe interobserver variability for recognizing the pres-

ence of LA abnormality showed agreement in 109 of120 cases (91%; Figure 3). Their results were cross-checked by each other and by another expert electro-cardiographer. LA abnormality was independently di-agnosed by the observers in 89% and 84% of cases,with a false-positive diagnosis in 11% and 16% pa-tients, respectively. The discrepancies (11%) were set-tled by consensus.

Sensitivity and specificity: With LV hypertrophy de-fined earlier by echocardiography, the performance ofobservers 1 and 2 were expressed in terms of sensi-tivity and specificity compared with the diagnosis ofLV hypertrophy by electrocardiogram in patients withLA abnormality. Sensitivity was 81% and 79% andspecificity 91% and 88% for observers 1 and 2, re-spectively (Table IV).

FIGURE 2. Clinical diagnosis of the patients: CAD 5 coronaryartery disease; CHD 5 congenital heart disease; CMP 5 cardio-myopathy; CPD 5 cardiopulmonary disease; HTP 5 hyperten-sion; VHD 5 valvular heart disease.

356 THE AMERICAN JOURNAL OF CARDIOLOGYT VOL. 85 FEBRUARY 1, 2000

Left atrial abnormality correlated with LV mass:There was significant difference in LV mass betweenthe 2 groups. Mean LV mass for group 1 patients(Figure 3) was 3206 82 (3366 72 for men, 296666 for women), and it was significantly diagnostic ofLV hypertrophy in 92% patients in group 1 comparedwith 6% of patients in group 2. The remaining 9patients in group 1 had marginally increased LA ab-normality (0.04 to 0.042 mV/s), and LV mass was 198to 216 g in 6 men and 196 to 198 g in 3 women. Ingroup 2 it was 1826 78 (1886 64 in men, 1786 57in women). Corrected by body surface area, it was2286 42 in men and 1886 30 in women in group 1,and 1626 46 in men and 1326 42 in women ingroup 2. However, when corrected with body surfacearea, LV mass was still high in 86% patients with LAabnormality. These differences were statistically sig-nificant (p,0.001).

Regression analysis delineated (Figure 4) a strongcorrelation between LA abnormality and LV mass(r 5 0.92; n5 120). Each 0.01-mV/s increase in LAabnormality gave an increase of 30 g of LV mass.Multivariate analysis also revealed LA abnormality asan independent predictor for increased LV mass afteradjusting for age, body mass index, body surface area,left-axis deviation, and QrS duration. Multivariate

analysis found age, body mass index, body surfacearea, left-axis deviation, and QrS duration significantpredictors of increased LV mass in men and women(Table II) with LA abnormality compared with con-trols.

Although LV mass of.225 g in men or 215 g inwomen predicted LV hypertrophy independently, gen-der lacked significance in predicting LV mass on

TABLE I Mean 6 Standard Deviation and Correlation Coefficients of Variables Predicting LV Hypertrophy

LVM Age (yrs) BMI BSA Axis QrS-D

Control 182 6 78 64 6 10.6 26 6 7 1.8 6 0.4 30 6 2 144 6 10With LAA 320 6 82;

r 5 0.9266 6 11*;

r 5 0.8627 6 8*;

r 5 0.881.9 6 0.1*;

r 5 0.80250 6 25*;

r 5 0.84158 6 12;

r 5 0.82

*p ,0.05 (see text) (chi-square analysis).n 5 120 for all variables.Axis 5 frontal plane axis; BMI 5 body mass index; BSA 5 body surface area; LAA 5 LA abnormality; LVM 5 LV mass; QRS-D 5 QrS duration.

TABLE II Bivariate Analysis Depicts that LA AbnormalityStrongly (in both genders) Predicts LV Mass

For Both Sexes Men Women

Likelihood ratio 106.5* 64.0* 52.0*Pearson 88* 54.0* 47.0*

*p 5 0.0001.

TABLE III Multivariate Analysis Showing Significance WithVariables

Without LAAbnormality With LA Abnormality

Chi-Square p Value Chi-Square p Value

LA abnormality 0.1 0.09 10 0.001Gender 3.8 0.6 1.8 0.3Age 2.5 0.12 5.5 0.01BMI 0.02 0.8 11 0.02BSA 0.02 0.8 8 0.01Axis 2.4 0.15 6 0.04QrS duration 3.0 0.2 8 0.02

Abbreviations as in Table I.

FIGURE 3. Comparison of LV mass (LVM) between 2 groups ofpatients. LV mass (mean 6 SD of 320 6 82 g) increased signifi-cantly when LA abnormality was present by electrocardiographywith LBBB. Dotted lines show minimum levels at which LV hyper-trophy was diagnosed (215 g in women, 225 g in men) byechocardiography.

TABLE IV Sensitivity, Specificity, Predictive Value, andAccuracy of Electrocardiographic Criteria for the Diagnosisof LV Hypertrophy in the Presence of LBBB

CriteriaSensitivity

(%)Specificity

(%)

PredictiveValue(%)

Accuracy(%)

Sokolow Lyon index 8.4 62 56 55Lewis index 0 90 0 15R in aVL .13 mm 10 72 40 42R in V5/V6 .25 mm 0 98 0 46Mean QrS axis ,230° 30 47 43 38QrS-D .155 ms 56 72 62 60LA abnormality 80 89 88 78

D 5 duration.

ARRHYTHMIAS AND CONDUCTION DISTURBANCES/LA ABNORMALITY PREDICTS LV HYPERTROPHY BY ECG 357

multivariate analysis (Table III). Predictions werethen compared with those judged clinically on actualcomputations of LV mass by echocardiography. Thus,the prediction equation for LV mass based on LAabnormality was used to obtain a predicted LV massfor each patient by multiple regression analysis, andLA abnormality was found to be a strong predictor ofLV hypertrophy.

Age correlated with LV mass: The mean age was66 6 11 versus 646 10.6 in patients in groups 1 and2, respectively. Correlation coefficient between ageand LV mass in group 1 was r5 0.86, n5 120, andhad high predictive value when compared with thecontrol group.

Body mass index correlated with LV mass: Meanbody mass index were significantly different (276 8and 266 7; p ,0.02) and a correlation coefficient ofr 5 0.88, n5 120 was a high predictive value in group1 compared with group 2 patients.

Body surface area correlated with LV mass: Themean difference between body surface area was sig-nificant (1.96 0.1 vs 1.86 0.40; p,0.01), and thecorrelation coefficient was of high predictive value(r 5 0.80; n5 120) in group 1 patients versus con-trols.

Frontal axis correlated with LV mass: Left-axis devi-ation was significantly common in group 1 patients (48%vs 30%) and the mean axis was2506 25 versus 3062; p,0.04. Correlation coefficient strongly predicted LVhypertrophy (r5 0.84, n5 120).

QrS duration correlated with LV mass: QrS durationwas significantly more prolonged (.155 ms) in group1 patients (61% vs 9%; p,0.02). The mean QrSduration was 1586 12 versus 1446 10. The corre-lation coefficient of QrS duration was r5 82 and n5120 in group 1 patients and was highly predictive ofLV hypertrophy compared with group 2 patients.

DISCUSSIONThere is a need to diagnose LV hypertrophy, al-

though LBBB makes its accurate diagnosis difficult.

Autopsy studies found much larger hearts in patientswith than without LBBB.1,2,24The conventional crite-ria of diagnosis of LV hypertrophy during normalconduction have very low sensitivity in the presenceof LBBB.24 This has been demonstrated best by ex-amples in the same patients who met criteria of LVhypertrophy and later developed LBBB on electrocar-diography. Patients who had high QrS voltage sugges-tive of LV hypertrophy before developing LBBB hadlower QrS voltage after their electrocardiogramshowed LBBB.25 In the study by Zymslinski et al,24

most patients met criteria for LV hypertrophy beforeLBBB, but then were unable to meet voltage criteriafor LV hypertrophy after LBBB developed. With re-gard to the important quest to derive as much infor-mation as possible from simple noninvasive diagnos-tic techniques, we have already reported LA abnor-mality to be an accurate electrocardiographic criteriato predict LV hypertrophy in various conditions.6,9

Evaluation of data herein strongly suggests that LAabnormality predicts LV hypertrophy in the presenceof LBBB.

One of the primary mechanisms by which the leftventricle adapts to increased pressure or volume over-load is muscular hypertrophy. The degree of hyper-trophy parallels the severity of the increased load,which in turn also affects the left atrium producing LAabnormality.26,27Hypertrophy is a predictor of cardio-vascular events and mortality.28 LV hypertrophy ischaracterized by an increase in LV mass, and our datareveal that in patients with LA abnormalities in thepresence of LBBB, 92% had increased LV mass (i.e.,LV hypertrophy).

Some textbooks use the conventional electrocar-diographic criteria for the diagnosis of LV hypertro-phy in the presence of LBBB3,29but Scott and Norris1and Havelda et al2 independently concluded that thesecriteria had poor correlation to the anatomic LV hy-pertrophy found by autopsy. Furthermore, Scott andNorris1 found these criteria to be unreliable because ofthe high incidence of false-negative diagnoses. In thepresent series LV hypertrophy was diagnosed only in11% patients by 6 singular conventional electrocar-diographic criteria, and therefore is poor criteria to beused for diagnosing LV hypertrophy in the presence ofLBBB. In comparison, LA abnormality was a predic-tor of LV hypertrophy in 92% of patients.

Previous reports5,9 noted satisfactory observer rec-ognition of LA abnormality. Interobserver variabilityevaluation of LA abnormality formed a part of thisstudy and the results obtained from 2 expert indepen-dent observers were highly acceptable.

Data presented herein provide support that the di-agnosis of LA abnormality by electrocardiogram canbe used to identify LV hypertrophy from normalhearts in the presence of LBBB. LA abnormality wasfound in the presence of LBBB to be superior toconventional criteria of LV hypertrophy in the ab-sence of LBBB.30 This is further supported by sensi-tivity and specificity observed in this study. With useof multivariable analysis, age, body mass index, bodysurface area, left-axis deviation, and QrS duration

FIGURE 4. Regression line between LA abnormality and LV mass.Dotted lines show SD. PTF 5 p terminal force.

358 THE AMERICAN JOURNAL OF CARDIOLOGYT VOL. 85 FEBRUARY 1, 2000

were significantly, associated with LV mass. Dataherein suggest that LA abnormality is an independentpredictor of LV hypertrophy in the presence of LBBB.

Data in this noninvasive study conclude that in thepresence of LBBB by electrocardiogram, LA abnor-mality is an independent predictor of LV mass/LVhypertrophy. It remains a predictor of LV mass/LVhypertrophy even on correction by body surface area.Increase in age, body mass index, body surface area,frontal axis, and QrS duration also independently pre-dict increased LV mass.

Acknowledgment: We are grateful for the construc-tive criticism and statistical analysis generously pro-vided by Gerald Hobbs, Jr., PhD, Chief Statistics/Department of Community Medicine. West VirginiaUniversity.

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