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Goldberger’s Electrocardiographic Triad in Patients WithEchocardiographic Severe Left Ventricular Dysfunction

Christina Lopez, MDa,b, Camelia C. Ilie, MDa,b, D. Luke Glancy, MDa,b,*, andRoberto E. Quintal, MD, PhDa,b

In 1982, Goldberger described an electrocardiographic triad (SV1 or SV2 � RV5 or RV6>3.5 mV, total QRS amplitude in each of the limb leads <0.8 mV, and R/S ratio <1 in leadV4) that was 70% sensitive and >90% specific for detecting severe left ventricular (LV)dysfunction. To confirm his sensitivity results, in 51 consecutive patients (36 men) aged 28to 84 years (mean 56) with LV ejection fractions <20%, the electrocardiographic triad wassought in the electrocardiogram (ECG) recorded closest in time to the echocardiographicstudy. All 51 patients had systemic arterial hypertension. Evidence of ischemia was presentin 7 and absent in 38, and in 6 patients, ischemic status was unknown. In 49 patients, NewYork Heart Association functional class was available: class II in 8, class III in 32, and classIV in 9. LV ejection fractions ranged from 4% to 20% (mean 14%), and LV internalend-diastolic diameters ranged from 5.7 to 8.6 cm (mean 6.6). Left atrial anteroposteriordiameters ranged from 2.9 to 6.1 cm (mean 4.7) and were >4.0 cm in 47 of the 51 patients.The right ventricular cavity was enlarged in 22 patients. SV1 or SV2 � RV5 or RV6 was>3.5 mV in 29 of the 51 ECGs; total QRS amplitude was <0.8 mV in each of leads I, II,and III in 10; and the R/S ratio was <1 in lead V4 in 37. Only 1 of the 51 ECGs met all 3criteria. In contrast to Goldberger’s finding of the triad to be 70% sensitive for severe LVdysfunction, in this study, the triad was found to be only 2% sensitive. The difference islikely due to his patients’ having idiopathic dilated cardiomyopathy, whereas those in thisstudy had hypertensive cardiomyopathy with or without ischemia. Also, in this study, 1specific ECG was used for each patient, whereas Goldberger reviewed all of the patients’ECGs looking for the triad. In conclusion, Goldberger’s triad is a sensitive or insensitivemarker for severe LV dysfunction depending on the patient population and the number ofECGs reviewed. © 2012 Elsevier Inc. All rights reserved. (Am J Cardiol 2012;109:

914–918)

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Thirty years ago Goldberger1 described an electrocardio-raphic triad (SV1 or SV2 � RV5 or RV6 �3.5 mV, total

QRS amplitude �0.8 mV in each of the extremity leads, andR/S ratio �1 in lead V4) with high specificity and sensitivityor severe left ventricular (LV) dysfunction. The triad ap-eared to be have positive predictive value �90% andpecificity �90% for severe LV dysfunction in controls andatients with a wide variety of cardiac diseases. The sensi-ivity of 70%, however, was determined solely in a group ofatients with idiopathic dilated cardiomyopathy.1 This studyas undertaken to assess the sensitivity of the triad in aifferent group of patients. Although currently echocardi-graphy is the prime tool for assessing LV function, the lessxpensive electrocardiographic study, if it has high sensi-ivity and specificity for detecting LV dysfunction, can helpuide the use of echocardiography.

aSection of Cardiology, Department of Medicine, Louisiana State Uni-versity, Health Sciences Center; and bSection of Cardiology, Departmentf Medicine, Interim LSU Public Hospital, New Orleans, Louisiana. Man-script received August 1, 2011; revised manuscript received and acceptedctober 28, 2011.

*Corresponding author: Tel: 504-450-5530; fax: 504-568-2127.

E-mail address: dglanc@lsuhsc.edu (D.L. Glancy).

002-9149/12/$ – see front matter © 2012 Elsevier Inc. All rights reserved.oi:10.1016/j.amjcard.2011.10.053

ethods

In 51 consecutive patients (36 men) aged 28 to 84 yearsmean 56) with LV ejection fractions (LVEFs) �20%,oldberger’s ECG triad (SV1 or SV2 � RV5 or RV6 �3.5

mV; total QRS amplitude in each of leads I, II, and III �0.8mV; and R/S ratio � 1 in lead V4) was sought in thelectrocardiogram (ECG) recorded closest in time to thechocardiographic study. Our not using all 6 extremity leadsor the second criterion, as Goldberger did, would, if any-hing, tend to increase the sensitivity of the triad.

Echocardiographic measurements and calculations wereade according to the recommendations of the American So-

iety of Echocardiography.2 Specifically, LV relative wallthickness (RWT) was calculated as 2 � LV diastolic posteriorwall thickness (WT)/LV diastolic internal diameter, and LVmass was calculated as 0.8 � {1.04[(LV diastolic internaldiameter � diastolic posterior WT � diastolic septal WT)3 �LV diastolic internal diameter)3]} � 0.6 g.

All 51 patients had diagnoses of systemic arterial hyper-tension, and 17 had diabetes mellitus. In 49 patients, NewYork Heart Association functional class was available: classII in 8, class III in 32, and class IV in 9. All 51 patients werebeing treated for cardiovascular disease. Evidence of isch-emia was present in 7 patients and absent in 38, and isch-

emic status was unknown in 6.

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915Methods/ECG Assessment of LV Systolic Dysfunction

Results

LVEFs ranged from 4% to 20% (mean 14%), and LVinternal diameters in diastole ranged from 5.7 to 8.6 cm(mean 6.6) and were higher than the reference ranges (3.9 to5.3 cm for women and 4.2 to 5.9 cm for men)2 in all 15women and 32 of the 36 men. Diastolic LV posterior WTsranged from 0.7 to 2.2 cm (mean 1.12), and diastolic ven-tricular septal WTs ranged from 0.5 to 1.9 cm (mean 1.10).Compared to reference ranges for gender (0.6 to 0.9 cm forwomen and 0.6 to 1.0 cm for men),2 LV posterior WTs wereormal in 19 patients and higher than normal in 32, andeptal WTs were lower than normal in 1 patient, normal in3, and higher than normal in 37. RWTs ranged from 0.20o 0.75 (mean 0.34). Compared to reference ranges forender (0.22 to 0.42 for women and 0.24 to 0.42 for men),2

RWTs were normal in 42 patients, low in 3, and high in 6.LV mass indexed to body surface area ranged from 82.5 to339.5 g/m2 (mean 178.3). Compared to reference ranges forgender (43 to 95 g/m2 for women and 49 to 115 g/m2 for

en),2 LV mass index was normal in 3 patients and elevatedin 48, severely so in 35 of these. A comparison of RWTwith LV mass index categorized the geometry of the leftventricle as normal in 3 patients, concentric hypertrophy in6, and eccentric hypertrophy in 42.2 Left atrial anteropos-

Figure 1. ECG from a 62-year-old man with an LVEF of 4%, an LV interncm. This patient was the only 1 of our 51 patients to meet all 3 of Goldbstudy. The average S wave in lead V2 (1.6 mV) plus the average R wave iIII was �0.8 mV. The R/S ratio in lead V4 was �1. Other findings were sechocardiography 5.2 cm), and repolarization changes of LV enlargement.striking voltage criteria for LV hypertrophy (SV2 � RV5 � 8.2 mV), witere had 1 (Figure 2) and 2 (Figure 3) of Goldberger’s criteria, respectivel

terior diameters ranged from 2.9 to 6.1 cm (mean 4.7), and (

were �4.0 cm in 47 of the 51 patients. The right ventricularcavity was enlarged in 22 patients.

In 29 of the 51 ECGs, SV1 or SV2 � RV5 or RV6 was3.5 mV; total QRS amplitude was �0.8 mV in each of

eads I, II, and III in 10 studies; and the R/S ratio was �1n lead V4 in 37 studies (Figures 1 to 3). Only 1 of the 51CGs met all 3 of Goldberger’s criteria (Figure 1). Com-lete left bundle branch block was present in 10 of the 51atients, incomplete left bundle branch block in 2, andonspecific intraventricular conduction defects in 2.

The sensitivity of Goldberger’s electrocardiographicriad for identifying an echocardiographically determinedVEF �20% in this study was 2%. The specificity andegative predictive value could not be calculated, becausehere could be no true-negatives (i.e., LVEFs �20%). Theositive predictive value was 100%; the only positive find-ng was a true-positive finding.

Because the component of Goldberger’s triad least fre-uently reached was total QRS amplitude �0.8 mV in eachf leads I, II, and III, the breakpoint was arbitrarily in-reased to �1.1 mV, and the number of ECGs with leads I,I, and II equal to or lower than this breakpoint increasedrom 10 to 25. The number of ECGs meeting all 3 ofoldberger’s criteria, however, increased only from 1 to 5

eter in diastole of 6.6 cm, and septal and posterior WTs in diastole of 1.1criteria in the ECG recorded closest temporally to the echocardiographic.0 mV) equaled 3.6 mV. The total QRS voltage in each of leads I, II, andhycardia, left atrial enlargement (left atrial anterior-posterior diameter onliest ECG in this patient was recorded 7 years before this one and showedher abnormality. Two ECGs recorded �6 months before the ECG showning out how data will differ depending on how many ECGs are examined.

al diamerger’sn V6 (2inus tacOur earh no ot

i.e., from 2% to 10% of the 51 patients).

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Discussion

In the retrospective portion of his study (27 patients withidiopathic congestive cardiomyopathy, 100 normal subjects,and 30 patients with severe aortic valve disease but normalLVEFs), Goldberger1 found his triad to have specificity of100%, sensitivity of 70%, positive predictive value of100%, and negative predictive value of 94% for severe LVdysfunction (LVEF �35%). In the prospective portion ofthe study, he discovered the triad in 32 of 2,000 consecutiveECGs (1.6%), and 29 of these 32 patients had evidence ofsevere LV dysfunction, for a positive predictive value of91%. Thus, Goldberger described findings more specificthan sensitive, a point he emphasized in a subsequent re-port3 and a situation that is true for most eponymous find-ngs. Nevertheless, 70% is high value for sensitivity.

Why then did we find the triad in only 1 of 51 patientsith severe LV dysfunction, for a sensitivity of 2%? There

re several potential answers. Goldberger1 actually de-cribed the electrocardiographic triad as being associatedith congestive heart failure, and in his retrospective androspective analyses, LV dysfunction was the dominanteature. In the retrospective portion of his study, from whichensitivity data were derived, all patients with true-positivendings had idiopathic dilated cardiomyopathy.1 As Hamby

and Raia4 had pointed out before Goldberger, and as he3 andthers5–9 subsequently showed, the ECGs of patients withdiopathic dilated cardiomyopathy show a transverse/frontallane voltage ratio that is higher than normal and above theatio in patients with ischemic cardiomyopathy.3,7,8 Gold-

Figure 2. An ECG, recorded 6 months earlier in the same patient whose tin lead V4). In addition, sinus tachycardia and changes of biatrial and LV

berger’s triad expresses this transverse/frontal plane voltage

discordance, as well as the posterior rotation of the QRSvector that occurs with marked LV enlargement (i.e., R/Sratio �1 in lead V4).

Although the cause of dilated cardiomyopathy is oftenmultifactorial, the dominant feature in our patients is thehistory of systemic arterial hypertension in each of them.Two recent studies of patients initially having concentricLV hypertrophy and normal LVEFs on echocardiography,who were followed for mean and median periods of 2.75and 7.5 years, showed progression to LV dysfunction of13% and 20%, respectively.10,11 The mean systolic systemicarterial pressure at baseline was elevated, 146 mm Hg10 and153 mm Hg,11 in each study. Compared to patients who

aintained stable LVEFs, those whose LVEFs decreaseduring follow-up had slightly lower LVEFs,10,11 higher di-

astolic and systolic LV internal diameters,10,11 lowerRWTs,10,11 higher systemic arterial impedance,10 and lon-er QRS durations10 at baseline. The differences were even

larger at follow-up.10,11 Interval myocardial infarction wassignificantly more common in those who progressed toreduced LVEFs than in those whose LVEFs remained sta-ble.10,11 Nevertheless, Milani et al10 found that 8% of theirpatients without interval infarcts progressed to low LVEFsduring their study’s mean follow-up of 2.75 years.

In Krishnamoorthy et al’s11 study, and possibly in that ofMilani et al,10 most patients who developed reduced LVEFswere classified as having concentric LV hypertrophy be-cause their left ventricles were not grossly dilated. Never-theless, compared to the patients with stable LVEFs, their

s shown in Figure 1, meets only 1 of Goldberger’s criteria (R/S ratio �1ll) enlargement can be seen.

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LV diameters were increased and their RWTs were de-

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917Methods/ECG Assessment of LV Systolic Dysfunction

creased at baseline, and the differences were more markedat follow-up. It is quite possible that if their LVEFs decreasefurther from �50% with only 7 of 45 patients �30%11 anda mean of 36%10 to �20% (mean 14%) as in our patients,the LV geometry will indicate eccentric hypertrophy, as itdid in most of our patients. Despite the preponderance ofeccentric hypertrophy in our patients, LV posterior WTswere higher than normal in 32 of the 51 patients, and septalWTs were higher than normal in 37.

Goldberger’s1 evaluation of his patients with idiopathicongestive cardiomyopathy was clinical and angiographic,nd assessments of LV WT and right ventricular chamberize were not available. Pathoanatomic5 and echocardio-

graphic12,13 studies of idiopathic dilated (congestive) car-iomyopathy have shown the right ventricle, as well as theeft, to be dilated in all5 or nearly all12,13 of the patients.

Echocardiographic studies have shown normal or decreasedventricular septal and LV posterior WT.12,13 Dilatation ofoth ventricles and normal to decreased LV WT are prob-bly the anatomic substrate of the increase in transverselane and decrease in frontal plane QRS voltages describedy Goldberger in idiopathic dilated cardiomyopathy.1,3 That

most of our patients had increased ventricular septal and LVposterior WTs and only a minority had right ventriculardilatation probably, in large part, accounts for only 10 of ourpatients having decreased frontal plane QRS voltage andonly 1 of the 51 having all 3 elements of Goldberger’s triad.

Our analyses were made on the ECGs recorded in clo-

Figure 3. An ECG recorded in the same patient between the tracings shownf leads I, II, and III �0.8 mV and R/S ratio �1 in lead V4). Sinus tachycaeen.

sest temporal proximity to the echocardiographic studies,

whereas Goldberger1 included patients if any of their ECGsrevealed the triad, a factor that would have increased thesensitivity, as shown in Figures 1 to 3. We and others haveound Goldberger’s triad1 and his transverse/frontal plane

QRS voltage ratio3 useful in recognizing cases of idiopathicilated cardiomyopathy with 4-chamber enlargement.14,15

The sensitivity of the triad for recognizing LV dysfunctionof other causes, however, is probably low and may depend,in part, on the number of ECGs examined.

This study had a number of limitations. First, it was aretrospective study attempting to correlate echocardio-graphic data with electrocardiographic and clinical data, andclinical data reviewed retrospectively are virtually never ascomplete as those collected in a planned prospective fash-ion. Second, we compared our echocardiographic LV ana-tomic and functional data with LV data collected primarilyangiographically in a study done 30 years ago. Finally, weassessed the sensitivity of just 1 set of electrocardiographiccriteria, albeit the gold-standard set, for detecting LV dys-function, without quantitatively addressing specificity orsuggesting a new set of criteria. Nevertheless, in attemptingto broaden the scope of the inexpensive, noninvasive elec-trocardiographic study, we think it important to define itsboundaries.

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ures 1 and 2 meets 2 of Goldberger’s criteria (total QRS amplitude in eacht atrial enlargement, and the Cornell criteria for LV enlargement are again

in Figrdia, lef

PA, Picard MH, Roman MJ, Seward J, Shanewise JS, Solomon SD,

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3. Goldberger AL, Dresselhaus T, Bhargava V. Dilated cardiomyopathy:utility of the transverse:frontal plane QRS voltage ratio. J Electrocar-diol 1985;18:35–40.

4. Hamby RI, Raia F. Electrocardiographic aspects of primary myocar-dial disease in 60 patients. Am Heart J 1968;76:316–328.

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7. Momiyama Y, Mitamura H, Kimura M. ECG differentiation of idio-pathic cardiomyopathy from coronary artery disease with left ventric-ular dysfunction. J Electrocardiol 1995;28:231–236.

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