3 Ventricular Enlargement - Chuyện y khoa · ated 10 ECG criteria for detecting LVH using ECG and echocardiographic measurements from 3351 adults.24 The best performer for evaluating

3 Ventricular Enlargement

Left Ventricular Enlargement(Hypertrophy and Dilation)VoltageIntrinsicoid DeflectionRepolarization AbnormalitiesOther ECG Changes in LVHPhysiologic Factors Affecting theReliability of Diagnostic Criteria

Pathologic States Affecting the Diagnosisof LVH

Assessment of the Severity of ValvularLesions Causing LVH

Presence of LBBB

Right Ventricular Hypertrophy andDilationThree Types of RVHRVH in Other Clinical Conditions

Combined Ventricular HypertrophyClinical and Anatomic Correlations

Before the advent of noninvasive methods capableof accurately estimating the dimensions, mass, andwall motion of cardiac chambers, electrocardiogra-phy in association with chest radiography andphysical examination played a prominent role inassessing the size of the cardiac chambers. Theelectrocardiographic theory underlying the recog-nition of hypertrophy or dilation rests on a numberof sound physical principles thatmay lead tomean-ingful correlations with the tissue mass, chamberdiameter, and intracardiac blood volume.1 Thereare, however, unavoidable limiting factors relatedto the variable orientation of the heart in the chest,variable properties of the volume conductor sur-rounding the heart, and nonspecificity of eachdepolarization and repolarization abnormalityused for diagnosing hypertrophy or dilation.

As early as the 1950s and 1960s a wealth ofautopsy and angiographic correlations firmly estab-lished the limits of the diagnostic accuracy of theelectrocardiogram (ECG). With regard to left ven-tricular hypertrophy (LVH), it has been establishedthat the ECG diagnosis is most accurate in patientswith hypertensive and pure left-sided valvularheartdisease in the absence of concomitant right ven-tricular hypertrophy (RVH), myocardial infarc-tion, intraventricular conduction disturbances,and treatment with drugs altering depolarizationand repolarization. Similar limiting factors play arole in the ECG diagnosis of RVH.

Left Ventricular Enlargement(Hypertrophy and Dilation)

In general, ECG criteria for the diagnosis of left ven-tricular enlargement are increased QRS amplitude

(voltage), intraventricular conduction delay mani-fested by delayed intrinsicoid deflection in theprecordial leads facing the left ventricle, widenedQRS/T angle, and a tendency to left axis deviation(Figure 3–1).

VOLTAGE

The increased voltage is attributed to one or moreof the following factors: increased left ventricularmass, increased left ventricular surface, increasedintracavitary blood volume, and close proximityof the enlarged ventricle to the chest wall.

Left Ventricular Mass

The increase in the left ventricular mass exagge-rates the leftward and posterior QRS forces.An increase in voltage may be due to theincrease in the number2 or size3 of the fibersin the hypertrophied ventricle. The importanceof fiber size was shown in the computer-gener-ated ECG model where the amplitude of the Rwave increased by 36 percent when the cellradius was increased by 15 percent withoutincreasing the number of cells.3 The enlargedcells and increased number of intercalated disksin the hypertrophied myocardium are believedto facilitate the intercellular current flow, whichmay be expected to increase the strength of theequivalent dipole generated by excitation ofmuscle layers. Consistent with this hypothesiswas the finding of increased voltage recordedin the intramural electrograms from a hypertro-phied human heart.4

In the presence of “pure” LVH (e.g., in chil-dren and young adults with isolated congenital

45

aortic stenosis), the maximum spatial QRS vectorsignificantly correlated with the peak left ventricu-lar systolic pressure.5 Because the QRS duration inthis patient group was not increased, the increasedvoltagewas believed to reflect an increased numberof fibers in the hypertrophied myocardium.2 Inmiddle-aged and elderly patients, a significant cor-relation was observed between the QRS voltageand the left ventricular mass estimated from angio-grams6 and echocardiograms.7–9

Myocardial Surface

Hypertrophy increases the area of ventricularmuscle in relation to the short-circuiting fluidsurrounding the heart.10 Increased surface areaand wall thickness may be expected to increasethe solid angle subtended by the precordial elec-trodes (see Chapter 1).

In a study of left ventricular angiograms in93 patients with LVH, wall thickening sufficientto result in an increased left ventricular massdid not result in increased QRS voltage indica-tive of LVH unless sufficient concurrent chamberdilation was present.11 This implied that there isa critical role for the geometric relation betweenwall thickness and chamber dilation, as wouldbe expected from application of the solid angletheorem. However, a strict correlation betweenthe left ventricular dimension and QRS voltageis not a universal finding. Thus Devereuxet al.12 found that the QRS voltage correlatedonly weakly with the size of the left ventricularchamber; for a given left ventricular mass, it

depended less on chamber dilation than on leftventricular weight, the depth of the left ventriclein the chest, and the patient’s age.

Intracavitary Blood Volume

The QRS amplitude may be expected to increasein the presence of an increased end-diastolicblood volume owing to a mechanism postulatedby Brody.13 The Brody effect predicts that anincrease in the intracardiac blood volume aug-ments the initial (i.e., radial) QRS vectors andattenuates the late (i.e., tangential) QRS vectors.The validity of this principle was documentedby correlating the R wave amplitude with theleft ventricular volume, which was altered bypacing the heart at various rates.14 Numerousstudies using ventricular angiography,6 nuclearimaging,15,16 and echocardiography8 have shownthat the correlation of the QRS voltage with the leftventricular volume was either poor or not as goodas the correlation with the left ventricular mass.

Proximity of the Heart to the Chest Wall

Feldman et al.17 have shown that the R waveamplitude increased as the left ventricular lateralwall moved closer to the V5 and V6 electrodesand that the proximity of the left ventricle to theanterior chest wall was a major determinant ofthe R wave amplitude. Moreover, echocardio-graphic studies showed that the correlationbetween the ECG criteria for LVH and left ventric-ular mass calculated from the echocardiogram

Figure 3–1 Typical left ventricular hypertrophy (LVH) pattern with secondary ST segment and T wave changes in a67-year-old man with long-standing hypertension, bilateral carotid artery disease, bilateral renal artery disease, nonobstruc-tive three-vessel coronary artery disease, and severe LVH but no history of myocardial infarction and no wall motionabnormalities. Q wave in lead III exemplifies a pseudoinfarction pattern. Note also the left atrial enlargement. PR interval,220 ms; QRS, duration 102 ms; QTc, 415 ms.

46 SECTION I � Adult Electrocardiography

could be improved by correcting for the distanceof the center of the left ventricular mass from thechest wall.18

INTRINSICOID DEFLECTION

In about 35 to 90 percent of LVH cases, thedelayed onset of intrinsicoid deflections occurs�45 ms after the onset of the QRS complex,10

which may be due to late activation of the hyper-trophied left ventricle. The finding is not specific,however, because late ventricular activation insubjects with LVH also correlated with rightventricular thickness.19

REPOLARIZATION ABNORMALITIES

Deviation of the ST segment and the Twave in thedirection opposite to the main QRS vector in thehorizontal and frontal planes causes widening ofthe QRS/T angle. The combination of increasedQRS amplitude and a wide QRS/T angle resultsin a pattern known as left ventricular strain. Eventhough the term “strain” is not appropriate tocharacterize an electrical event, use of this termhas become entrenched in clinical practice. TheST and T changes in the left ventricular strainpattern are secondary to delayed propagation ofthe impulse in the conducting system, the hyper-trophied myocardium, or both (see Chapter 23).

Diagnostic Criteria for Patients Aged40 Years or Older

In most studies, high voltage in the precordialleads was the most sensitive criterion for thediagnosis of LVH. A recognition rate of up to56 percent may be achieved, although it also

was most frequently responsible for false-positivediagnoses.

If the duration of the QRS complex is <0.12second, the following criteria are used for thediagnosis of LVH. They are based mainly on thestudies of Sokolow and Lyon.20

The limb lead criteria are as follows:1. R wave in lead I þ S wave in lead III

>2.5 mV2. R wave in aVL >1.1 mV3. R wave in aVF >2.0 mV4. S wave in aVR >1.4 mVPrecordial lead criteria are as follows:5. R wave in V5 or V6 >2.6 mV6. R wave in V6 þ S wave in V1 >3.5 mV7. Largest R wave þ largest S wave in the

precordial leads >4.5 mVThe most commonly used voltage criteria in

the more recent literature are as follows:

S in V1 þ R in V6 >3.5 mVS in V2 þ R in V6 >4.3 mVS in V1 >2.4 mVS in V6 >2.8 mVR in aVL >1.3 mV

in addition to the Cornell criteria of:R in aVL þ S in V3 >2.0 mV for femalesand >2.8 mV for males

Supporting criteria include the following:8. Onset of the intrinsicoid deflection in V5

or V6 �0.05 second9. ST segment depression and T wave inver-

sion in the left precordial leads and inthe limb leads in which major QRS deflec-tion is upright in the presence of one ormore of the above findings

Romhilt and Estes21 proposed a point-scoresystem that uses a combination of the variousfindings listed in Table 3–1. LVH is considered

TABLE 3–1 Point-Score System

Measurement Points

Amplitude: any of the following 3Largest R or S wave in the limb leads �20 mmS wave in V1 or V2 �30 mmR wave in V5 or V6 �30 mmST segment and T wave changes (typical pattern of leftventricular strain with the ST segment and T wave vector shiftedin a direction opposite to the mean QRS vector)

Without digitalis 3With digitalis 1Left atrial involvement: terminal negativity of the P wavein V1 is �1 mm in depth with a duration of �0.04 second

3

Left axis deviation of �30 degrees or more 2QRS duration �0.09 second 1Intrinsicoid deflection in V5 and V6 �0.05 second 1

473 � Ventricular Enlargement

present if the points total 5 or more and is prob-ably present if the points total 4.

Echocardiographic Criteria

Casale et al.22 used the echocardiographicallydetermined left ventricular mass measurementsin 414 subjects as a standard to develop newECG criteria for LVH and tested various corre-lations prospectively in an additional 129subjects. The best criteria consisted of a combi-nation of the sum of R amplitude in aVL and Samplitude in V3 to be >2.8 mV in men and>2.0 mV in women, associated with increasedT wave amplitude in lead V1. This combinationhad a sensitivity of 49 percent and a specificityof 93 percent, which was better than the respec-tive values of 33 percent and 94 percent for theSokolow-Lyon voltage criteria and 30 percentand 93 percent for the Romhilt-Estes score of4 points or more. In the same study, ECG cri-teria based on a multiple logistic regressionequation developed in the learning series andtested prospectively achieved 51 percent sensi-tivity, 90 percent specificity, and 76 percentoverall accuracy for diagnosis of LVH. Theinnovative feature of these criteria is the separa-tion by gender. A more accurate correlation wasfound subsequently using the product of eitherthe Cornell voltage or 12-lead voltage systemand the QRS duration.23

Framingham Heart Study investigators evalu-ated 10 ECG criteria for detecting LVH usingECG and echocardiographic measurements from3351 adults.24 The best performer for evaluatingmen was the Cornell voltage criterion multipliedby the QRS duration; for women, it was the volt-age criteria in the limb leads. The sensitivity ofthe best criteria was about 95 percent, and thespecificity varied from 32 to 51 percent. Theauthors found also that incorporation of obesityand age in gender-specific ECG algorithms con-sistently enhanced their performance for detect-ing hypertrophy.

Sensititivity and Specificity of CombinedCriteria

To evaluate the sensitivity of the combined cri-teria, Scott and associates25 studied 100 casesof isolated LVH with increased heart weightand left ventricular wall thickness at autopsy.Using one or more of the criteria listed previ-ously (except criterion 7), 85 percent of thecases were correctly diagnosed. In this study,however, ST segment and T wave changes alonewere also considered as indicative of LVH. Intwo later investigations26,27 the sensitivities were60 percent and 85 percent, respectively.

To test the specificity of listed criteria (exceptcriterion 7), Chou et al.28 reviewed the autopsyfindings of 100 cases diagnosed as LVH by ECGless than 3 months before death. Cases with STsegment and T wave changes alone were notincluded. Taken together, 44 cases had isolatedLVH, and 45 had combined ventricular hypertro-phy. A false-positive diagnosis of LVH was madein 11 cases (11 percent). Selzer and associates27

reported a slightly higher incidence (15 percent)of false-positive diagnoses. The point-score sys-tem,21 tested in 360 autopsied hearts by thechamber dissection technique, gave a sensitivityof 54 percent, with only 3 percent false-positivediagnoses.

Sensitivity and Specificity of IndividualCriteria

Mazzoleni and co-workers29 examined the reli-ability of several of the individual criteria inthe autopsied hearts with the chamber dissectiontechnique. In 185 unselected adult patients, ana-tomic LVH was recognized in 22 percent by thecriterion RV5 or V6 þ SV1 >3.5 mV and in 17percent by the criterion RaVL >1.0 mV.

A group of Cornell investigators30 correlatedantemortem ECGs with a left ventricular massat autopsy in 220 patients. LVH was defined asan LV mass index > 118 g/m 2 in men and>104 g/m 2 in women . They fo und that the prod-uct of the QRS duration and a 12-lead voltage(voltage-duration product) identified LVH moreaccurately than the voltage criteria alone, QRSduration criteria alone, or the Romhilt-Estespoint score.

One of the most extensive anatomic correlationstudies using the chamber dissection techniquewas conducted by Romhilt and associates.32 A totalof 33 ECG criteria for LVH were evaluated. Themost sensitive (45 percent) was the R þ S ampli-tude >4.5 mV. In other studies, increased QRSvoltage correlated to variable degrees with thesum of the thickness of the septum and theposterior wall,33–35 the posterior wall thicknessalone,36 or the calculated left ventricular mass.37

ST Segment and T Wave Changes

The two most commonly used repolarization cri-teria for the diagnosis of LVH are a QRS/T angle>100 degrees and a Twave that is upright in V2

and more negative than �0.1 mV in V6. Theclassic ST and T wave changes in LVH consistof ST segment depression with upward convexityand T wave inversion in the left precordial leads(Figures 3–1 to 3–4). Reciprocal changes arepresent in the right precordial leads with ST


segment elevation and a tall T wave. In the limbleads, the direction of the ST and T vectors isalso directed opposite to the main QRS forces.Therefore ST segment depression and T waveinversion are seen in leads I and aVL when theQRS axis is horizontal and in leads II, III, andaVF when the QRS axis is vertical. These classicST and T wave changes are usually found inpatients with fully developed LVH.

If high QRS voltage and the secondary repo-larization changes are both present, a false-positive diagnosis of LVH is seldom made.27 Lesspronounced repolarization changes, such as

slight ST segment depression or flat T waves inthe left precordial leads, which usually precedefrank ST segment deviation and Twave inversionduring development of LVH, are also helpful,particularly when the voltage is increased.

A common diagnostic difficulty encounteredin practice is recognition of the ST segment andTwave abnormalities caused by myocardial ische-mia in the presence of the left ventricular strainpattern in patients with high-voltage QRS com-plexes suggestive of LVH. In theory, if the QRSarea is strictly proportional to the ventricularmass and if the hypertrophy does not alter the

Figure 3–2 Typical left ventricular hypertrophy pattern with sharply inverted T waves suggestive of myocardial ischemiain a 78-year-old woman with hypertensive heart disease, intermittent atrial fibrillation, nonobstructive coronary artery dis-ease, and no history of myocardial infarction suggested by the Q wave in aVL. There is poor R wave progression and leftatrial enlargement. PR interval, 183 ms; QRS duration, 74 ms; QTc, 403 ms.

Figure 3–3 Left ventricular hypertrophy (LVH) with inverted U waves in a 33-year-old man with severe hypertension,cardiomegaly, and congestive heart failure. ECG shows high QRS voltage and notching of the R wave in lead V3. Withthe addition of ST segment and T wave changes, the tracing is highly suggestive of LVH. U waves are inverted in leadsV4–V6 and perhaps in leads V2 and V3. The P waves suggest left atrial enlargement.


relation between the sequence of repolarizationand the sequence of activation, the ventriculargradient should remain unchanged. This patternoccurs with uncomplicated hypertrophy, but thegradient does change when the ST and T wavechanges are due to associated myocardial ische-mia, which may be present even in the absenceof coronary artery disease because of the follow-ing: (1) the increase in coronary artery diameterdoes not match the increased heart weight; (2)the unchanged capillary/fiber ratio increases themean diffusion distance; and (3) the coronaryvascular reserve is reduced owing to increasedcoronary vascular resistance.38

The morphology of the secondary T wavechanges is distinctly different from that of theprimary T wave changes and is suggestive ofischemia in about two thirds of the cases. Inthe remaining third of patients with documentedLVH and normal coronary arteries, the negativeTwaves do not have the characteristic asymmet-ric configuration of secondary T waves (seeChapter 23) but instead resemble the primaryterminally inverted T waves with an isoelectricor horizontally depressed ST segment, such asin the presence of subacute or chronic myocar-dial ischemia39 (see Figures 3–2 and 3–4). Insuch cases one cannot use repolarization criteriato support the diagnosis of LVH. Repolarizationchanges attributed to myocardial ischemia canbe distinguished from the secondary repolariza-tion abnormalities caused by LVH if, instead ofthe expected secondary ST segment elevationand upright T wave, one encounters ST segmentdepression and T wave inversion in leads V1

and V2 (see Chapters 7 and 8). Favoring a

diagnosis of myocardial ischemia is the rapidappearance and disappearance of repolarizationabnormalities in patients with coexisting coro-nary artery disease. It should be mentioned thattransient or permanent T wave inversion in theright precordial leads in patients with LVH areoccasionally caused by “right heart strain.”

OTHER ECG CHANGES IN LVH

Incomplete Left Bundle Branch Block

In patients with LVH, Q waves often decrease insize or are absent (Figures 3–5 and 3–6). The Qwave was absent in about 50 percent of autop-sied hearts with LVH resulting from variouscauses (T.C. Chou, 1960, unpublished data).The absence of the Q wave in the left precordialleads is related to leftward displacement of theinitial QRS forces, which is also partly responsi-ble for the decrease in the R wave in the rightprecordial leads.

When high QRS voltage and ST and T wavechanges in LVH are accompanied by anincreased QRS duration up to 0.11 second, anabsence of Q waves with a delay in the onset ofthe intrinsicoid deflection in the left precordialleads, and (occasionally) notching of the QRSin the mid-precordial lead, the often-raised ques-tion is whether incomplete left bundle branchblock (LBBB) coexists with hypertrophy. Theproblem is seldom of practical importancebecause incomplete LBBB is nearly always asso-ciated with marked LVH and therefore has thesame significance as the LVH pattern withsecondary ST and T wave changes.

Figure 3–4 Aortic valve disease with left ventricular hypertrophy in a 61-year-old man with aortic stenosis and insuffi-ciency. A peak systolic pressure gradient of 88 mmHg across the aortic valve was demonstrated during cardiac catheteriza-tion. Aortography revealed 3þ to 4þ aortic insufficiency. The coronary arteries were normal. The ECG shows high QRSvoltage and the classic “strain pattern” of the ST segment and T waves. The P waves are suggestive of left atrial enlargement.


Abnormal Left Axis Deviation

When used alone, an abnormal left axis devia-tion of �30 degrees or more is a relatively insen-sitive, nonspecific sign of LVH. Grant40 found nocorrelation between heart weight and left axisdeviation.

Poor R Wave Progression in Precordial Leads

Poor progression of the R wave in the rightand mid-precordial leads occurs commonly withLVH41 and is associated with a leftward shift ofthe transitional zone in the precordial leads(i.e., R/S ratio <1 in V5). Occasionally, R waves

Figure 3–5 Coarctation of the aorta in a 36-year-old man who died shortly after unsuccessful correction of this congenitallesion. At autopsy there was also evidence of a healed dissecting aneurysm of the ascending aorta. The heart weighed 545 gand had marked left ventricular hypertrophy (LVH) and a moderate degree of dilatation. Left ventricular wall thickness was25 mm. Coronary arteries revealed mild focal atherosclerosis with no significant narrowing of the lumen. Myocardiumshowed no evidence of fibrosis or infarction. Aortic valve was monocuspid with a centrally located orifice approximately7 mm in diameter. This ECG was recorded 1 day before surgery. It shows rather typical changes of LVH. The QS deflectionsin leads III and aVF suggest inferior wall myocardial damage and, in view of the autopsy findings, represent a pseudoinfarc-tion pattern. The poor progression of the R waves in the precordial leads also suggests the possibility of anterior myocardialdamage, which was absent.

Figure 3–6 A, Left ventricular hypertrophy pattern with incomplete left bundle branch block (LBBB) (QRS, 110 ms; absentQ wave in lead V6) in a 35-year-old man with alcoholic dilated cardiomyopathy (left ventricular ejection fraction 10 per-cent). B, Six months later the LBBB is complete. Standardization is half-normal. QRS duration is 156 ms. Pattern of left atrialenlargement and first-degree atrioventricular block are present in both A and B.


are absent in leads V1, V2, and even V3, resultingin a QS deflection in these leads that mimics ante-roseptal myocardial infarction (see Figures 3–2and 3–5; also see Chapter 9).

Abnormal Q Wave in Inferior Leads

Occasionally, an abnormal Q wave is recorded inleads III and aVF and less often in lead II, mim-icking inferior myocardial infarction. Examplesare shown in Figures 3–1 and 3–5. The mecha-nism of this pseudoinfarction pattern is not clear.

Notching and Prolongation of QRS Complex

In some patients the normal QRS complex isslightly prolonged and notched, especially in themid-precordial leads, probably as a result of anintraventricularconduction defect (see Figure 3–3).

U Wave

The amplitude of a normal positive U wave maybe increased in the right precordial leads, but theincrease appears to be proportional to the overallincrease in the amplitude of the ventricular com-plex. The U wave is often negative in the leftprecordial leads in patients with LVH, particu-larly when the latter is caused by systemic hyper-tension or regurgitation of the mitral or aorticvalve (see Figure 3–3).42

Anatomic Correlations

Reichek and Devereux43 found that the left ven-tricular mass estimated from M-mode echocardi-ography correlated well with the postmortemleft ventricular weight in 34 subjects, and therespective sensitivities of the Romhilt-Estes pointscore and the Sokolow-Lyon voltage criteria were50 percent and 21 percent, with a specificity of 95percent for both criteria.

Several echocardiographic studies confirmedthat the sensitivity and the specificity of the leftventricular strain pattern or of the Romhilt-Estespoint score (particularly when the score was >5)was superior to the voltage criteria alone. Thepoint score of Romhilt and Estes correlated withan increased left ventricular mass and was asso-ciated with a sensitivity of 57 percent and a speci-ficity of 81 percent.44 In two other studies45,46 theleft ventricular strain pattern had a sensitivity of52 percent and a specificity of 95 percent.

Crow et al.47 tested the performance of eightECG criteria with the echocardiographic leftventricular mass index in a biracial populationof men and women enrolled in the Treatment

of Mild Hypertension Study. The ECG LVH sen-sitivity at 95 percent specificity was <34 per-cent. The Cornell voltage criteria showed thehighest average sensitivity (17 percent). TheECG correlations with the LV mass index wereconsistently improved by including non-ECGvariables, such as blood pressure and body massindex. The authors47 thought that further refine-ment of the ECG criteria alone in Caucasianmen was unlikely to improve its relation to theleft ventricular mass. More recently, Budhwaniet al.48 correlated several traditional ECG cri-teria with the increased left ventricular massestimated by echocardiography in 608 patients.Increasing number of the ECG criteria was asso-ciated with a greater mean left ventricular mass,but increased wall thickness and ventriculardiameter did not influence significantly the fre-quency of any of the ECG criteria.

Echocardiographic studies exposed the short-comings of the ECG in its ability to differentiateamong concentric hypertrophy, eccentric hyper-trophy, and dilation without hypertrophy anddemonstrated that the QRS voltage may beincreased in the presence of an increased leftventricular diastolic diameter and normal thick-ness of the left ventricular wall.34 It appears thatnone of the tested criteria, such as the magnitudeof the maximal QRS vector in the horizontalplane,35 the QRS amplitude in the scalar ECG, orTwave changes, can distinguish reliably betweenconcentric LVH and isolated left ventricular dila-tion. Echocardiography also showed that fora diagnosis of asymmetric LVH, the presence ofprominent abnormal Q waves attributed to septalhypertrophy was a poor predictor of increasedseptal thickness or the septal wall/free wallratio31,49 (see Chapter 12). The echocardiogramis also superior to the ECG for detecting LVH inthe presence of a ventricular conduction defect.

Systolic and Diastolic Overloadof the Left Ventricle

Cabrera and Monroy introduced the concept ofsystolic and diastolic overload of the left ventri-cle.50 Later writers used the terms pressure over-load and volume overload. The ECG pattern ofleft ventricular systolic overload includes highvoltage of the R wave and the classic secondaryST segment and Twave changes in the left precor-dial leads (see Figures 3–3 and 3–5). It occurswith such conditions as aortic stenosis, systemichypertension, and coarctation of the aorta whenthe left ventricle contracts against increased resis-tance. With diastolic overload of the left ventricle,which is seen in patients with aortic insufficiency,


mitral insufficiency, and patent ductus arteriosus,the ECG usually exhibits high voltage of theR waves with prominent Q waves in the left pre-cordial leads (Figure 3–7). The ST segment isusually elevated, with an upright, peaked Twave.

Although the concept of systolic and diastolicoverload has enjoyed some popularity, its clini-cal application often has been disappointing,especially in patients with advanced acquiredheart disease, severe dilatation, and hypertrophy.In young patients with congenital heart disease,correlation of the hemodynamic state and the

ECG pattern usually is better, particularly inpatients with a ventricular septal defect withoutpulmonary hypertension whose ECG often showsa prominent Q wave followed by a tall R waveand an upright T wave (Figure 3–8).

PHYSIOLOGIC FACTORS AFFECTINGTHE RELIABILITY OF DIAGNOSTICCRITERIA

Most of the present ECG criteria for LVH havebeen developed for populations with a high

Figure 3–7 Severe mitral insufficiency in a 52-year-old man with 4þ mitral regurgitation demonstrated by left ventricularangiography. The ECG reveals deep Q waves and tall R waves in the left precordial leads. ST segments and T waves arewithin normal limits. P wave changes are suggestive of left atrial enlargement. This tracing is a typical diastolic overloadpattern of left ventricular hypertrophy.

Figure 3–8 Ventricular septal defect in a 29-year-old man proved by cardiac catheterization. The ECG shows deep Qwaves in leads I, aVL, and V4–V6. There are tall R waves in the left precordial leads. The ST segment is slightly elevated,and the T waves are tall and peaked in most of the precordial leads. The findings are consistent with diastolic overloadingof the left ventricle. An R1 is present in lead V1, suggesting possible right ventricular hypertrophy or incomplete right bundlebranch block.


prevalence of heart disease. The Bayes theorempredicts that these criteria would result in a highincidence of false-positive ECG interpretationsin a population with a low prevalence of heartdisease. Indeed, in such populations none ofthe ECG signs of LVH are specific, and no QRSvoltage criteria have more than 46 percent accu-racy for the diagnosis of LVH.51

A common vexing problem stems from varia-tions in precordial voltage. Such variationsmay be due to changes in electrode positionbut may also occur in the same individual at24-hour intervals, even independent of electrodeposition, perhaps due to changes in respirationor heart rate.52 The ST and Twave abnormalitiesare even less specific than the voltage. Moreover,the combination of increased voltage and a wideQRS/T angle can be present without hypertrophydue to delayed conduction in the left bundlebranch system. This can be shown by applyingearly premature atrial stimuli, which causesa delay in the left bundle branch. The LVHpattern produced in this manner can be normal-ized by delaying conduction in the right bundlebranch.53

Age

Age is one of the most important factors to beconsidered in the ECG diagnosis of LVH. Mostof the voltage criteria were derived and testedagainst the older population. It is well known,however, that the QRS voltage is higher in ado-lescents and young adults than in older indivi-duals (Figure 3–9). For example, from age 20to 29 years, the normal 99th percentile for

SV1 þ RV5 or V6 is 5.3 mV.54 The voltage ofSV2 þ RV5 is more than 3.5 mV in 32 percentof normal men 20 to 39 years of age (T.C. Chou,1960, unpublished data). It has been estimatedthat the amplitude of the maximum spatial QRSvector decreases by 6.5 percent for each decadeof life from age 20 to 78.55

During routine interpretation of the ECG,LVH must be diagnosed with caution in patientsunder age 40 if only the voltage criteria are met,unless the amplitude is extremely high. Even thecombination of high QRS voltage and ST andT wave changes, which is reliable in older sub-jects, cannot be applied with equal confidencein young subjects. The ST and Twave abnormal-ities may be due to other causes in the youngpatient, and the high amplitude of the QRSmay be normal for the particular body build. Itis therefore advisable to look for some other sup-porting evidence in the QRS complex such asabnormal left axis deviation, a delay in the onsetof the intrinsicoid deflection in leads V5 and V6,an increase in QRS duration to 0.11 second, thepresence of notching of the QRS complex inthe mid-precordial leads, and especially poorprogression of the R wave in the right and mid-precordial lead. Because most normal indivi-duals have taller R waves in lead V5 than in leadV6, reversal of this order also is suggestive of anabnormality.

The correlation between the ECG and the leftventricular wall thickness in the elderly wasdetermined in 671 autopsies of patients 65 to116 years of age. The correlation was notaffected by age in subjects younger than 85 yearsbut was blunted in those older than 85.56

Figure 3–9 ECG with high QRS voltage recorded from a healthy 22-year-old male medical student. RV5 þ SV1 ¼ 46 mm;RV5 þ SV2 ¼ 49.5 mm.


Body Habitus

The voltage is reduced in persons with largebreasts. A significant increase in R amplitude inleads V1–V5 occurred after left mastectomy andin leads V3R and V1 after right mastectomy.57

On the basis of increased voltage, LVH wouldbe erroneously diagnosed in nearly 50 percentof women after mastectomy.57 Other factors thatmay alter voltage in the absence of hypertrophyare hematocrit, intraventricular conduction dis-turbance, and perhaps myocardial ischemia.A low hematocrit increases the QRS voltageand a high hematocrit decreases it because ofchanges in blood resistivity.58

Kilty and Lepeschkin51 examined the effect ofbody build on the QRS voltage of the ECG.Using the ponderal index (height in inchesdivided by the cube root of weight in pounds)as a measure of body build, they found a highlysignificant correlation between body build andthe voltage of R1 þ S3, largest R þ S in theprecordial leads, and largest R þ S in a single pre-cordial lead. The precordial lead criterion R þ S>4.5 mV underdiagnoses LVH in obese peopleand overdiagnoses it in thin people. Others havealso noted that most false-positive diagnoses ofLVH occur in emaciated individuals.51 Theincreased amount of adipose or muscle tissue inthe chest wall affects the voltage as a result of anincreased distance between the precordial elec-trode and the heart. An accumulation of adiposetissue around the heart of overweight personsmay produce a similar effect 59 (see Figure 1–2 3).

The Cornell investigators60 found that theability of ECG criteria to detect LVH differsdepending on the method used to index the leftventricular mass for body size and with the pres-ence or absence of obesity. When the left ventric-ular mass was indexed to the body surface areaor to height, the sensitivity of the Cornell prod-uct criteria increased from 39 to 52 percent witha matched specificity of 95 percent.

Gender and Race

Gender has a significant effect on the amplitudeof the QRS complex. Men have higher ampli-tudes than women in both the limb leads andprecordial leads, but especially in the latter.59

In women it is sometimes important to knowwhether lead V4 was recorded with the electrodeon or underneath the breast. A significant reduc-tion in voltage may occur if the electrode isplaced on a large breast (Figure 3–10).

African-American subjects are reported to havehigher QRS voltage than Caucasian subjects. In a

study of 114 healthy adolescents61 the upper limitfor the S wave amplitude in lead V1 was 3.4 mV inblackmales, 3.2 mVinwhitemales, 2.6 mVin blackfemales, and 1.6 mV in white females. Thecorresponding values for the R amplitude in leadV6 were 3.0, 2.4, 2.2, and 2.4 mV.62

In another study of 15- to 19-year-old adoles-cents61 the sum of S in V1 and R in V6 ampli-tudes averaged 3.69 mV in black males and3.13 mV in white males. No significant differ-ences were found between black and whitefemales. The echocardiograms showed that theleft ventricular posterior wall was thicker andthe distance between the anterior chest walland the mid-left ventricle was shorter in blackmales than in white males. No such racial differ-ences were observed in females.

The Chicago Heart Association DetectionProject in Industry collected data from 1391black men and 19,216 white men.63 The preva-lence of an ECG LVH pattern was significantlyhigher in black men than in white men in eachage group. The difference remained significantafter adjustment for all possible risk factors. Exam-ination of the data fromNational Health andNutri-tion Surveys64 also showed that black racialbackgroundwas associatedwith amore than three-fold excess of LVH by the Cornell voltage criteria.

In a smaller study of 196 African-Americans,ages 54 to 100 years, Arnett et al.65 found thatthe application of ECG algorithms was associatedwith misclassification of LVH and overestimationof the left ventricular mass by echocardiography.The diagnostic accuracy of the Cornell criteriain African-Americans was comparable to theaccuracy reported in white subjects.

PATHOLOGIC STATES AFFECTING THEDIAGNOSIS OF LVH

The lung is a poor electrical conductor andattenuates the QRS voltage. In patients withchronic obstructive pulmonary disease (COPD),the voltage of the QRS complex may be markedlyreduced. The presence of LVH often is not recog-nized in such patients. Pericardial effusion mayalso mask a ventricular hypertrophy patternbecause of the short-circuiting effect of the peri-cardial fluid. Pulmonary edema may reduce thebody surface potential by its short-circuitingeffect.66 A reduction of the amplitude of the com-plexes is also seen in patients with pleural effu-sion, generalized anasarca, or pneumothorax.

Myocardial damage in patients with coronaryartery disease, secondary myocardial diseasesuch as amyloidosis, or scleroderma-associatedheart disease is often accompanied by low


voltage, which makes diagnosing LVH difficult.The presence of myocardial infarction did notaffect ECG recognition of LVH by the voltage cri-teria in an autopsy series,67 although changes inQRS amplitude during the acute stage are oftenpresent (see Chapter 7).

In most patients with RVH secondary to leftventricular disease, the effect is minimal andthe diagnosis of LVH is not affected. WhenRVH is severe, however, the LVH pattern maynot be apparent because of the canceling effectof the rightward forces.

ASSESSMENT OF THE SEVERITY OFVALVULAR LESIONS CAUSING LVH

Most attempts to correlate the ECG with theseverity of a valvular lesion have been made in

patients with valvular aortic stenosis. Hugenholtzand associates68 studied 95 patients (ages 6 weeksto 20 years) with congenital aortic stenosis. Aboutthree fourths of the patients with severe lesionsand one fourth of those with mild lesions hadevidence of LVH. Braunwald and associates69

reported hemodynamic and ECG findings in 100patients with congenital aortic stenosis. Theirages ranged from 2 to 51 years, with 36 patientsyounger than 10 years. No single ECG changewas found to be reliable for determining theseverity of the obstruction. The ECG was morehelpful in patients younger than age 10 than inolder individuals.

Roman and associates70 correlated the ECG,echocardiographic, and radionuclide angiographicfindings in 95 adults with severe, pure, chronicaortic insufficiency and no evidence of coronary

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Figure 3–10 Difference in voltage in leads V3–V6 resulting from electrode placement under a large breast (top) and overthe breast (bottom) in the ECG of a 60-year-old obese woman. The two ECGs were recorded 1 hour apart. Note the absenceof an appreciable change in voltage in leads other than V3–V6.


artery disease. The correlation between the QRSvoltage and the degree of left ventricular dilatationand dysfunction was weak.70 In patients withchronic aortic regurgitation and massive cardio-megaly (heart weighing 1 kg or more), the usualQRS criteria for LVH were often absent.43

In patients with mitral insufficiency, the correla-tion between the severity of the mitral lesion andthe ECG changes is generally poor. In a series of65 cases of dynamically significant mitral insuffi-ciencywithout significantmitral stenosis confirmedat surgery or autopsy, the ventricular complex wasnormal in 50 percent and suggestive of LVH in 30percent, RVH in 15 percent, and combined ventric-ular hypertrophy in 5 percent of cases.71

LVH and Systemic Hypertension

In the early reports from the Framingham Study72

the ECG was normal in almost half, borderline inone fifth, and definitely abnormal in one third ofa group of 154 patients with a clinical diagnosisof hypertensive cardiovascular disease.72 Duringthe follow-up73 the incidence of an LVH ECGpattern over a 14-year period of observation rosein proportion to the blood pressure elevation inall age groups. About half the patients with sys-tolic pressures above 200 mmHg had or devel-oped an LVH ECG pattern during the 14 years.

Ashizawa and associates74 reported a 26-yearfollow-up study of 601 patients with hypertensionand ECG changes of LVH with both high QRS volt-age and ST segment and T wave changes. Thepatients were examined at 2-year intervals. In 60subjects the ECG signs of LVH developed duringthe observation period. In 37 of the subjects, highQRS voltage appeared first, followed by ST and Twave changes. In 10 patients the ST and T wavechanges occurred first; in the other 13 patients theQRS and STsegment and Twave changes appearedsimultaneously. In 72 of the 601 subjects the LVHpattern regressed. The QRS voltage became nor-mal in 36, ST segment and Twave changes disap-peared in 25, and both high QRS voltage and STsegment and T wave changes disappeared in 11patients. In about half of these 72 subjects, regres-sion of the abnormal ECG findings, usually theQRS voltage, was associated with lowering theblood pressure. Regression of the ECG abnormal-ities during antihypertensive therapy was asso-ciated with lower morbidity and mortality.75,75a

Prognostic Value of ECG Changes

The ECG is of limited value for predicting theseverity of the hypertension in individual patients.It is believed, however, that in the presence of both

ST segment and T wave changes and high QRSvoltage, patients usually have a higher bloodpressure than those with high QRS voltage alone.76

In a study of 227 patients with untreateddiastolic hypertension before the advent of echo-cardiography, the left ventricular mass was pre-dicted by combining the surface area, gender,age, the S voltage in leads V1 and V4, and theduration of the terminal P wave component inlead V1.

77 In the Framingham study78 the mor-tality of hypertensive patients with a definitiveLVH pattern (tall R wave, ST segment depres-sion, flattened or inverted Twave, increased ven-tricular activation time in the left precordialleads) was much higher than in subjects withoutsuch findings, even though the blood pressurewas the same. In an analysis of 4824 patientsby Sullivan et al.,79 the ECG pattern of LVHhad an independent adverse effect on survival,even in patients without coronary artery disease.

In a study of 923 Caucasian untreated hyper-tensive patients80 in whom the prevalence ofechocardiographic LVH was 34 percent, the spec-ificity of ECG for LVH was >90 percent and thesensitivity varied between 9 percent and 33percent. The highest sensitivity was found whenthree highly specific criteria (Cornell voltage,Romhilt-Estes score, left ventricular strain pat-tern) were combined. Combination of these cri-teria was also most predictive of cardiovascularevents in 1717 Caucasian hypertensive patientsfollowed prospectively for up to 10 years.81 In along-term Losartan Intervention for EndpointReduction (LIFE) in Hypertension study of 8696hypertensive subjects, ECG LV strain pattern iden-tified patients at increased risk of developingcongestive heart failure and dying, even in thesetting of aggressive blood pressure lowering.82

PRESENCE OF LBBB

Klein et al.83 used echocardiograms to developcriteria for diagnosing LVH in patients withLBBB. They found that the sum of the S ampli-tude in V2 and the R amplitude in V6 exceeding4.5 mV had an 86 percent sensitivity and 100percent specificity for LVH, and that the diagno-sis of LVH was supported by the findings of leftatrial enlargement and QRS duration >160 ms.

Right Ventricular Hypertrophyand Dilation

Right ventricular forces normally are directedanteriorly and rightward but are mostly maskedby the dominant left ventricular potential. An


increase in the right ventricular muscle massmodifies the resultant forces proportional tothe severity of the hypertrophy. In mild cases,no apparent change may be detected in theECG. If the RVH is severe, the normally domi-nant left posterior QRS forces may be replacedby prominent right anterior forces, and theQRS patterns in the left and right precordialleads are reversed. Intermediate degrees ofabnormality may be observed when the hyper-trophy is moderate. Because lead V1 is moreproximal to the right ventricular mass, it isthe most sensitive lead for recording thechanges. Tall R wave, small S wave, or a changein the R/S ratio may be observed. The onset ofthe intrinsicoid deflection in this lead may bedelayed because of delayed activation of theright ventricular epicardium,84,85 but the delayis seldom sufficiently pronounced to be of diag-nostic usefulness.85

In some instances the increased rightwardforces are directed posteriorly instead of ante-riorly. In such cases no apparent abnormality isseen in lead V1, but the left precordial leadsmay reveal deep S waves, and the increasedrightward forces may be recognized in the limbleads as right axis deviation.

Secondary T wave change often occurs. TheT waves are directed opposite to the main QRSvector (i.e., inverted in the right precordialleads and upright in the left precordial leads).These secondary T wave abnormalities may beaccompanied by secondary deviations of theST segment. In some instances, the ST and Tchanges may be seen without apparent QRSabnormalities and are attributed to myocardialischemia of the right ventricle, or right ventric-ular strain.

THREE TYPES OF RVH

It is useful to subdivide the ECG manifestationsof RVH and right ventricular dilation into threetypes: (1) typical RVH pattern with anteriorand rightward displacement of the main QRSvector; (2) incomplete right bundle branchblock (RBBB); and (3) posterior and rightwarddisplacement of the main QRS axis, predomi-nantly in patients with chronic lung disease.

Typical RVH Pattern

The typical RVH pattern is a mirror image of theLVH pattern, with right axis deviation in the frontalplane, tall R waves in the right precordial leads,deep S waves in the left precordial leads, anda slight increase in QRS duration (Figure 3–11).This pattern is characteristically present in patientswith congenital pulmonary stenosis, tetralogy ofFallot, primary pulmonary hypertension, and otherconditions in which the right ventricular masstends to approach or exceed the left ventricularmass. The earliest portion of the QRS complex isusually unchanged because septal activation is nor-mal. The anterior displacement of the main QRSvector manifested by tall R waves in the right pre-cordial leads is attributed to a longer activation timeof the hypertrophied right ventricular free wall.86,87

Intraoperative epicardial mapping of patientswith RVH undergoing pulmonary thromboen-darterectomy showed that right ventricular acti-vation was delayed by an average of 36 ms.84

In addition, the latest right ventricular epicardialactivation occurred significantly later than thelatest left ventricular activation (i.e., average of75 ms vs. average of 64 ms). In some casesthere was no discrete early right ventricular

Figure 3–11 Typical right ventricular hypertrophy pattern with right axis deviation and negative T waves in leads V1–V4 ina 26-year-old man who had undergone corrective surgery for transposition of the great vessels during childhood.


breakthrough, but in these cases the latest rightventricular activation also occurred significantlylater than the left ventricular activation.

Sensitivity and Specificity of Criteria for RVH

The sensitivity and the specificity of various cri-teria are generally inversely related.88 The earlycriteria of Myers and associates89 and Sokolowand Lyon90 included the following:

1. R in V1 >0.7 mV2. S in V1 <0.2 mV3. S in V5 or V6 >0.7 mV4. Sum of R in V1 and S in V5 or V6

>1.05 mV5. R in V5 or V6 <0.5 mV6. R/S ratio in V5 or V6 <17. R in aVR >0.5 mV8. R/S ratio in V5 divided by R/S ratio in

V1 <0.49. R/S ratio in V1 (or V3R) >1

10. qR pattern in V1 (or V3R)Supporting criteria include the following:11. Onset of intrinsicoid deflection in V1

later than 0.04 second12. Negative T wave in V1 in the presence of

R >0.5 mV13. Right axis deviation >110 degreesThese criteria have high specificity but low

sensitivity.91,92 In the autopsy series in whichthe anatomic diagnosis was based mainly onright ventricular wall thickness, the ECG metone or more of the criteria in 23 to 100 per-cent.93 Roman and colleagues94 examined 118hearts with an ECG diagnosis of RVH. Therewas a false-positive diagnosis in 60 percent ofthe cases. The criteria of R in V1 þ S in V5 orV6 >1.05 mV and S in V5 or V6 >0.7 mV wereresponsible for most of the erroneous diagnoses.Chou et al.95 studied 97 patients in whom thepresence of RVH was supported by hemody-namic data. The sensitivity of the ECG was 66percent.

Burch and de Pasquale96 found that none ofthe RVH criteria were satisfied in 40 percent ofcases of autopsy-proven RVH due to cor pulmo-nale. Kilcoyne et al.97 found that only 28 percentof 81 patients with cor pulmonale had an RVHpattern on the ECG.

Milnor97a modified the Sokolow and Lyon cri-teria and limited the variables to: QRS duration<0.12 second and a frontal axis of þ110 toþ 180 degrees or � 91 to � 180 degrees; or anR/S or R 1/S ratio in V1 > 1.0, wi th R or R1 ampli-tude >0.5 mV. These criteria have the advantageof applicability in the presence of incompleteRBBB. They predicted RVH correctly in 24 of 32autopsy-proven cases. A 79 percent sensitivity

and 73 percent specificity for diagnosing RVHwas reported by Holt et al.98 using the 12-dipoleECG derived from recordsmade at 126 body sites.

Behar et al.99 evaluated the usefulness of theButler-Legget criteria for diagnosing RVH. Thesecriteria are as follows: (1) P wave amplitude>0.25 mV in any of leads II, III, aVF, V1, or V2;(2) R wave amplitude ¼ 0.2 mV in lead I; (3) Aþ R – PL ¼ 0.7 mV, where A (anteriorly directeddeflection) is derived from lead V1 or V2, R(rightward deflection) is the S amplitude in leadI or V6, and PL (posterolateral deflection) is theS amplitude in lead V1. In patients with pulmo-nary hypertension, these criteria achieved 66percent sensitivity for mitral stenosis, 97 percentsensitivity for pulmonary arterial obstructive dis-ease, and 79 percent sensitivity for pulmonarydisease. The specificity of these criteria wasenhanced by ruling out posterior myocardialinfarction using the Selvester QRS scoring sys-tem (see Chapter 8).

The explanation for the marked differences inthe results probably lies in the patient populationsampled. The lower sensitivity was obtainedmostly from unselected adult patients in a generalhospital.92 In these patients, RVH most com-monly develops as a result of left ventricular dis-ease. The degree of hypertrophy usually is mildand likely to be masked by the dominant left ven-tricle. The higher sensitivity values mostly camefrom centers with large numbers of patients withcongenital heart disease and a high incidence ofsevere RVH.100

Flowers and Horan101 used the chamber dis-section technique to examine 819 apparentlyunselected hearts, including 178 with RVH.The sensitivity and specificity of the individualcriteria are summarized in Table 3–2, whichindicates that the sensitivity of the individualcriterion is low, generally less than 20 percent.The more sensitive signs, such as those basedon changes in the left precordial leads, usuallyare associated with a larger number of false-positive diagnoses. By comparison, criteria basedon abnormalities in lead V1 are more specific butless sensitive.

Echocardiographic Correlations

Good correlations were found between the mea-surements of right ventricular wall thickness onthe echocardiogram and autopsy findings.102

The echocardiogram was reported to be moresensitive for detecting RVH than the ECG.103

For increased right ventricular wall thickness,the sensitivity and the specificty of the echocar-diogram were 93 percent and 95 percent, respec-tively. The corresponding values for the ECG


were 31 percent and 85 percent, respectively.103

When the ECG and the echocardiogramwere com-pared in 134 patients with RVH and in 78 patientswithout RVH, the ECG had 27 percent sensitivityand 88 percent specificity. In more than half thepatients the diagnosis of RVHwas difficult to estab-lish on the ECG because of conduction distur-bances or old myocardial infarction.103

Differential Diagnosis

Abnormal Right Axis Deviation. Other thanRVH, the situations in which right axis deviationmay be seen are as follows:

1. Normal young or slender adults2. Chronic obstructive pulmonary disease

(COPD) without cor pulmonale3. Lateral myocardial infarction4. Left posterior fascicular blockRight axis deviation occurs normally in

infants and children. The mean QRS axis duringthe first 4 weeks of life is þ110 degrees ormore.104 After 1 month the average axis is lessthan þ90 degrees (although a significant num-ber of children still have a QRS axis of up toþ110 degrees). In the adult population, talland slender subjects tend to have a rightwardQRS axis. Hiss and colleagues105 reported that2 percent of normal subjects 20 to 30 years ofage have an axis of þ105 degrees. A frontalplane QRS axis of more than þ110 degrees inolder individuals is uncommon, however, andusually suggests abnormality. Even an axis

within the range from þ90 to þ110 degreesmay indicate an abnormality in older patients,particularly if other ECG abnormalities coexist.

In patients with COPD the frontal plane axismay be within a range from þ90 to þ110 degreesin the absence of pulmonary hypertension. Therecognition or exclusion of RVH in these patientsis difficult. In patients with chronic lung diseasewithout RVH, the amplitude of the entire QRScomplex in lead I tends to be small.

In patients with lateral wall myocardial infarc-tion, the loss of leftward forces may result in arightward shift of theQRS vector. In these patientsthe initial R wave in lead I is usually absent, how-ever, and abnormal Q waves are often observedalso in the left precordial leads. Inverted Twavesin leads I, aVL, V5, and V6 are often present inpatients with lateral myocardial infarction butare uncommon in patients with pure RVH.

Abnormal right axis deviation also is seen inpatients with left posterior fascicular block.The differentiation of abnormal right axis devia-tion due to RVH from that secondary to left pos-terior fascicular block may not be possiblewithout clinical information. If the P waves aresuggestive of right atrial enlargement, however,the presence of RVH may be inferred. Left poste-rior fascicular block is favored if signs of inferioror posterior myocardial infarction are evident.

Tall R Wave, Small S Wave, Increased R/SRatio in Lead V1 in Conditions Other thanRVH. One or more of the findings of a tall R

TABLE 3–2 Sensitivity, Specificity, and Correctness of ECG Criteria for Diagnosisof Right Ventricular Hypertrophy

Criterion Sensitivity (%)Specificity(False-Positives) (%) Correctness (%)

Right axis deviation �110 degrees 12 4 78R/S V1 (or V3R) >1 6 2 78RV1 �7 mm 2 1 78SV1 �2 mm 6 2 78qR in V1 5 1 79RV1 þ SV5 or V6 >10.5 mm 18 6 77R/S V5 or V6 <1 16 7 77OID in V1 (or V3R) ¼ 0.035–0.055second

8 6 76

RSR1 in V1 with R0 >10 mm 0 0 78aVR �11.5 mm 0 0 78RV5 (or RV6) <5 mm 13 13 71SV5 (or SV6) �7 mm 26 10 76

Adapted from Flowers NC, Horan LG: IV. Hypertrophy and infarction: subtle signs of right ventricular enlargement and theirrelative importance. In: Schlant RC, Hurst JW (eds): Advances in Electrocardiography. Orlando, Grune & Stratton, 1972.

OID ¼ onset of intrinsicoid deflection.


wave, a small S wave, or an increased R/S ratio inlead V1 may be seen in the following:

1. Normal young adults2. True posterior infarction3. Intraventricular conduction disturbances

attributed to left septal fascicular block4. Displacement of the heart due to pulmo-

nary disease5. Wolff-Parkinson-White patternA tall R wave with or without a small S wave

in lead V1 is a frequent finding in normal chil-dren. The average amplitude of the R wave inV1 is more than 0.7 mV in children younger than8 years.106 The amplitude exceeds 0.7 mV in 20percent of children between ages 8 and 12 andin 11 percent of those between ages 12 and 16.An amplitude of up to 1.6 mV may be seen innormal adolescents. The R/S ratio in V1 is morethan 1 in most children under 1 year of age,106

but the ratio progressively decreases as ageincreases. In adults an R/S ratio of 1 or morewas reported in fewer than 1 percent of the nor-mal population.107 Personal observations suggestthat such a pattern is much more common, par-ticularly among the younger and the obesepopulations. In lead V2 an R/S ratio of >1 wasobserved in as many as 10 percent of adults.108

In patients with true posterior myocardialinfarction, the polarity of the T wave in V1 oftenis helpful in the differential diagnosis. Althoughexceptions do occur, an inverted T wave usuallyis seen in patients with RVH (see Figures 3–11and 3–12; see also Figure 2–4), whereas anupright T wave in V1 is likely to be associatedwith posterior myocardial infarction. The coexis-tence of abnormal right axis deviation in the

frontal plane favors RVH. Occasionally, however,right axis deviation is observed in patients withposterior myocardial infarction when it is com-plicated by left posterior fascicular block.Because true posterior myocardial infarction isseldom encountered in the absence of inferioror lateral wall infarction, the differential diagno-sis is usually not difficult.

An R wave of 0.7 mV or more occasionally isseen in lead V1 in patients with autopsy-provenisolated LVH.108 In such cases the S wave ampli-tude in lead V1 is usually large. The cause of thetall R wave is unclear. In some cases it is asso-ciated with hypertrophic cardiomyopathy. Thesesubjects often have a prominent R wave inthe right precordial leads107 and a small S wavein lead V1, resulting in an R/S ratio of >1. DeepQ waves are usually present in the left precordialleads and in leads II, III, and aVF. Hypertrophy ofthe interventricular septum is probably responsi-ble for these abnormal forces.

Rightward displacement of the heart as aresult of disease of the lung or pleura, such asmassive pleural effusion or pneumothorax, maybe accompanied by a tall R wave in lead V1

(Figures 3–13 and 3–14) because lead V1 isbelieved to record left, rather than right, ventric-ular potential. In the absence of structural heartdisease, the T wave in V1 is upright in the caseof a displaced heart, whereas in patients withRVH the T wave in this lead is often inverted.

In patients with the Wolff-Parkinson-Whitepattern, the anterior direction of the delta waveresulting in an R or Rs pattern in lead V1 is pres-ent in most subjects with posterior and leftwardinsertions of the atrioventricular bypass tract.

Figure 3–12 Severe mitral stenosis in a 47-year-old man with severe mitral stenosis proved at surgery. On the ECG the Pwaves are consistent with biatrial enlargement. The abnormal right axis deviation with an R/S ratio of >1 in lead V1 and theT wave inversion in the right precordial leads are consistent with right ventricular hypertrophy.


qR Pattern in Lead V1. The qR complex in V1 isone of the most specific signs of severe RVH (seeFigure 3–14). When the earliest part of the QRScomplex is isoelectric, abnormal depolarizationof the interventricular septum probably isresponsible for the initial negativity of the com-plex.109 It is possible that the right septal forcesare now greater than those on the left, and theresultant vector is directed toward the left(opposite to the normal orientation). It has beenalso suggested that this complex is a manifesta-tion of an enlarged right atrium that transmitsto the right precordial leads the intracardiacpotential from the right ventricle.90 Indeed, inpatients with this pattern the right atrium is fre-quently enlarged, and tricuspid regurgitation iscommonly present. Others have ascribed thisqR morphology to the extreme rotation of theheart such that the forces arising from the leftventricle are now recorded in the V1 position.

Some normal adults have a QS rather than an rSdeflection in leadV1. If such an individual developsRBBB, a qR rather than an rSR1 pattern will berecorded. If the QRS duration is 0.12 second ormore, the conduction defect usually can be readilyrecognized. If the bundle branch block is incom-plete with a QRS duration of 0.11 second or less,the differentiation becomes difficult. A similarproblem exists in patientswith anteriormyocardialinfarction and RBBB. The qR complex in thesepatients usually is accompanied by abnormalQ waves in the adjacent precordial leads.

Deep S Wave, Small R Wave, R/S Ratio <1 inLeads V5 and V6. In patients with COPD, theleft precordial leads often display small R waves,deep S waves, and an R/S ratio of <1. Thesechanges may be observed in the absence of pul-monary hypertension or cor pulmonale. Whenthe lung disease is not associated with RVH,

Figure 3–13 Tall R waves in the right precordial leads due to dextro displacement in a 28-year-old man with completecollapse of the right lung as a result of Hodgkin’s disease. At autopsy the heart weight was normal, and there was no evi-dence of ventricular hypertrophy or myocardial damage.

Figure 3–14 Right ventricular hypertrophy caused by Eisenmenger syndrome. The patient is a 24-year-old man with aventricular septal defect and severe pulmonary hypertension proved by cardiac catheterization. Abnormal right axis devia-tion with a qR pattern is apparent on the ECG in lead V1, and T wave changes are visible in the right precordial leads.


however, the amplitude of the QRS complexes inthe left precordial leads tends to be low.

A similar pattern in the left precordial leadsmaybe seen in normal subjects and with various condi-tions associated with cardiomegaly and markedleftward shift of the transition zone. An rS patternin leads V5 and V6 may be seen in patients withanterior myocardial infarction110 (see Figure 4–7)and in those with left anterior fascicular block.111

ST Segment and T Wave Changes in RVH.With RVH, ST segment depression and T waveinversion are seen most commonly in the rightprecordial leads (see Figures 3–12 and 3–14).These changes also may be seen in leads II, III,and aVF. If the T waves are biphasic in the rightprecordial leads, it is useful to note whether theconfiguration is of the positive-negative ornegative-positive type. A negative-positive biphasicT wave is abnormal and often is seen in patientswith RVH112,113 (Figure 3–15), whereas the posi-tive-negative configuration may be normal.

Systolic and Diastolic Overload Patterns. Cab-rera and Monroy50 called attention to the differ-ent ECG changes during systolic and diastolicoverloading of the right ventricle. With systolicoverloading, which was called pressure overload-ing by later investigators, lead V1 exhibits a tallmonophasic R wave or a diphasic RS, Rs, or qRcomplex. The T wave usually is inverted in thislead. This pattern typically is seen in patientswith pulmonary stenosis, tetralogy of Fallot, orpulmonary hypertension (see Figures 3–14 and3–15). With diastolic, or volume, overload of

the right ventricle, lead V1 usually shows anrSR1 pattern. This is the typical QRS complex inpatients with an atrial septal defect, partial anom-alous pulmonary venous return, or tricuspidinsufficiency. The anatomic alteration consistsmainly of a dilated right ventricle instead ofhypertrophy as in the case of systolic overload.

The clinical application of this concept is ofquestionable value. As a rule, the hemodynamiccorrelation of these two ECG overload patternsis more satisfactory in congenital than acquiredheart disease.114

S1S2S3 Pattern as a Manifestation of RVH. TheS1S2S3 pattern is a frequently used descriptiveterm during ECG interpretation. It is seenin normal individuals and in patients withpulmonary emphysema or RVH. Chou et al.112

proposed the criterion of an R/S ratio of <1 inleads I, II, and III or the S waves in these leadsthat exceed the upper limits of normal for thevarious age groups as defined by Simonson.115*

S waves of low amplitude are more likely to beseen in normal subjects and deeper S waves inpatients with RVH (Figure 3–16). Additionally,in patients with RVH and the S1S2S3 pattern,the prominent late QRS forces are directedrightward and superiorly. The S wave amplitudeis usually greater in lead II than in lead III.

*Upper limits of the normal amplitude of the S waves inleads I, II, and III:

Age 20–29: S1, 0.4 mV; S2, 0.5 mV; S3, 0.6 mVAge 30–39: S1, 0.4 mV; S2, 0.4 mV; S3, 0.9 mVAge 40–49: S1, 0.3 mV; S2, 0.4 mV; S3, 0.8 mV

Figure 3–15 Severe pulmonary stenosis in a 19-year-old man. The right ventricular peak systolic pressure was132 mmHg. On the ECG, the findings suggestive of right ventricular hypertrophy are an abnormal right axis deviation andan R/S ratio >1 in V1. The R wave in lead aVR is >5 mm. Note the negative-positive biphasic T wave in lead V1.


Inco mplete RBBB

Inco mplete RBBB, mani fested by th e rSR 1 patternin the right preco rdial leads, is attri buted tode layed acti vation of the hypert rophied rightve ntricular outflo w tract (see C hapter 5). Thispa ttern is most freque ntly due to factors otherth an RVH. It can signi fy hypert rophy, dilation, oroverl oad of th e right ventric le, perhap s mostcommonly in mitral valve disease with pulmonaryhypertension (Figure 3–17) and atrial septal defect(see Chapter 12). In patients with pulmonic valvu-l ar s te no si s, t h e R 1 v o lt ag e c o r re la te s w it h t heseverity of stenosis116 (Figure 3–18). The prompt

disappearance of this pattern observed in manycases within days after corrective surgery suggeststhat incomplete RBBB may result from slowing ofintraventricular conduction due to stretching ofthe peripheral conducting system in the dilatedventricle (see Chapter 5).

In additi on to RVH, an rSR1 pattern in lead V1

with the duration of t he QRS compl ex <0.1 2second is also seen in: (1) normal indivi duals;(2) acute right ventricular dilatation; (3) trueposterior myocardial infarction; and (4) extra-cardiac abnormalities such as pectus excavatum.Further differential diagnoses of the incompleteRBBB pattern is discussed in Chapter 5.

Figure 3–16 RVH resulting from chronic cor pulmonale in a 67-year-old man with severe pulmonary emphysema andchronic cor pulmonale proved at autopsy. There was severe right ventricular hypertrophy and dilatation. Mild atherosclerosisof the coronary arteries was present without evidence of myocardial fibrosis or infarction. On the ECG the P wave is consis-tent with right atrial enlargement. There is an S1S2S3 pattern, with the QRS axis in the frontal plane directed rightward andsuperiorly. The QS deflection in the right precordial leads with T wave inversion mimics anterior wall myocardial infarction.The R/S ratio in leads V5 and V6 is <1.

Figure 3–17 Right ventricular hypertrophy pattern with incomplete right bundle branch block in a 52-year-old man withmitral stenosis, mitral regurgitation, and pulmonary artery pressure of 100/42 mmHg. Left ventricular function and coronaryarteriogram were normal. The QRS axis is intermediate. The P wave suggests left atrial enlargement.


Patterns in the Presence of ChronicLung Disease

The characteristic ECG pattern in patients withCOPD is attributed to changes in the spatial orien-tation of the heart and the insulating effect of theoveraerated lungs.96 The changes induce peakedP waves in leads II, III, and aVF; a low R waveamplitude in all leads; and a late QRS vector ori-ented superiorly and to the right resulting in awide, slurred S wave in leads I, II, III, V4, V5,and V6.

96,118,119 Pathognomonic of emphysema inthe absence of myocardial infarction is low voltagewith a posteriorly and superiorly oriented QRSvector and an axis of the P wave>60 degrees in thelimb leads.117 Atrial repolarization may becomemore prominent, as evidenced by depression of

the Ta wave in lead II.121 In the presence of anrSr1 pattern in the right precordial leads, a slurredS wave in the left precordial leads and a prominentR wave in lead aVR may indicate superimposedRVH.117,120

Severity of Chronic Lung Disease

The best criteria for judging the severity ofCOPD are (1) R in V6 <0.5 mV; (2) R/S inV6 <1.0; and (3) increased P wave amplitudein leads II and III122 (Figure 3–19). In theorthogonal leads, low R wave amplitude andlow R/S amplitude in the X lead, low voltagein the X and Y leads, and a rightward shiftof the P axis identified COPD correctly in75 percent of patients, with only 8 percent being

Figure 3–18 Incomplete right bundle branch block with increased R1 amplitude in a 23-year-old man with moderatelysevere pulmonary valvular stenosis. Right ventricular pressure was 54/4 mmHg.

Figure 3–19 ECG pattern suggestive of severe respiratory insufficency in a 63-year-old man with chronic obstructive lungdisease, as described in the text. Premature atrial complexes are conducted with aberration.


false-positive diagnoses.123 The best reportedindicators of deteriorating pulmonary functionin patients with COPD are (1) progressive reduc-tion of the R wave and the R/S ratio in orthogo-nal lead X (may be applied to lead I), (2)progressive shift of the QRS axis in the superiordirection, and (3) rightward shift of the P waveaxis.

In a study of 263 cases of COPD followed for13 years after an exacerbation of respiratory fail-ure, Incalzi et al.123 identified the strongest pre-dictors of death to be an S1S2S3 pattern, “rightatrial overload” (defined as a P wave axis ofþ90 degrees or more), and an alveolar-arterialO2 gradient >48 mmHg. The median survivalof patients having either of these two ECG signswas 2.7 years; of those having both ECG signs,1.33 years.

Chronic Cor Pulmonale

In an effort to detect early cor pulmonale, Kil-coyne and co-workers surveyed 200 patientswith COPD.97 One or more of the followingECG trends were suggested as indicators of rightventricular abnormality or dilation: (1) shift ofthe mean QRS axis to the right of þ30 degrees;(2) T wave inversion in the right precordialleads; (3) ST segment depression in leads II, III,and aVF; and (4) transient appearance of RBBB.These ECG manifestations usually were asso-ciated with an arterial oxygen saturation of lessthan 85 percent and a mean pulmonary arterialpressure of 25 mmHg or more.

The sensitivity of the ECG for diagnosing RVHin patients with chronic autopsy-proven cor pul-monale is about 60 to 70 percent,94,124–128

whereas in clinical studies the rate of recognitionmay be only 28 percent. With moderate RVH theprecordial leads display deep S waves in leads V5

and V6, but the R waves in the right precordial

leads are not prominent. In the most severe casesof cor pulmonale, the QRS forces are orientedanteriorly and rightward, and tall R waves appearin the right precordial leads (Figure 3–20).Patients with cor pulmonale secondary to pulmo-nary thromboembolism, idiopathic pulmonaryhypertension, or obesity hypoventilation syn-drome are more likely to have a tall R wave inV1 than are those with pulmonary emphy-sema128,129 (Figures 3–21 and 3–22). The latter,however, more often have deep S waves in leadsV4, V5, and V6.

RVH IN OTHER CLINICALCONDITIONS

Pulmonary Hypertension in Mitral Stenosis

In the absence of RVH secondary to pulmonaryhypertension, the only ECG abnormality inpatients with mitral stenosis is left atrial enlarge-ment. In the experience of Chou,130 the criteriafor an RVH diagnosis, in descending order of fre-quency, are an R/S ratio in V1 >1; a delay ofonset of the intrinsicoid deflection in V1;RV1 þ SV5,6 >1.05 mV; S wave in V1 <0.2 mV;R in V1 > 0.7 mV; R/S ratio in V5 or V6 �1; rightaxis deviation �þ110 degrees; rSR0 in V1; RaVR�0.5 mV; and qR in V1. Although exceptionsoften occur, there is correlation between thedegree of pulmonary hypertension in mitralstenosis and the appearance of RVH on theECG. Fowler and associates131 found thatwhen the mean pulmonary arterial pressureexceeded 42 mmHg, nearly all the patientsexhibited a hypertrophy pattern, as indicatedby an abnormal R/S ratio with delayed intrinsi-coid deflection in lead V1. Such evidencewas not found in patients with a pulmonaryartery pressure <28 mmHg. Others have shown

Figure 3–20 Severe chronic cor pul-monale with right heart failure second-ary to pulmonary emphysema in a 54-year-old man. Note the qR pattern inlead V1.


that when the ECG displayed evidence of RVH,the mean pulmonary arterial pressure was uni-formly 33 mmHg or higher, and the total pulmo-nary vascular resistance exceeded 800 or 1000dynes�sec�1�cm�5.132–134 The finding of a mean

QRS axis that exceeded þ90 degrees is thoughtby some to indicate moderate or severe pulmo-nary hypertension,133 whereas incomplete RBBBor an rSR0 pattern is not a reliable indicator ofthe severity of the vascular obstruction. A

Figure 3–21 Chronic cor pulmonale secondary to recurrent pulmonary embolism in a 56-year-old woman with a 6-yearhistory of recurrent thrombophlebitis of the legs and pulmonary embolism. The diagnosis was verified at autopsy. The heartshowed severe right ventricular hypertrophy and dilatation with marked right atrial hypertrophy. The ECG shows first-degreeatrioventricular block. There is an S1S2S3 pattern. The R/S ratio in lead V1 is >1. Deep S waves are present in the left precor-dial leads. ST segment and T wave changes are present in the right and mid-precordial leads. The patient was not receivingdigitalis at the time.

Figure 3–22 Chronic cor pulmonale in a 37-year-old woman with obesity-hypoventilation (pickwickian) syndrome. Herbody weight ranged between 250 and 300 pounds, and she had a history of sleep apnea and syncope. There was clinicalevidence of right ventricular failure. The pulmonary arterial pressure obtained during cardiac catheterization was at the sys-temic level. On the ECG the P waves are tall and peaked in leads II, aVF, and V1–V3, suggestive of right atrial enlargement.The abnormal right axis deviation, R/S ratio in lead V1 >1, and inverted T waves in leads V1–V4 are highly suggestive of rightventricular hypertrophy (RVH). T wave inversion in the inferior leads also is related to RVH.


monophasic R wave or qR complex in lead V1 withT w a ve i nv er si on i s un co mm on in pa tie nt s w it hmitral stenosis, but its presence signifies advanceddisease.

Conge nita l Hear t Diseas e

The ECG diagnos is of RVH in congenital heartdisea se is general ly accura te in more than 90pe rcent of cases. 93 The higher rate of RVH recog-niti on in congeni tal heart disea se th an inacq uired heart disease is due mainly to a higherright ven tricular systoli c pressure, greater rightve ntricular thickne ss, and the frequent absenceof LVH in the congeni tal heart disea se group.135

The relation betwee n the ECG findings ofRVH and the hemody namic find ings has beenstud ied in patie nts with isolated pulmo nary ste-nosi s by severa l investigato rs. 136–139 Acc ordingto Burch and DePasqua le, 137 the ECG is norma lin about 50 percent of patie nts with mild pulmo -nary steno sis an d a pe ak right ventric ularsy stolic pressure < 60 mmH g. When the rightve ntricular pressure is eleva ted modera tely orseverely, most patien ts have an RVH pattern. Amono phasic R wave or qR complex with T waveinvers ion in V1 usual ly is seen in patients withsevere lesion s, whereas the less typi cal rSR 1 pa t-tern is encount ered more often in those withmild disease 136,138 (see Figure 3–1 8).

With an atrial septal defect, the basic pattern ofrSR1 in lead V1 is common in patients who havemean pulmonary arterial pressures <20 mmHg,whereas most patients with a qR or rSR1S1 complexhave higher pressures.137,140 Additional discussionof the ECG findings with an atrial septal defect isincluded in Chapter 12.

Combin ed Ventricular Hypertrophy

Partial c ancel lati on o f op positel y dire c ted fo rcesgenera ted by LVH and RVH may result in a nor-mal ECG pattern. For e xample, the develop -ment of RVH due to pulmonary hypertensionsometimes o bscures the previous LV H pattern.M ore often, however, re cognition o f t he concur-re nt p resence o f LV H a nd RV H is p ossi blebecause of the asynchrony of ventricular depo-larization and because the semidirect pre co rdialleads pre ferentially re flect the local potentialsunderlying the respective elec trodes. A co m-bined pattern of RV H and LV H is fre quentl yp res ent in p atie nts with ventric ula r s epta ld efect or patent ductus arteriosus in the pre s-ence of pulmonary hypertension (Eise nmenger

syndro me). In such cases, tall R waves may bepres ent in b oth lef t and right p rec ord i al le ad swith a tall biphasic QRS in the mid-precordialleads (Katz-Wachte l pattern).141

Rig ht axis deviation in the frontal plane in th epresenc e of an LVH pattern sugge sts associatedright ventricu lar enlargement. A les s reliableindicato r of possibl e right ventric ular dilationin the presenc e of an LVH pattern is a shift ofthe transition zone in the preco rdial lea ds tothe left. In ad ults with rheumatic heart disea se,biventric ular hypertrophy may be suspecte din the presenc e of tall R wave s in the left precor-dial leads and disproportionately smal l S waves(i.e., <1 mV in lea d V1 ) or inverte d T waves inthe right precordial leads . Such a pattern is char-acteristica lly present in patie nts with mitral ste-nosis and pulmon ary hypert ensi on who als ohave mitra l regurgitation or aortic valve disea se.

CLINICA L AND ANA TOMICCORRELA TIONS

One of t he follow ing ECG crit eria has beenapplied in a limit ed number of correlationstudies:

1. ECG pattern meets one or more of thediagnos tic crit eria for isolated RVH orLVH.

2. Precordial leads show signs of LVH, butthe QRS axis in the frontal plane is morethan þ90 degrees.142

3. The R wave is greater than the Q wave inlead aVR, and the S wave is greater thanthe R wave in lead V5, with T wave inver-sion in lead V1 in conjunction with signsof LVH.143

In general, these criteria have low sensitivityfor recognizing combined ventricular hypertro-phy. In 172 cases of anatomic combined ventric-ular hypertrophy studied by four groups ofinvestigators, the ECG was diagnostic in only17 percent of cases.143–146 It showed signs ofisolated LVH or RVH in 28 percent of the cases.The secondary RVH in patients with left-sidedheart disease is usually masked by the dominantLVH (Figure 3–23). Conversely, LVH, which isoften seen in patients with chronic cor pulmo-nale, usually is not detectable on the ECG(Figure 3–24).

The specificity of the ECG diagnosis of com-bined ventricular hypertrophy is also limited.In a small autopsy series examined by Chou,130

only 10 of 22 cases (45 percent) with an ECGdiagnosis of combined hypertrophy had ana-tomic combined ventricular hypertrophy, with


the remainder showing isolated LVH. Jainet al.147 studied 69 patients with biventricularhypertrophy identified by echocardiography.Among them, 17 (25 percent) had ECG findingscompatible with biventricular hypertrophy, 25(36 percent) had an LVH pattern, and 14 (20percent) had an RVH pattern. An S wave in leadsV5 and V6 >0.7 mV was the most frequent

finding in the 17 patients with the ECG criteriafor biventricular hypertrophy. The sensitivityof the ECG criteria for biventricular hyper-trophy was 24.6 percent and the specificitywas 86.4 percent. Figures 3–23 to 3–26 illustratethe spectrum of ECG changes seen inpatients with anatomic combined ventricularhypertrophy.

Figure 3–23 Anatomic com-bined ventricular hypertrophy witha left ventricular hypertrophy (LVH)pattern on the ECG in a 40-year-old man with advanced hyperten-sive cardiovascular disease andsevere congestive heart failure. Atautopsy the heart weighed 550 g,with marked hypertrophy and dila-tation of all the heart chambers.The ECG shows left atrial enlarge-ment and LVH. No evidence is seenof right ventricular hypertrophy.

Figure 3–24 Combined ventricular hypertrophy with a right ventricular hypertrophy (RVH) pattern on the ECG in a25-year-old extremely obese woman (400 lb). She was believed to have the pickwickian syndrome with chronic cor pulmo-nale and recurrent pulmonary embolism. At autopsy the heart weighed 615 g, with marked RVH and moderate left ventric-ular hypertrophy (LVH). The right ventricular wall was 9 mm thick, and the left ventricular wall was 19 mm thick. There alsowas marked right atrial hypertrophy and dilatation. On the ECG the P waves are consistent with right atrial enlargement. Anabnormal right axis deviation with deep S waves in the left precordial leads suggests RVH. There is no evidence to suggestcoexisting LVH.


REFERENCES

1. Surawicz B: Electrocardiographic diagnosis of chamberenlargement. J Am Coll Cardiol 8:711, 1986.

2. Linzbach AJ: Heart failure from the point of view of quan-titative anatomy. Am J Cardiol 5:370, 1960.

3. Thiry PS, Rosenberg RM, Abbott JA: A mechanism for theelectrocardiogram response to left ventricular hypertro-phy and acute ischemia. Circ Res 36:92, 1975.

4. Durrer D: The human heart: some aspects of its excitation.Transact Stud Coll Physicians Phila 33:159, 1966.

5. Hugenholtz PG, Gamboa R: Effect of chronically increasedventricular pressure on electrical forces of the heart. Cir-culation 30:511, 1964.

6. Baxley WA, Dodge HT, Sandler H: A quantitative angiocar-diographic study of left ventricular hypertrophy and theelectrocardiogram. Circulation 37:509, 1968.

Figure 3–25 Rheumatic heart disease with combined ventricular hypertrophy in a 29-year-old man with severe aortic andmitral valve disease proved at cardiac catheterization and surgery. On the ECG the P waves are consistent with biatrialenlargement. The frontal plane QRS axis is þ90 degrees. This finding, in the presence of signs of left ventricular hypertrophy,suggests coexisting right ventricular hypertrophy.

Figure 3–26 Combined ventricular hypertrophy demonstrated on the ECG in a 63-year-old man with severe mitral andaortic stenosis and mild aortic insufficiency. At autopsy the heart weighed 850 g, with hypertrophy and dilatation of allchambers. The left ventricular wall was 20 mm thick, and the right ventricular wall was 9 mm thick. Coronary arteries werepatent, and there was no evidence of myocardial infarction. The ECG shows atrial fibrillation. The abnormal right axis devi-ation and the RSR1 pattern in lead V1 suggest right ventricular hypertrophy. The voltage of the R waves and the ST segmentand T wave changes in the left precordial leads suggest left ventricular hypertrophy. Some of the ST and T changes are theresult of a digitalis effect.


7. McFarland TM, Alam M, Goldstein S, et al: Echocardio-graphic diagnosis of left ventricular hypertrophy. Circu-lation 57:1140, 1978.

8. Inoue H, Takenaka K, Murayama M, et al: Effects ofacute changes in left ventricular size on surface potentialin man. Jpn Heart J 23:279, 1982.

9. Wollam GL, Hull WD, Porter VD, et al: Time course ofregression of left ventricular hypertrophy in treatedhypertensive patients. Am J Med 75:100, 1983.

10. Lepeschkin E: Modern Electrocardiography. The P-Q-R-S-T-U Complex, Baltimore, Williams & Williams, 1951.

11. Antman EM, Green LH, Grossman W: Physiologic deter-minants of the electrocardiographic diagnosis of left ven-tricular hypertrophy. Circulation 60:386, 1979.

12. Devereux RB, Phillips MC, Casale PN, et al: Geometricdeterminants of electrocardiographic left ventricularhypertrophy. Circulation 67:907, 1983.

13. Brody DA: A theoretical analysis of intracavitary bloodmass influence on the heart-lead relationship. Circ Res4:731, 1956.

14. Daniels S, Iskandrian AS, Hakki AH, et al: Correlationbetween changes in R wave amplitude and left ventric-ular volume induced by rapid atrial pacing. Am HeartJ 107:711, 1984.

15. Battler A, Froelicher V, Slutsky R, et al: Relationship ofQRS amplitude changes during exercise to left ventricu-lar function and volumes and the diagnosis of coronaryartery disease. Circulation 60:1004, 1079.

16. Deanfield JE, Davies G, Mongiardi F, et al: Factors influ-encing R wave amplitude in patient with ischaemic heartdisease. Br Heart J 49:8, 1983.

17. Feldman T, Childers RW, Borow KM, et al: Change inventricular cavity size: differential effects on QRS and Twave amplitude. Circulation 72:495, 1985.

18. Horton JD, Sherber HS, Lakatta EG: Distance correctionfor precordial electrocardiographic voltage in estimatingleft ventricular mass. Circulation 55:509, 1977.

19. Carter WA, Estes EH Jr: Electrocardiographic manifesta-tions of ventricular hypertrophy, a computer study ofECG-anatomic correlations in 319 cases. Am Heart J68:173, 1964.

20. Sokolow M, Lyon TP: The ventricular complex in ven-tricular hypertrophy as obtained by unipolar precordialand limb leads. Am Heart J 37:161, 1949.

21. Romhilt DW, Estes EH: Point-score system for the ECGdiagnosis of left ventricular hypertrophy. Am Heart J75:752, 1968.

22. Casale PN, Devereux RB, Kligfield P, et al: Electrocardio-graphic detection of left ventricular hypertrophy: devel-opment and prospective validation of improved criteria.J Am Coll Cardiol 6:572, 1985.

23. Okin PM, Roman MJ, Devereux RB, et al: Electrocar-diographic identification of increased left ventricularmass by simple voltage-duration products. J Am CollCardiol 23:417, 1995.

24. Norman JE, Levy D: Improved electrocardiographicdetection of echocardiographic left ventricular hypertro-phy: results of a correlated data base approach. J Am CollCardiol 26:1022, 1995.

25. Scott RC, Seiwert VJ, Simon DL, et al: Left ventricularhypertrophy: study of accuracy of current electrocar-diographic criteria when compared with autopsy find-ings in one hundred cases. Circulation 11:89, 1955.

26. Rosenfeld I, Goodrich C, Kassebaum G, et al: The elec-trocardiographic recognition of left ventricular hypertro-phy. Am Heart J 63:731, 1962.

27. Selzer A, Ebnother CL, Packard P, et al: Reliability ofelectrocardiographic diagnosis of left ventricular hyper-trophy. Circulation 17:255, 1958.

28. Chou TC, Scott RC, Booth RW, et al: Specificity of thecurrent electrocardiographic criteria in the diagnosis ofleft ventricular hypertrophy. Am Heart J 60:371, 1960.

29. Mazzoleni A, Wolff R, Wolff L, et al: Correlation betweencomponent cardiac weights and electrocardiographicpatterns in 185 cases. Circulation 30:808, 1964.

30. Molloy TJ, Okin P, Devereux RB, et al: Electrocardio-graphic detection of left ventricular hypertrophy by thesimple QRS voltage-duration product. J Am Coll Cardiol20:1180, 1992.

31. Savage DD, Drayer HM, Henry WL, et al: Electrocardio-graphic findings in patients with obstructive and nonob-structive hypertrophic cardiomyopathy. Circulation58:402, 1978.

32. Romhilt DW, Bove KE, Norris RJ, et al: A criticalappraisal of the electrocardiographic criteria for the diag-nosis of left ventricular hypertrophy. Circulation 40:185,1969.

33. Cohen A, Hagan AD, Watkins J, et al: Clinical correlatesin hypertensive patients with left ventricular hypertro-phy diagnosed with echocardiography. Am J Cardiol47:335, 1981.

34. Toshima H, Koga Y, Kimura N: Correlations betweenelectrocardiographic, vectorcardiographic, and echocar-diographic findings in patients with left ventricular over-load. Am Heart J 94:547, 1977.

35. Browne PJ, Sridhar S, Dresser KB, et al: Hypertrophy ordilatation? A vectorial analysis of echocardiographicallydetermined left ventricular enlargement. J Electrocardiol11:117, 1978.

36. Geva B, Elkayam U, Fisman W, et al: Determination ofleft ventricular wall thickening in patients with chronicsystemic hypertension: correlation of electrocardiogra-phy and echocardiography. Chest 76:557, 1979.

37. Bennet DH, Evans DD: Correlation of left ventricularmass determined by echocardiography with vectorcar-diographic and electrocardiographic measurements. BrHeart J 36:981, 1974.

38. O’Keefe DD, Hoffman DT, Cheitlin R, et al: Coronaryblood flow in experimental canine left ventricular hyper-trophy. Circ Res 43:43, 1978.

39. Huwez FU, Pringle SD, Macfarlane PW: Variable patternsof ST-T abnormalities in patients with left ventricularhypertrophy and normal coronary arteries. Br Heart J67:304, 1992.

40. Grant RP: Left axis deviation. Circulation 14:233, 1956.41. Barker JM: The Unipolar Electrocardiogram: A Clinical

Interpretation. Norwalk, CT, Appleton-Century-Crofts,1952, p. 375.

42. Kishida H, Cole JS, Surawicz B: Negative U wave:a highly specific but poorly understood sign of heart dis-ease. Am J Cardiol 49:2030, 1982.

43. Reichek N, Devereux RB: Left ventricular hypertrophy:relationship of anatomic, echocardiographic and electro-cardiographic findings. Circulation 63:1391, 1981.

44. Kansal S, Roitman DI, Sheffield LT: A quantitative rela-tionship of electrocardiographic criteria of left ventricu-lar hypertrophy with echocardiographic left ventricularmass. Clin Cardiol 6:456, 1983.

45. Devereux RB, Reichek N: Repolarization abnormalitiesof left ventricular hypertrophy: clinical, echocardio-graphic and hemodynamic correlates. J Electrocardiol15:47, 1982.

46. Devereux RB, Casale PN, Eisenberg RR, et al: Electrocar-diographic detection of left ventricular hypertrophy usingechocardiographic determination of left ventricular massas the reference standard: comparison of standard criteria,computer diagnosis and physician interpretation. J AmColl Cardiol 3:82, 1984.


47. Crow RS, Prineas RJ, Rautaharju P, et al: Relationbetween electrocardiography and echocardiography forleft ventricular mass in mild systemic hypertension(results from treatment of mild hypertension study).Am J Cardiol 75:1233, 1995.

48. Budhwani N, Patel S, Dwyer EM Jr: Electrocardiographicdiagnosis of left ventricular hypertrophy: the effect of leftventricular wall thickness, size, and mass on the specificcriteria for left ventricular hypertrophy. Am Heart J149:709, 2005.

49. Moro C, Tascon J, Muela A: Correlation between electri-cal and echocardiographic data in hypertrophic cardio-myopathy. Int J Cardiol 3:381, 1983.

50. Cabrera CE, Monroy JR: Systolic and diastolic loading ofthe heart. II. Electrocardiographic data. Am Heart J43:669, 1952.

51. Kilty SE, Lepeschkin E: Effect of body build on the QRSvoltage of the electrocardiogram in normal men: its sig-nificance in the diagnosis of left ventricular hypertrophy.Circulation 31:77, 1965.

52. Larkin H, Hunyor SN: Precordial voltage variation in thenormal electrocardiogram. J Electrocardiol 13:347, 1980.

53. Piccolo E, Raviele A, Delise P, et al: The role of left ven-tricular conduction in the electrogenesis of left ventricu-lar hypertrophy: an electrophysiologic study in man.Circulation 59:1044, 1979.

54. Manning GW, Smiley JR: QRS-voltage criteria for leftventricular hypertrophy in a normal male population.Circulation 29:224, 1964.

55. Pipberger HV, Goldman MJ, Littman D, et al: Correla-tions of the orthogonal electrocardiogram and vectorcar-diogram with constitutional variables in 518 normal men.Circulation 35:536, 1967.

56. Yamashita S, Dohi Y, Miyagawa K, et al: Reliability of theelectrocardiogram for detecting left ventricular hypertro-phy in elderly. Am J Cardiol 81:650, 1998.

57. LaMonte CS, Friedman AH: The electrocardiogram aftermastectomy. Circulation 32:746, 1965.

58. Rosenthal A, Restiaux NJ, Feig SA: Influence of acutevariations in hematocrit on QRS complex of the Frankelectrocardiogram. Circulation 44:456, 1971.

59. Levy D, Labib SB, Anderson KM, et al: Determination ofsensitivity and specificity of electrocardiographic criteriafor left ventricular hypertrophy. Circulation 81:815,1990.

60. Okin PM, Roman MJ, Devereux RB, et al: Electrocar-diographic identification of left ventricular hypertrophy:test performance in relation to definition of hypertrophyand presence of obesity. J Am Coll Cardiol 27:124, 1996.

61. Rao S: Racial differences in electrocardiograms and vec-torcardiograms between black and white adolescents.J Electrocardiol 18:309, 1985.

62. Bailey MA, Su JJ, Guller B: Racial and sexual differencesin the standard electrocardiogram of black vs white ado-lescents. Chest 75:474, 1979.

63. Xie X, Liu K, Stamler J, et al: Ethnic differences in elec-trocardiographic left ventricular hypertrophy in youngand middle-aged employed American men. Am J Cardiol73:564, 1994.

64. Rautaharju PM, Zhou SH, Calhoun HP: Ethnic differ-ences in ECG amplitudes in North American white,black and Hispanic men and women: effect of obesityand age. J Electrocardiol 27(Suppl):20, 1994.

65. Arnett DK, Rautaharju P, Sutherland S, et al: Validity ofelectrocardiographic estimates of left ventricular hyper-trophy and mass in African Americans (The CharlestonHeart Study). Am J Cardiol 79:1289, 1997.

66. Rudy Y, Wood R, Plonsey R, et al: The effect of high lungcapacity on electrocardiographic potentials. Circulation65:440, 1982.

67. Scott RC: Ventricular hypertrophy. Cardiovasc Clin5:220, 1973.

68. Hugenholtz PG, Lees MM, Nadas AS: The scalar electro-cardiogram, vectorcardiogram, and exercise electrocar-diogram in the assessment of congenital aortic stenosis.Circulation 26:79, 1962.

69. Braunwald E, Goldblatt A, Aygen MM, et al: Congenitalaortic stenosis. I. Clinical and hemodynamic findings in100 patients. Circulation 27:426, 1963.

70. Roman MJ, Kligfield P, Devereux RB, et al: Geometricand functional correlates of electrocardiographic repolar-ization and voltage abnormalities in aortic regurgitation.J Am Coll Cardiol 9:500, 1987.

71. Bentivoglio LG, Urricchio JF, Waldow A, et al: An elec-trocardiographic analysis of sixty-five cases of mitralregurgitation. Circulation 18:572, 1958.

72. Dawber TR, Kannel WB, Love DE, et al: The electrocar-diogram in heart disease detection: a comparison of themultiple and single lead procedures. Circulation 5:559,1952.

73. Kannel WB, Margolis JR: Electrocardiographic leftventricular hypertrophy and risk of coronary heartdisease: the Framingham study. Ann Intern Med72:813, 1970.

74. Ashizawa N, Seto S, Kitano K, et al: Effects of blood pres-sure changes on development and regression of electro-cardiographic left ventricular hypertrophy: a 26-yearlongitudinal study. J Am Coll Cardiol 13:165, 1989.

75. Okin PM, Devereux RB, Jern S, et al: Regression of elec-trocardiographic left ventricular hypertrophy duringantihypertensive treatment and the prediction of majorcardiovascular events. JAMA 292:2343, 2004.

75a. Wachtell K, Okin PM, Olsen MH, Dahlof B, Devereux RB,Ibsen H, Kjeldsen SE, Lindholm LH, Nieminen MS,Thygesen K. Regression of electrocardiographic left ven-tricular hypertrophy during antihypertensive therapyand reduction in sudden cardiac death: the LIFE Study.Circulation 116(7):700–5, 2007.

76. Pringle SD, MacFarlane PW, McKillop JH, et al: Patho-physiologic assessment of left ventricular hypertrophyand strain in asymptomatic patients with essential hyper-tension. J Am Coll Cardiol 13:1377, 1979.

77. De Vries SO, Heesen WF, Beltman FW, et al: Prediction ofleft ventricular mass from the electrocardiogram in sys-temic hypertension. Am J Cardiol 77:974, 1966.

78. Kannel WB, Gordon T, Offutt D: Left ventricular hyper-trophy by electrocardiogram: prevalence, incidence, andmortality in the Framingham study. Ann Intern Med71:89, 1969.

79. Sullivan JM, Zwaag RV, El-Zeky F, et al: Left ventricularhypertrophy: effect on survival. J Am Coll Cardiol22:508, 1993.

80. Schillaci G, Verdecchia P, Borgioni C, et al: Improvedelectrocardiographic diagnosis of left ventricular hyper-trophy. Am J Cardiol 74:714, 1994.

81. Verdecchia P, Schillaci G, Borgioni C, et al: Prognosticvalue of a new electrocardiographic method for diagnosisof left ventricular hypertrophy in essential hypertension.J Am Coll Cardiol 31:383, 1998.

82. Okin PM, Devereux RB, Nieminen MS, et al: Electrocar-diographic strain pattern and prediction of new-onsetcongestive heart failure in hypertensive patients. TheLosartan intervention for endpoint reduction in hyper-tension (LIFE) study. Circulation 113:67, 2006.


83. Klein RC, Vera Z, De Maria AN, et al: Electrocar-diographic diagnosis of left ventricular hypertrophy inthe presence of left bundle branch block. Am Heart J108:502, 1984.

84. Chen PS, Moser KM, Dembitsky WP, et al: Epicardialactivation and repolarization patterns in patients withright ventricular hypertrophy. Circulation 83:104, 1991.

85. Wallace AG, Spach MS, Estes EH, et al: Activation ofthe normal and hypertrophied human right ventricle.Am Heart J 75:728, 1968.

86. Durrer D: The human heart: some aspects of its excita-tion. Transact Stud Coll Physicians Phila 33:159, 1966.

87. Kyriacopoulos JD, Conrad LL, Cuddy TE, et al: Activationof the free wall of the right ventricle in experimentalright ventricular hypertrophy with and without rightbundle branch block. Am Heart J 67:81, 1964.

88. Selzer A: Limitations of the electrocardiographic diag-nosis of ventricular hypertrophy. JAMA 195:1051, 1966.

89. Myers GB, Klein HA, Stofer BE: The electrocar-diographic diagnosis of right ventricular hypertrophy.Am Heart J 35:1, 1948.

90. Sokolow M, Lyon TP: The ventricular complex in rightventricular hypertrophy as obtained by unipolar precor-dial and limb leads. Am Heart J 38:273, 1949.

91. Murphy ML, Thenebudu PN, Blue LR, et al: Descriptivecharacteristics of the electrocardiogram from autopsiedmen free of cardiopulmonary disease: a basis for evalu-ating criteria for ventricular hypertrophy. Am J Cardiol52:1275, 1983.

92. Walker JC Jr, Helm RA, Scott RC: Right ventricularhypertrophy. I. Correlation of isolated right ventricularhypertrophy at autopsy with the electrocardiographicfindings. Circulation 11:215, 1955.

93. Scott RC: The electrocardiographic diagnosis of rightventricular hypertrophy: correlation with the anatomicfindings. Am Heart J 60:659, 1960.

94. Roman GT Jr, Walsh TJ, Massie E: Right ventricularhypertrophy: correlation of electrocardiographic andanatomic findings. Am J Cardiol 7:481, 1961.

95. Chou TC, Masangkay MP, Young R, et al: Simple quan-titative vectorcardiographic criteria for the diagnosis ofright ventricular hypertrophy. Circulation 48:1262, 1973.

96. Burch GE, de Pasquale NP: The electrocardiographicdiagnosis of pulmonary heart disease. Am J Cardiol11:622, 1963.

97. Kilcoyne MM, Davis AL, Ferrer I: A dynamic electrocar-diographic concept useful in the diagnosis of cor pul-monale. Circulation 42:903, 1970.

97a. Milnor WR: Electrocardiogram and vectorcardogram inright ventricular hypertrophy and right bundle branchblock. Circulation 16:348, 1957.

98. Holt JH, Barnard AC, Lynn MS, et al: A study of thehuman heart as a multiple dipole electrical source. III.Diagnosis and quantitation of right ventricular hyper-trophy. Circulation 40:711, 1969.

99. Behar JV, Howe CM, Wagner NB, et al: Performance ofnew criteria for right ventricular hypertrophy and myo-cardial infarction in patients with pulmonary hyperten-sion due to cor pulmonale and mitral stenosis. JElectrocardiol 24:231, 1991.

100. Woods A: The electrocardiogram in the tetralogy of Fal-lot. Br Heart J 14:193, 1952.

101. Flowers NC, Horan LG: IV. Hypertrophy and infarction:subtle signs of right ventricular enlargement and theirrelative importance. In Schlant RC, Hurst JW, editors:Advances in Electrocardiography, Orlando, Grune &Stratton, 1972.

102. Prakash R: Determination of right ventricular wallthickness in systole and diastole: echocardiographicand necropsy correlation in 32 patients. Br Heart J40:1257, 1978.

103. Prakash R: Echocardiographic diagnosis of right ven-tricular hypertrophy: correlation with ECG and nec-ropsy findings in 248 patients. Catheter CardiovascDiagn 7:179, 1981.

104. James FW, Kaplan S: The normal electrocardiogram inthe infant and child. Cardiovasc Clin 5:295, 1973.

105. Hiss RG, Lamb LE, Allen MF: Electrocardiographicfindings in 67,375 asymptomatic subjects. X. Normalvalues. Am J Cardiol 6:200, 1960.

106. Ziegler RF: Electrocardiographic Studies in NormalInfants and Children, Springfield, IL, Charles C Thomas,1951.

107. Wigle ED, Baron RH: The electrocardiogram in muscu-lar subaortic stenosis: effect of a left septal incisionand right bundle-branch block. Circulation 34:585,1966.

108. Chou TC, Scott RC, Booth RW, et al: Specificity of thecurrent electrocardiographic criteria in the diagnosisof left ventricular hypertrophy. Am Heart J 60:371,1960.

109. Fowler NO, Westcott RN, Scott RC: The Q wave in pre-cordial electrocardiograms overlying the hypertrophiedright ventricle: intracavity leads. Circulation 5:441,1952.

110. Goodwin JF: The influence of ventricular hypertrophyupon the cardiogram of anterior cardiac infarction. BrHeart J 20:191, 1958.

111. Rosenbaum MB, Elizari MV, Lazzari JO: The Hemi-blocks. Oldsmar, FL, Tampa Tracings, 1970, p. 94.

112. Chou TC, Co P, Helm RA: Vectorcardiographic analysisof T-wave inversion in the right precordial leads. AmHeart J 78:75, 1969.

113. McCaughan D, Primeau RE, Littmann D: The precor-dial T wave. Am J Cardiol 20:660, 1967.

114. Kamper D, Chou TC, Fowler NO, et al: The reliabilityof electrocardiographic criteria of chronic obstructivelung disease. Am Heart J 80:445, 1970.

115. Simonson E: Differentiation Between Normal and Abnor-mal in Electrocardiography, St. Louis, Mosby, 1961.

116. Ellison RC, Miettinen OS: Interpretation of RSR0 in pul-monic stenosis. Am Heart J 88:7, 1974.

117. Selvester RH, Rubin HB: New criteria for the electrocar-diographic diagnosis of emphysema and cor pulmonale.Am Heart J 69:437, 1965.

118. Schmock CL, Pomerantz B, Mitchell RS, et al: The elec-trocardiogram in emphysema with and without chronicairway obstruction. Chest 60:328, 1971.

119. Silver HM, Calatayud JB: Evaluation of QRS criteria inpatients with chronic obstructive pulmonary disease.Chest 59:153, 1971.

120. Padmavati S, Raizada V: Electrocardiogram in chroniccor pulmonale. Br Heart J 34:658, 1972.

121. Wasserburger RH, Ward VG, Cullen RE, et al: TheTa wave of the adult electrocardiogram. An expres-sion of pulmonary emphysema. Am Heart J 54:875,1975.

122. Kerr A, Adicoff A, Klingeman JD, et al: Computer anal-ysis of the orthogonal electrocardiogram in pulmonaryemphysema. Am J Cardiol 25:34, 1970.

123. Incalzi RA, Fuso L, De Rosa N, et al: Electrocar-diographic signs of chronic cor pulmonale: a negativeprognostic finding in chronic obstructive pulmonarydisease. Circulation 99:1600, 1999.


124. Armen RN, Kantor M, Weiser NJ: Pulmonary heart dis-ease: with emphasis on electrocardiographic diagnosis.Circulation 17:164, 1958.

125. Caird FI, Wilcken DEL: The electrocardiogram inchronic bronchitis with generalized obstructive lungdisease: its relation to ventilatory function. Am J Car-diol 10:5, 1962.

126. Millard FJC: The electrocardiogram in chronic lung dis-ease. Br Heart J 29:43, 1967.

127. Phillips RW: The electrocardiogram in cor pulmonalesecondary to pulmonary emphysema: a study of 18cases proved by autopsy. Am Heart J 56:352, 1958.

128. Burwell CS, Robin ED, Whaley RD, et al: Extreme obe-sity associated with alveolar hypoventilation: a pick-wickian syndrome. Am J Med 21:811, 1956.

129. Fowler NO, Daniels C, Scott RC, et al: The electrocar-diogram in cor pulmonale with and without emphy-sema. Am J Cardiol 16:500, 1965.

130. Chou TC: Electrocardiography in Clinical Practice.Adult and Pediatric. 4th ed. Philadelphia, Saunders,1996, p 63.

131. Fowler NO, Noble WJ, Giarratano SJ, et al: The clinicalestimation of pulmonary hypertension accompanyingmitral stenosis. Am Heart J 49:237, 1955.

132. Booth RW, Chou TC, Scott RC: Electrocardiographicdiagnosis of ventricular hypertrophy in the presenceof right bundle branch block. Circulation 18:169, 1958.

133. Scott RC, Kaplan S, Fowler NO, et al: The electrocar-diographic pattern of right ventricular hypertrophy inchronic cor pulmonale. Circulation 11:927, 1955.

134. Semler HJ, Pruitt RD: An electrocardiographic estima-tion of the pulmonary vascular obstruction in 80patients with mitral stenosis. Am Heart J 59:541, 1960.

135. Goodwin JF, Abdin ZH: The cardiogram of congenitaland acquired right ventricular hypertrophy. Br Heart J21:523, 1959.

136. Bassingthwaighte JB, Parkin TW, DuShane JW, et al:The electrocardiographic and hemodynamic findingsin pulmonary stenosis with intact ventricular septum.Circulation 28:893, 1963.

137. Burch GE, DePasquale NP: Electrocardiography in theDiagnosis of Congenital Heart Disease. Philadelphia,Lea & Febiger, 1967, p 322.

138. Cayler GG, Ongley P, Nadas AS: Relation of systolicpressure in the right ventricle to the electrocardiogram:a study of patients with pulmonary stenosis and intactventricular septum. N Engl J Med 258:979, 1958.

139. Gamboa R, Hugenholtz PG, Nadas AS: Corrected(Frank), uncorrected (cube), and standard electrocar-diographic lead systems in recording augmented rightventricular forces in right ventricular hypertension.Br Heart J 28:62, 1966.

140. Barboza ET, Brandenburg RO, Swan HJC: Atrial septaldefect: the electrocardiogram and its hemodynamic cor-relations in 100 proved cases. Am J Cardiol 2:698,1958.

141. Katz LN, Wachtel H: The diphasic QRS type of electro-cardiogram in congenital heart disease. Am Heart J13:202, 1937.

142. Soulie P, Laham J, Papanicolis I, et al: Les principauxtypes electrocardiographiques de surcharge ventricu-laire combinee. Arch Mal Coeur 42:791, 1949.

143. Pagnoni A, Goodwin JF: The cardiographic diagnosis ofcombined ventricular hypertrophy. Br Heart J 14:451,1952.

144. Fraser HRL, Turner R: Electrocardiography in mitralvalvular disease. Br Heart J 17:459, 1955.

145. Levine HD, Phillips E: An appraisal of the newer elec-trocardiography: correlations in one hundred and fiftyconsecutive autopsied cases. N Engl J Med 245:833,1951.

146. Lipsett MB, Zinn WJ: Anatomic and electrocar-diographic correlation in combined ventricular hyper-trophy. Am Heart J 45:86, 1953.

147. Jain A, Chandna H, Silber EN, et al: Electrocardiogra-phic patterns of patients with echocardiographicallydetermined biventricular hypertrophy. J Electrocardiol32:269, 1999.


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