Value of other electrocardiological techniques

Macfarlane et al. (1981) postulated that hybrid criteria derived from a 12‐lead ECG plus three orthogonal leads would produce a sensitivity ranging from 55% to 65%. However, this scoring system has not been popularized. Pipberger et al. (1982) used a new classification system for epidemiological studies that increased sensitivity at the expense of specificity. It may be useful to carry out the preliminary screening.

Acute right ventricular dilation

We will now examine the ECG changes found when abrupt right ventricular overload accompanied by pulmonary hypertension induce right ventricular dilation. This includes cases of decompensated cor pulmonale and pulmonary embolism.

Decompensated cor pulmonale

Patients with cor pulmonale often present with acute hypoxemic episodes accompanied by pulmonary hypertension that are generally reversible but accompanied by alterations in the right ventricular structure or function. In these cases, right ventricular dilation can appear without ventricular wall hypertrophy, at least in the initial stages. Dilation of the right ventricle may therefore be the initial, and sometimes the only, sign of cor pulmonale (Kilcoyne et al. 1970).

Criterion		Sensitivity (%)	Specificity (%)
V1	R/S V1 ≥ 1	6	98
	R V1 ≥ 7 mm	2	99
	qR in V1	5	99
	S in V1 < 2 mm	6	98
	IDT in V1 ≥ 0.35 sec	8	98
V5 − V6	R/S V5 − V6 ≥ 1	16	93
	R V5 − V6 < 5 mm	13	87
	S V5 − V6 > 7 mm	26	90
V1 + V6	R V1 + S V5 − V6 > 10.5 mm	18	94
ÂQRS	ÂQRS ≥ 110°	12–19	96
	SI SII SIII	24	87

There are certain ECG changes that lead us to suspect that the degree of pulmonary hypertension varies abruptly as a consequence of decompensation in patients with cor pulmonale. These include:

• ÂQRS changes, oriented more than 30° to the right of its usual position, with RS or rS persisting until V6.
  
• Presentation of a flattened or negative T wave in the right precordial leads due to associated pulmonary affection that disappears when the affection is over (Figure 10.14). A negative T wave in the right precordial leads can also be seen in ischemic heart disease (see Chapter 13), in which case it is usually not so transient and is sometimes accompanied by a QS morphology that may also be found in right ventricular dilation (usually only in V1). The marked differences in clinical setting help to establish the diagnosis.

  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  

  Sign	Points
  1. Ratio reversal (R/S V5: R/S V1 ≤ 0.4)	5
  2. qR in V1	5
  3. R/S ratio in V1 > 1	4
  4. S in V1 < 2 mm	4
  5. R in V1 + S in V5 or V6 > 10.5 mm	4
  6. Right axis deviation >110°	4
  7. S in V5 or V6 ≥ 7 mm and each ≥2 mm	3
  8. R/S in V5 or V6 ≤ 1	3
  9. R in V1 ≥ 7 mm	3
  10. S1, SII and SIII each ≥1 mm	2
  11. SI and OIII each ≥1 mm	2
  12. R′ in V1 earlier than 0.08 and ≥2 mm	2
  13. R peak in V1 or V2 between 0.04 and 0.07	1
  14. S in V5 or V6 ≥ 2 mm but <7 mm	1
  15. Reduction in V lead R/S ratio between V1 and V4	1
  16. R in V5 or V6 < 5 mm	1

  
  

  Interpretation of point score:

  
  

  
  
  • 10 points: Right ventricular enlargement
    
  • 7–9 points: Probable right ventricular enlargement or hemodynamic overload
    
  • 5–6 points: Possible right ventricular enlargement or hemodynamic overload.

  
  

  These criteria do not take into account serial electrocardiographic comparisons. Such additional data may be the interpreter’s impression of the likelihood of fixed enlargement or dynamic overload.

  
  
• Deviations of the ST segment in frontal and/or horizontal plane leads.
  
• Appearance of RBBB morphology. A depressed or even elevated ST with a new RBBB pattern may be found in patients with important pulmonary hypertension. With adequate treatment, clinical outlook and ECG alterations may improve.

Right ventricular enlargement in children

In the neonatal period, it is difficult to diagnose RVE because there is already a physiological RVE. Nonetheless, any of the following criteria suggest the existence of abnormal RVE in the newborn (Burch and DePasquale 1967; Moss and Adams 1968; Rowe and Mehrizi 1968; Fretz et al. 1992):

• qR in V1,
  
• solitary R in V1 over 20 mm,
  
• S in V6 greater than 11 mm after the 2nd day of life, positive T in V1 after the 4th day, as long as T is also positive in the left precordials, and
  
• P wave taller than 4 mm.

Later on and until adulthood, some of these signs undergo modifications. RVE is then suggested by:

• R/S ratio over 1 in V1 at 2 or 3 years of age, with intrinsicoid deflection time (IDT) ≥0.03 sec (except for post‐term infants) or
  
• an rSr′ morphology in V1 may be a normal variant, frequently due to bad location (V1 too high) of V1 electrode. May also be seen in pectus excavatum and other thoracic abnormalities. It is especially more indicative of RVE when: (i) R′ has a high voltage, (ii) the morphology does not vary with respiration (see Figure 7.40), (iii) it is accompanied by a marked S in V6, and (iv) ÂQRS is right‐deviated beyond +120°.

Indirect signs of right ventricular enlargement

We consider the following to be indirect signs of RVE:

• clear signs of right atrial enlargement in the absence of tricuspid atresia;
  
• signs of left atrial enlargement in the presence of mitral stenosis; or
  
• atrial fibrillation accompanying mitral stenosis.

Regression of ECG signs

Regression of RVE signs is frequently seen post‐surgery in patients with congenital heart diseases such as ASD or pulmonary stenosis (Figure 10.11). After correction of Fallot’s tetralogy, post‐operative ECG often shows advanced RBBB (see Chapter 11) (Figure 11.12), masking the regressive changes of the RVE.

Differential diagnosis of right ventricular enlargement with dominant R or rSr′ morphology in V1

A differential diagnosis should be made with all cases that present with prominent R in V1, as a result of an anterior and mainly right‐oriented loop (Table 10.3).

• Normal variant. Prominent R (RS) or rSr′ in V1 is seen with some frequency in 2.5% of normal adults, particularly in those with extreme counterclockwise rotation (RS) or thoracic abnormalities (rSr′), such as pectus excavatum or straight back syndrome. A low‐voltage RS morphology in V1 may be seen in post‐term newborns, even into adulthood (see Chapter 7). As we have already commented, the location of V1 lead too high, usually originates a QRS pattern with final r′ in V1. Therefore, the valve of PtfV1 as abnormal P wave indices is controversial (see Chapter 9).

• Sometimes prominent R, especially in V2, can result from positional changes (extreme counterclockwise rotation, massive pleural effusion, etc.). In these cases, the T wave is usually positive in V1 if there is no coexistent heart disease.
  
• Right bundle branch block. Regardless of whether the RBBB is partial or advanced, a dominant R morphology can be seen in V1, V2. The rsR′ morphology with QRS <0.12 sec, corresponding to classic, isolated partial RBBB, may be identical to the morphology observed in RVE. This morphology typically appears in ASD, but it can also be seen in mitral stenosis and early‐stage congenital heart diseases with systolic overload, such as pulmonary stenosis. This rsR′ morphology usually represents a less important degree of RVE than the presence of solitary R morphology (Figure 10.2). Therefore, the same patient can show first, one morphology and then the other in the course of the disease (see Figure 10.4).

  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  

  Clinical setting	R or RN(r′) morphology in V1	QRS width	P wave morphology in V1
  1. No heart disease Electrode misplacement Hypermature Normal variant: Fewer Purkinje fibers in anteroseptal zone or extreme counter clockwise rotation Thorax abnormalities (pectus excavatum) (see Figure 7.16)		<0.12 sec	P– in 2° IS P+ or ± In 4° IS
  		<0.12 sec	Normal
  		<0.12 sec	Final negativity
  2. Classical RBBB		From <0.12 to >0.12 sec	Normal
  3. Atypical RBBB Ebstein’s disease Arrhythmogenic RVD/C Low voltage in V1 or ∑ wave Brugada syndrome (see Table 21.9)		Usually ≥0.12 sec	Usually peaked and/or ±
  		May be 0.12 sec	Usually pathologic
  		Sometimes ≥0.12 sec	Normal
  4. Right or biventricular enlargement (athletes) or even LVH (Hypertrophic or others CM)		<0.12 sec	Usually tall and peaked. Sometimes ±
  5. Wolff–Parkinson–White syndrome		From <0.12 to >0.12 sec	Normal P wave with short PR
  6. Lateral MI		<0.12 sec	Usually normal
  7. Block of middle fibers (especially if the pattern is transient (see Chapter 11)?	Prominent R in V1 or more frequently V2	<0.12 sec	Usually normal

  
  
• Atypical RBBB. These include the ECG pattern seen in some congenital (Ebstein’s disease) and inherited heart diseases (arrhythmogenic right ventricular dysplasia, some Brugada pattern).
  
• Cases of LV or biventricular enlargement including athletes. Also in some cases of hypertrophic cardiomyopathy (HCM), or other types of cardiomyopathy with isolated LVE involving the septum, a tall R wave in V1 (>7 mm), usually with a deep S in the same lead, may be seen. An increase in the first vector due to septal hypertrophy is probably responsible, although there is not always a deep Q wave in V5–V6 because the enlarged first vector is directed more forward than to the right.
  
• Type II and III WPW pre‐excitation. There is no problem if initial slurrings are visible (δ wave) and the PR interval is short. When there is an important degree of pre‐excitation, an exclusive R morphology in V1 may be seen (see Figure 12.2).
  
• Lateral infarction (see Figures 13.72 and 13.76). The QRS pattern in V1 may present with prominent R (rR, RS) with a usually positive T wave (Bayés de Luna et al. 2006). It has been very well demonstrated with ECG‐MR correlations that prominent R in V1 in patients with ischemic heart disease, is due to lateral MI, not to posterior MI that now we know, does not exist (Bayés de Luna et al. 2015). The QRS is consistently less than 0.12 sec. The differential diagnosis between RVE and lateral infarction can be difficult with conventional electrocardiography alone. Lateral myocardial infarction is supported by the presence of positive and an especially tall and symmetric T wave in V1–V2 and often abnormal Q waves in II, III, and aVF of associated inferior myocardial infarction. RVE is favored by a negative T wave in V1–V2, a right ÂQRS, and atrial signs of right atrial enlargement.
  
• Block of middle fibers. In the absence of lateral infarction or RVE, the presence of transient prominent R in V1–V2 may be explained by a block of left bundle middle fibers (see Chapter 11, Anteroseptal middle fiber block. Myth or reality? Figures 11.44–11.47).

Differential diagnosis of right ventricular enlargement with rS or Qs morphology in V1

The presence of a QRS complex without final anterior forces and consequently with rS morphology in V1 or even QS (see Figure 10.2VI), or, at most, rSr′ with a low‐voltage r′ (Figure 10.2VII), sometimes with a much deeper S wave in V2, can cause confusion between this type of RVE and left ventricular or biventricular hypertrophy, septal infarction, or zonal right ventricular block, a frequently associated pathology. We will discuss the most important ECG characteristics in these cases.

In this type of RVE, the S waves are prominent until V6, there is dominant R in V3 R–V4R and in aVR there is a terminal R because often the final vector is oriented backward, but also upward and to the right (see Figure 10.3C and D). Sometimes there is a shallow S in V1 with greater voltage of S in V2, with an RS pattern until V6. In biventricular hypertrophy, a deep S in V2 with small S in V1 (shallow S inV1) may also exist, but in left precordials, there is a R or Rs pattern.

In LVH, the forces are directed backward and to the left, originating a tall R wave in V5–V6 and usually a deep S in right precordials, V3R and V4R. Moreover, in the frontal plane, ÂQRS is deviated to the left and in aVR, the terminal r is minimal or not found.

Biventricular enlargement diagnosis is possible when there is a much larger S wave in V2 than in V1, with R or Rs morphology in V6, and SI, SII, SIII morphology, or right ÂQRS in the frontal plane.

In chronic septal infarction a negative post‐ischemic T wave is seen from V1 to V2, V3, frequently with QS or qrS in the same leads, and with an R/S ratio in V6 > 1 and a generally normal P wave.

The C loop of Figure 10.3(“SI, RII, RIII”‐type) (Figure 10.12) should be distinguished from inferoposterior hemiblock (IPH) of the left bundle branch (see Chapter 11). In IPH, the q of III and aVF is more marked, the R/S ratio in V6 > I, and the atriogram is not suggestive of right atrial enlargement.

The D loop of Figure 10.3(“SI, SII, SIII”‐type) (Figure 10.13) is explained by the existence of zonal right ventricular block and/or RVE (see Chapter 11). In patients with COPD, this type of loop is usually due to associated RVE with a certain degree of zonal conduction delay in the right ventricle (Bayés de Luna et al. 1987). However, the presence of the SI, SII, SIII pattern in normal individuals is likely to be caused more by a variation in the distribution of the right ventricular Purkinje fibers with some physiological delay of conduction than by a true right peripheral block (see Figure 11.19). In addition, the differential diagnosis between the SI, SII, SIII pattern and hemiblock of the superoanterior division of the left bundle branch must be made. The morphology is that of SI, SII, SIII in RVE and/or peripheral right ventricular block, with SII ≥ SIII and a low‐voltage R in I (Figure 10.3D), while in left superoanterior hemiblock (SAH), there is an exclusive R wave in lead I with high voltage and SII < SIII.

Differential diagnosis of right ventricular enlargement in the presence of ST/T changes

These changes may be seen as the most evident findings in cases of RVE, especially in acute dilation of the right ventricle. The clinical setting may be very useful to rule out other etiologies, especially ischemic heart disease.

Advanced RBBB

In the presence of advanced RBBB (QRS ≥ 0.12 sec) (Figure 11.13A), RVE is suggested when the following are found:

• rsR’ morphology is extended beyond V2. This is seen especially in right ventricular dilation (ASD, etc.).
  
• High‐voltage R’. The taller the R′, the greater the likelihood of associated RVE. However, there are instances of RBBB with tall R′ without RVE, and vice versa.
  
• Solitary R in V1. This results from the anterior orientation of the whole loop. Sometimes there is a solitary R of low voltage in emphysematous subjects (Figure 11.13A). It is frequently associated with the absence of “q” in V6.
  
• ‘rS’ morphology in I and ‘qR’ in III. In this case, the possibility of inferoposterior division hemiblock added to the advanced RBBB must be ruled out.
  
• P wave criteria of right atrial enlargement.

Advanced LBBB

In the presence of advanced LBBB (QRS ≥ 0.12 sec), RVE is suggested (Figure 11.13B) when the following are found:

• ÂQRS is to the right, with an RS morphology in lead I that may not be explained by other causes (see Figure 11.27).
  
• There is evident “r” in V1 in the absence of myocardial infarction.
  
• In precordial leads, the transition to an Rs pattern goes beyond V4.

Changes in the QRS complex (Figures 10.19–10.25)

• The maximum loop vector increased in voltage is directed to the left, generally farther to the back than normal and more upward. When we discuss the diagnostic criteria of LVH, we will comment on the voltage limits of QRS for this diagnosis. In any case, the LVH explains the taller R wave in the left precordial leads and in leads I and aVL, and the deep S wave in the right precordials leads V1, V2, or V3. In V4, there is a deep S wave, a transitional morphology, or a tall R wave.

  

  

  

  
  

  When septal hypertrophy (especially in the apical zone) predominates over that of the left ventricular free wall (asymmetric septal HCM), or when there is biventricular enlargement, the maximum loop vector can be fairly anterior (at about 0°), and the QRS may even show an RS pattern in lead V2 or even V1 (Figures 10.19E and 10.25). This morphology can be confused with isolated levorotation, or all causes of high R in V1 and/or V2 in the absence of RVE (see Table 10.3).

  
  
• A delay in recording the maximum loop vector, accounting for increased IDT (time till the take‐off of QRS) in the left precordial leads and usually in aVL. The IDT is not of value in classical bipolar leads (I, II, III). The IDT is considered to be increased when it exceeds 0.045 sec. Occasionally, slightly higher values are seen in athletes or vagal overdrive, for example. In LVE with the loop onset to the left and forward (left ventricular strain pattern), IDT measurement is useless because the right initial forces are reduced. Classically, it was thought that cases with severe but not long‐standing aortic regurgitation that frequently present with a normal onset of ventricular activation to the right (q in I and V6) have a larger IDT (Figure 10.20) than those with aortic stenosis of similar severity and characteristics (Figure 10.21). This is explained because loops with the initial forces to the left are seen less frequently in patients with not long‐standing aortic regurgitation (Figure 10.19A) (see below).

  

  

  

  
  
• Slightly longer QRS loop. The duration of the QRS complex, which is normally around 0.10 sec, is extended to 0.11 sec. The presence of QRS ≥ 0.12 sec is explained by associated advanced LBBB.
  
• Direction of the initial forces. The initial forces, especially in patients with long‐standing aortic valve disease and severe and long‐standing LVE, are frequently directed forward and to the left because of associated partial LBBB (Piccolo et al. 1979) and/or septal fibrosis (Bayés de Luna et al. 1983). The latter has been demonstrated in patients with aortic valve disease with septal biopsy performed during open heart surgery. The results of septal biopsy show that the q wave in V5–V6 is related more to the degree of septal fibrosis than to the type of hemodynamic overload (systolic or diastolic) (Cabrera and Monroy 1952). The greater the septal fibrosis, the smaller the q wave. Every case with a “q” wave <1 mm or absent presented with more than 10% septal fibrosis, and vice versa (Figures 10.22 and 10.23). Since aortic stenosis presents with more septal fibrosis than aortic regurgitation, a conspicuous q wave is more often seen in the latter. However, in the long follow‐up of cases of aortic regurgitation, the “q” wave in V5–V6 is not usually recorded or is seen to have decreased markedly (Figure 10.20). The initial forces to the right (“q” wave) frequently seen in cases of ventricular enlargement of severe but not long‐standing aortic regurgitation are frequently more marked than normal and are followed by a high‐voltage R wave. This is due to septal hypertrophy in the absence of septal fibrosis and/or a delay in impulse conduction in the peripheral portions of the left intraventricular conduction system that is greater than by the proximal portion. The septal forces are more evident because the left ventricular wall vector takes longer to form.

  

  
  

  Very conspicuous “q” waves are observed in 10–35% of cases of HCM, with the “q” wave sometimes more prominent than the “R” wave, with QS or QR patterns appearing (Figures 10.19D and 10.24). However, the presence of a prominent Q wave attributed to septal hypertrophy is a poor predictor of septal thickness (Moro et al. 1995). It is essential to rule out the “Q” wave of necrosis. The Q waves of HCM are thinner and, although they may be deep, they are usually followed by positive T waves (Figure 10.24) (see Chapter 13).

  
  
• QRS loop in the frontal plane (Figure 10.19). Because the heart frequently assumes a horizontal position in LVH, the QRS loop usually rotates counterclockwise in the frontal plane, deviating a little more to the left than normal. This may explain an rS morphology in III and an aVF and the slightly left ÂQRS deviation that may be seen, especially in long‐standing aortic stenosis (Figure 10.21). However, if the loop rotates clockwise, as is often the case in congenital aortic stenosis with vertical heart, a dominant R may appear in the QRS complex in II, III, and aVF (Figure 10.19B).
  
• The terminal portion of the loop remains on the left (Figure 10.19). Due to the final predominance of left ventricular depolarization over right (opposite to normal), the terminal portion of the loop remains in the positive hemifield of I, V6, and at times V5. As a result, no S waves are found in these leads.

Changes in ST and T (Figures 10.19, 10.25, 10.26, and 10.27B)

Two factors contribute to the appearance of repolarization alterations: the severity of the lesion and the duration of its evolution (Figures 10.19, 10.25, 10.26, and 10.27B). In valvular disease, as well as in hypertension or cardiomyopathies, the ST–T changes are determined especially by the duration of evolution.

• In heart diseases with more or less important LVH but not long‐standing, there is usually no clear ST segment depression and the T loop conserves its normal orientation (it is sometimes more anterior), although it is generally more symmetric. The T wave is still positive, but it is more symmetric and has a straight ST segment, even in moderate or severe but not long‐standing LVH. Its morphology differs somewhat according to the type of hemodynamic overload and is typically taller in diastolic overload (aortic regurgitation). The latter case usually shows a more evident q wave (Figure 10.26B,C). This relatively unaltered ECG does not mean that the valvular heart disease is mild, but that it is not very long‐standing if it is severe (Figures 10.20 and 10.26B,C). These morphologies are sometimes similar to those seen in healthy lean adolescents and adults. However, in the latter, the junction of ST and the T wave is smooth, and the T wave is asymmetrical with a slow upward slope (Figure 10.27A).
  
• As LVH increases, in part conditioned by the elapsed years of evolution but also because of the severity of the heart disease (especially the severity of aortic stenosis that increases with time), whether or not the LVH is secondary to systolic or diastolic hemodynamic overload, the T wave evolves from the positive morphology to the typical pattern of ST segment depression convex with respect to the baseline, with a final negative T wave with asymmetric branches (Figure 10.26A–C). This so‐called “strain pattern” occurs because the repolarization of the free wall starts in the subendocardium. The ST vector and T loop are therefore opposite to QRS and the initial part of the T loop is recorded more slowly (Figures 10.19A,B and 10.26A–C). The presence or not of a small “q” wave is more related to the degree of septal fibrosis and/or partial LBBB than to the type of hemodynamic overload (Figures 10.22, 10.23, and 10.26A–C). The partial LBBB may also help to explain the appearance of repolarization abnormalities (Bisteni 1977).

  

  
  
• The T wave and ST segment changes secondary to depolarization abnormalities, in this case LVH (secondary changes), are also associated to primary changes (prolonged AP duration) that may be related to ischemia or the effects of digitalis or other drugs, originating a mixed morphology with a more homogeneously recorded T wave and/or a more important ST depression, especially in long‐standing cases. The T wave is thus deeper and/or more symmetric and the deviation of ST from the baseline is more conspicuous and less convex (Figure 10.28). The contribution of both primary (QT prolongation–AP prolongation) and secondary (reduced conduction velocity) changes to the ECG pattern of LVH has been recently studied using an analytical computer model (Bacharova et al. 2010).
  
• It has been suggested (De Piccoli et al. 1987) in an ECG–echocardiographic study that patients with systolic overload of the left ventricle and negative ST–T have normal ventricular geometry, while patients with diastolic overload of the left ventricle and negative ST–T have an abnormal geometry of the left ventricle.
  
• The presence of a very deep negative and symmetric T wave in leads with an exclusively tall R wave is very suggestive of an apical type of HCM. In this case, the abnormal repolarization may appear early on in the evolution of the disease.

ECG criteria based on QRS voltage

The ECG diagnosis of LVH is based mainly on the increase of the QRS voltage generated by the increase of left ventricular mass. The voltage criteria correlates better with ventricular wall thickness than with left ventricular mass, and the sensitivity of the ECG criteria declines with cavity dilation. As with many diagnostic techniques, specificity of these criteria is better than sensitivity. Table 10.4shows many of the voltage criteria with its sensitivity, specificity, and accuracy. We will now comment on the most used criteria.

The best‐known QRS voltage criteria and voltage × duration products are as follows:

• The Sokolow–Lyon criteria (Sokolow and Lyon 1949) in which there is a LVE when SV1 + RV5–6 ≥ 35 mm. Nonetheless, although it is very specific (≈90–95%) (very few false positives), as happens with other voltage criteria, it has a low sensitivity (≈20–25%).
  
• The ECG criterion RVL + SV3 > 24 mm for men and >20 mm for women (Cornell voltage criteria) (Devereux et al. 1984; Casale et al. 1985, 1987). This is no more sensitive than the Sokolow–Lyon criterion, with mild higher specificity (>95%). With the Cornell product, a modified Cornell voltage criterion, a higher sensitivity without compromising specificity is obtained (Mulloy et al. 1992; Okin et al. 1995). The calculations, however, are tedious. Furthermore, in other series, the sensitivity is found to be lower. Even in those studies that corrected the Cornell voltage with the inclusion of body mass index (Norman and Levy 1993), sensitivity does not increase to above 50%.
  
• The sum of 12‐lead voltage has been used in aortic valve disease patients with necropsic and hemodynamic correlations (Siegel and Roberts 1982) and in hypertension patients with echocardiographic correlations (Koito and Spodick 1989; Rodriguez Padial 1991) (see Chapter 21).
  
• Talbot et al. (1976) studied the utility of diverse scalar and orthogonal ECG criteria for diagnosis of LVE, and the repercussions of associated diseases (myocardial infarction and ventricular block) on the usefulness of these criteria. The criterion R in aVL ≥ 11 mm in the absence of left axis deviation was found to be the most specific one in every group (92% in isolated LVE with a sensitivity of 10%), while in the presence of SAH, the voltage of R ≥ 16 mm in aVL had similar specificity for LVE (see later). Almost the same results were obtained when myocardial infarction was found to be associated.
  
• Murphy et al. (1983) studied the sensitivity of 30 ECG criteria for LVH alone or combined with RVE in four scenarios (ischemic heart disease, systemic hypertension, valvular heart disease, and cardiomyopathy). Some ECG criteria frequently showed a high sensitivity for one disease but not for others. Precordial voltage criteria were more sensitive for those with hypertension and valvular disease.
  
• High QRS voltage is determined by the relationship between ventricular wall thickness and cavity radius. If the product of the two exceeds 300 mm, the Sokolow index is always ≥35 mm. This explains how a large dilation with thin walls and a small radius with thick walls both produce large QRS voltage.
  
• The importance of the degree of LVH. The sensitivity of ECG for diagnosing LVH (Van der Wall et al. 1999) varies from 21% to 54%, with sensitivity increasing as the degree of hypertrophy increases, although this is not apparent in all ECG–LVH criteria. According to Devereux et al. (1984), the sensitivity of the ECG when using the Cornell voltage criteria for ECG–LVH increased from 27% for mild LVH to 57% for severe cases, with a specificity of 97% that indicated a low risk of false‐positive readings. These data are fairly consistent with other studies, such as the Perugia score (Figure 10.29). On the other hand, methods using combinations of various criteria also demonstrated improved sensitivity. Each of the results shown in Table 10.4has to be contemplated in light of this. The sensibility, especially of different criteria, varies widely according to population, the grade of hypertrophy, and the methodology used. We have shown the different sensitivity values of Cornell voltage criteria and Perugia score according to the severity of LVH. In addition, the Romhilt–Estes score ≥4 has an SE of 54% in the original paper (necropsic study) (Romhilt and Estes 1966); in a recent paper using CMR as a standard and in other types of population, it was only 15.9% (Jain et al. 2010).

Point score systems

Romhilt–Estes score

Romhilt and Estes (1966) devised a score (Table 10.5) that attained a global specificity of 97% and a sensitivity of ≈55% in a post‐mortem series of mostly hypertensive and coronary patients. Compared with the voltage criteria, this system is somewhat more accurate (see Table 10.4). In this series, 58% of hypertrophic patients scored 5 points and 62% at least 4 points, while only 2 patients (3%) without hypertrophy scored 5 points. In patients with hypertension, sensitivity was 45% and in coronary patients it was 55%. When hypertension and coronary disease coexisted, sensitivity was 88%.

Although an objective demonstration has yet to be carried out, the Romhilt–Estes point system would probably improve in sensitivity with little loss of specificity if the following additions or modifications would be performed: (i) ST–T vector opposite to QRS with digitalis = 2 points instead of 1; (ii) other repolarization alterations (flattened or negative T, straightened ST, negative U) = 1 point; and (iii) atrial flutter or fibrillation = 2 points. As mentioned above, however, in other group of populations that are based on standards of echocardiography or CMR for validating LVH, the sensitivity of this score is much lower while maintaining a very high specificity (≈100%).

A. Criteria based on QRS modifications
1. Voltage criteria	3 points
One of the following should be present: R or S in the FP ≥ 20 mm S in V1–V2≥ 30 mm R in V5–V6 ≥ 30 mm
2. ÂQRS at −30° or more to the left	2 points
3. Intrinsicoid deflection in V5–V6 ≥ 0.05	1 point
4. QRS duration ≥0.09 sec	1 point
B. Criteria based on ST‐T changes
1. ST‐T vector opposite to QRS () without digitalis	3 points
2. ST‐T vector opposite to QRS () with digitalis	1 point
C. Criteria based on P wave abnormalities
1. Negative terminal P mode in V1 ≥ 1 mm in depth and 0.04 sec in duration	3 points

Regression models

Regression equations for estimating left ventricular mass were used to identify LVH. Table 10.4 shows the most common models. However, they are not used in clinical practice, although they may be implemented in automatic interpretation. The accuracy in detecting LVH and evaluating risk of cardiovascular death is similar to the best voltage or score systems (see Table 10.4).