Cardiol Clin 24 (2006) 401411

Is Electrocardiography Still Useful in the Diagnosis of Cardiac Chamber Hypertrophy and Dilatation?
Peter W. Macfarlane, DSc, FESC, FRCPa,b
a

Division of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow G12 8QQ, Scotland, UK b Royal Inrmary, 10 Alexandra Parade, Glasgow G31 2ER, Scotland, UK

With the ubiquitous availability of the echocardiograph, it is nowadays the case that a hospital physician will seek to obtain an echocardiogram for detailed information on ventricular function when appropriate and in so doing obtain information on the presence or absence of cardiac chamber hypertrophy or enlargement. In addition, family practitioners are more easily able to refer patients to a local hospital or cardiology practice for an echocardiogram, although steps are having to be taken, at least in the United Kingdom, to minimize unnecessary referrals, particularly in patients who have suspected heart failure, by rst assessing the ECG and measuring B-type natriuretic peptide (BNP). In other health care systems, it is possible that patients may be referred directly to a cardiologist for echocardiographic investigation as required. Notwithstanding, an ECG is always part of a cardiologic work-up, and the question posed is whether there is still value in reviewing the ECG for evidence of changes related to chamber enlargement when an echocardiogram can be obtained if required. Atrial enlargement The P wave of the ECG is one of the smallest components of the ECG waveform. For this reason, accurate measurement is dicult, and many criteria for P-wave abnormality are nonspecic as a result. It is generally accepted that right atrial depolarization contributes to the initial part of the P wave, whereas left atrial

E-mail address: peter.w.macfarlane@clinmed.gla.ac.uk

depolarization is responsible for the terminal P-wave appearances. Thus, if there is any form of right atrial abnormality, the P- wave duration should not be increased, and the initial component of the P wave may be increased in amplitude. On the other hand, if there is a left atrial abnormality, the duration of the P wave may be lengthened, and in some leads there will be a more obvious division of the P wave into two components. Fig. 1 shows in schematic form how these dierent changes may appear in lead II and lead V1 of the 12-lead ECG. There is some dispute over the terminology to be used in cases of atrial abnormality. Left atrial enlargement is said to arise from atrial dilatation or pressure overload [1] or indeed from abnormal intra-atrial conduction [2]. Thus, a term such as left atrial abnormality can be used to cover different forms of atrial pathology. Waggoner and colleagues [3] reviewed ECG criteria for left atrial enlargement and compared ndings against two-dimensional echocardiograph measures. They found that of 39 patients who had false-positive ECG diagnoses of left atrial abnormality according to echocardiograph criteria, only 2 (5%) were free of organic heart disease. Thus, their conclusion was that the ECG detected left atrial abnormality rather than left atrial enlargement. Waggoner and colleagues [3] had used criteria such as P duration in lead II of 120 milliseconds or longer, (negative P duration in V1)/(PR segment duration) of 1.0 or longer, and the P terminal force in V1 greater than 3 mVms. The second of these criteria is a form of modied Macruz index, dened as P duration/PR segment (ie, end P to QRS onset) [4]. P terminal force in V1 is dened as the duration
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Fig. 1. Atrial abnormalities. (A) If there is right atrial enlargement, then the initial component of the P wave is enlarged. (B) If there is left atrial enlargement, there may be P-wave widening with an M-shaped P wave in lead II and an increased P terminal force in V1.

of the negative (terminal) component of the P wave times the amplitude of this component referred to baseline. P mitrale is dened as an M-shaped P wave in lead II with an increased P duration (Fig. 1). The name suggests that this abnormality is found in mitral valve disease, which is sometimes the case, but this type of P wave also can be found in patients who have constrictive pericarditis or when there is an intra-atrial conduction defect. In a study of 53 patients who had uncomplicated essential hypertension [5], ECG criteria of left atrial abnormality such as P duration greater than 0.12 milliseconds, P amplitude greater than 0.25 mV in lead II, Macruz index greater than 1.6 in lead II, and P terminal force in V1 of 4 mVms or less were assessed. (P terminal force more negative than 4 mVms where the P terminal amplitude is expressed as a negative value.) Echocardiograph measurements of left atrial dimensions were obtained together with Doppler estimates of left ventricular (LV) lling. The Macruz index had a sensitivity of 58.5% in detecting left atrial abnormality and was the best of the ECG measures. The authors concluded that ECG signs of left atrial abnormality were related more to an increased atrial workload, possibly secondary to impaired ventricular lling, than to left atrial enlargement [5]. Right atrial abnormality Right atrial abnormality is not commonly reported on an ECG. It can manifest as a tall P wave in V1 with the P amplitude being greater

than an age-dependent value around 0.2 mV. It may be found in patients who have congenital heart disease, pulmonary hypertension, or obstructive airways disease. Classically, a patient who has chronic obstructive airways disease may have so-called P pulmonale characterized by a tall, peaked P wave of at least 0.25-mV amplitude in lead II. There have been few studies in patients who have this abnormality, and most ECG criteria for right atrial abnormality are nonspecic and somewhat insensitive [68]. On occasions peaked P waves may be found in inferior leads in the absence of any demonstrable right atrial enlargement or dilatation, and in this case the term pseudo P pulmonale is used. It has been suggested that if left-sided heart disease is present, such an ECG nding might reect an increase in left atrial dimensions [9]. Kaplan and colleagues [10] evaluated ECG criteria for right atrial enlargement against two-dimensional echocardiograms in 100 patients who had right atrial enlargement according to echocardiography and in 25 control patients. The most powerful predictors of right atrial enlargement were QRS axis greater than 90 , P amplitude in V2 greater than 0.15 mV, and R/S greater than 1 in V1 in the absence of complete right bundlebranch block (RBBB). The combined sensitivity of these criteria was 49% with 100% specicity. On the other hand, classic criteria for P pulmonale were only 6% sensitive. Bi-atrial enlargement Occasionally an ECG may show P-wave abnormalities suggestive of both right and left atrial enlargement, and in this case the term bi-atrial enlargement may be used. Thus, criteria for biatrial enlargement are essentially a combination of those for right and left atrial enlargement. Use of the signal-averaged ECG In the last decade, there has been interest in using the signal-averaged ECG to measure P-wave duration and in using this parameter as an indicator of atrial enlargement and even as a prognostic index for the development of atrial brillation. Dixen and colleagues [11] showed that the signal-averaged P-wave duration was signicantly correlated with the left atrial diameter in 74 patients in whom a signal-averaged ECG and echocardiogram had been recorded. The left atrial volume, the right atrial volume, and in particular

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the total atrial volume were more strongly correlated to the signal-averaged P-wave duration, however. On the other hand, Merckx and colleagues [12] looked at correlations between the P-wave duration on the signal-averaged ECG and estimates of atrial activation time derived from Doppler tissue imaging. They showed that there was a significant correlation between the signal-averaged ECG P-wave duration and atrial activation times determined from the Doppler method, which was much quicker to use than a signal-averaged ECG when an echocardiogram was being recorded in any event. Approximately 1 additional minute was required. The conclusion was that this echocardiographic estimate of atrial activation time could be useful in detecting those patients prone to develop atrial brillation. In an interesting study using fractal measures, Peters [13] showed that course F waves in patients who had atrial brillation seemed to be more related to a larger left atrial size (R4.6 cm) than were smaller brillatory waves. Atrial abnormalitiesdconclusion There are few areas where the ECG holds any advantage over an echocardiogram in elucidating atrial enlargement. Widened P waves as found in intra-atrial conduction defects may, however, be the only way of determining that there is some form of atrial abnormality. Furthermore, the signal-averaged ECG may be of some prognostic value in predicting those patients at increased risk of developing atrial brillation when an echocardiogram is not available.

Table 1 Classication of left ventricular enlargement Left Ventricular Volumea Normal Left Ventricular Massb Normal Normal Abnormal

Abnormal

Concentric left ventricular hypertrophy Isolated left Eccentric left ventricular ventricular volume hypertrophy overload

a Abnormal left ventricular volume is dened as volume greater than 90 mL/m2. b Abnormal left ventricular mass is dened as mass greater than 131 g/m2 in men and mass greater than 108 g/m2 in women where indexing is with respect to body surface area. From Huwez FU, Pringle SD, Macfarlane PW. A new classication of left ventricular geometry in patients with cardiac disease based on M-mode echocardiography. Am J Cardiol 1992;70:687.

appearances in a group of 202 cardiac patients failed to elicit any ECG criteria that could separate the dierent types of LV geometry, however [15]. Echocardiography itself is not without its diculties in estimating LV mass. On the other hand, Rautaharju and colleagues [16] introduced several equations for the calculation of LV mass from the ECG. One set of equations for white men and women is as follows: LV mass men 0:026 CV 1:25 W 34:4 LV mass women 0:020 CV 1:12 W

Left ventricular enlargement No ECG criteria have ever successfully separated the dierent forms of LV abnormality (ie, LV hypertrophy [LVH] caused by an increase in muscle thickness or LV dilatation with increased LV cavity volume). Huwez and colleagues [14] introduced a new classication of LV geometry using M mode ECG. This classication was based on the use of an indexed LV mass greater than 131 g/m2 in men and 108 g/m2 in women together with a knowledge of indexed LV volume, which was regarded as abnormal if it exceeded 90 mL/m2. This classication led to four groupings based on normal or abnormal indexed LV mass and normal or abnormal indexed LV volume. Table 1 shows the classications. Extensive investigation of ECG

36:2 where LV mass equals LV mass in grams, CV equals Cornell voltage (RaVL SV3) in microvolts [17], and W equals weight in kilograms. By using these equations, Padmanabhan and colleagues [18] have shown that there are signicant heritable eects for ECG measures used in LV mass estimation. Inuence of constitutional variables on ECG criteria for left ventricular hypertrophy Age and sex It has been known for many years that normal ECG voltages vary both with age and sex (eg, see

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[19]). Voltages are highest in adolescence, particularly in males, and decrease with increasing age, with a leveling beyond approximately 50 years of age. A similar trend can be seen for women, although this is less marked. Signicant dierences in upper limits of normal QRS voltages exist between men and women of similar age, as can be seen in Fig. 2. These dierences mean that any criteria for ECG LVH and ECG right ventricular hypertrophy (RVH) should be age and sex dependent and explains why some ECG criteria for ventricular hypertrophy that are not age and sex adjusted perform in a suboptimal way. QRS duration is approximately 7 milliseconds longer in women than in men, but criteria that use QRS widening as an index of LVH generally fail to acknowledge this simple observation [19]. A fuller discussion of normal limits of ECG measures can be found elsewhere [19]. Other factors Other factors that may aect voltage include race. Blacks tend to have higher precordial voltages than whites [20], and in turn it has been shown that Chinese individuals have lower voltages than whites [2123] and hence also lower

voltages than blacks. Furthermore, increasing body mass index is inversely linked with precordial voltage, resulting in lower sensitivity and higher specicity of precordial voltage criteria for LVH in overweight individuals [24]. Selected criteria for left ventricular hypertrophy Sokolow and Lyon index Perhaps the best known of all ECG criteria for LVH is that of Sokolow and Lyon introduced in 1949 [25]. These authors actually listed four criteria, but the most commonly used amplitude criterion is SV1 plus maximum (RV5, RV6) of 3.5 mV or greater. It will be seen that this simple criterion is neither age nor sex dependent and probably has remained in use because the majority of patients in whom LVH is likely to be found are over 50 years of age. It therefore is a very nonspecic criterion in younger individuals, particularly men. More recently, Alfakih and colleagues [26] suggested new thresholds of 3.8 mV for men and 3.4 mV for women for reporting LVH, giving a combined sensitivity of 20.3% at 95% specicity. In the same study, the Cornell product (as discussed later) was 24.5% sensitive at the same specicity of 95%. The author and colleagues data [27] suggest that in persons older than 50 years the upper limit of normal should be 4.6 mV for men and 3.6 mV for women. Clearly, application of such thresholds would reduce sensitivity even further. Interestingly, the same data indicate that SV1 plus RV5 always has a higher mean value in men and women than SV1 plus RV6 (ie, for all age ranges and both sexes). This could explain why the Sokolow and Lyon criterion is often reduced to SV1 RV5 R 3.5 mV. Cornell index Two sets of criteria for LVH were published by the group at Cornell University [17,28]. The second of these, published in 1987, provided a simpler set of criteria, as follows: RaVL SV3 O 2:8 mV in men RaVL SV3 O 2:0 mV in women The Cornell group then introduced a voltage times duration product known as the Cornell product. In this case, the Cornell voltage was multiplied by the overall QRS duration, and this product showed improved accuracy in reporting LVH [29,30]. Of particular importance is the fact

Fig. 2. (A) The mean of SV1 RV5 in 725 male and 585 female adult healthy volunteers. (B) The upper normal limits in the same data set.

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that these ECG criteria can follow changes in echocardiographic LV mass [31] and accurately assess prognosis [32]. The opportunity to use this more readily available index to track LV mass may reduce the need for repeat echocardiograms. Note that in the Losartan Intervention for Endpoint (LIFE) reduction in hypertension study, the actual criteria used were adjusted on the basis of recruitment experience to use a dierential of 600 mV (rather than 800 mV, as given previously) between men and women; that is, in women 600 mV was added to RaVL plus SV3 before deriving the Cornell product. The threshold for abnormality was set at 244 mVms [32]. Secondary ST-T changes and left ventricular hypertrophy Although it is possible to diagnose LVH on the basis of QRS changes only, as is evident from the foregoing criteria, one particularly important aspect of the ECG in assessing LVH is the presence of so-called secondary ST-T wave changes, which have a classic morphology as shown in Fig. 3. Patients who have such abnormalities caused by LVH have been shown to have a lengthened time interval from minimum cavity dimension to mitral valve opening and a reduced rate of early diastolic wall thinning and dimension increase [33]. The importance of these ECG changes is that they are well known to aect prognosis adversely [3436]. In fact, these changes can add signicantly to the Cornell product as well as to the Sokolow and Lyon voltage for the prediction of cardiovascular mortality and

myocardial infarction in hypertensive patients [36]. Furthermore, ST depression itself in V5 and V6 has been shown to be a strong independent predictor of LVH and increased LV mass [37]. In short, the presence of secondary ST-T changes on the ECG is an independent predictor of a poorer prognosis than might exist in the absence of such a nding and shows that the ECG can provide information that is complementary to the echocardiogram. In many hypertensive patients who have secondary ST-T changes, coronary artery disease is present. Pringle and colleagues [38] in a study involving 23 such patients, 20 of whom had concentric LVH, found that 8 (40%) had signicant coronary artery disease at cardiac catheterization. This nding suggests that secondary ST-T changes in ECGs from hypertensive patients need to be interpreted as caused by hypertrophy with or without myocardial ischemia. Composite criteria for left ventricular hypertrophy Romhilt Estes criteria The fact that ST-T changes are additive to voltage criteria was recognized many years ago by Romhilt and Estes [39] who introduced a point scoring system for the ECG diagnosis of LVH. Their criteria, although dicult to apply manually, can be used by computer programs, which can also adapt voltage criteria for age and sex. Table 2 shows in summary form the main criteria used in this point score system. The Romhilt Estes criteria also make use of the frontal plane QRS axis, QRS duration, and intrinsicoid deection

Fig. 3. An ECG showing the typical features of LVH with secondary ST-T changes in the lateral leads in an 87-year-old woman. Note the broad, deep, inverted terminal portion of the P wave in V1, left axis deviation, the very high Cornell voltage, and the typical secondary ST-T changes, particularly in I and aVL. The QS in V2 may be caused by the LVH.

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Table 2 Romhilt-Estes point score system for ECG diagnosis of left ventricular hypertrophy* Criteria Any limb-lead R or S R 2.0 mV or SV1 or SV2 R 3.0 mV or RV5 or RV6 R 3.0 mV ST-T is typical of LVHa no digitalis with digitalis Left atrial involvement P terminal force V1 O 4 mVms LAD R 30 QRS duration R 90 ms Intrinsicoid deection V5 or V6 R 50 ms Points 3

Bundle-branch block and left ventricular hypertrophy An accurate diagnosis of LVH or LV mass in patients who have left bundle-branch block (LBBB) is essentially impossible. On the other hand, in a large series of over 1400 hearts examined at post mortem, Havelda and colleagues [42] noted that 93% of 70 hearts with ECG LBBB had LVH. Thus, the presence of LBBB itself in many ways is indicative of the presence of LVH with high specicity. In the presence RBBB, some ECG criteria for LVH can still be applied, notably those involving left atrial abnormality [43,44]. Regression Regression of LVH in patients receiving antihypertensive therapy has been detected by assessing the Cornell product after 1 year of treatment. Those patients in whom the Cornell product reduced in value had a higher probability of regression of echocardiographic LVH independent of changes in the systolic and diastolic blood pressure [31]. Thus, the ECG can indeed also be used to monitor LVH underlining the value of a baseline ECG in patients with newly diagnosed hypertension. Prognosis of ECG left ventricular hypertrophy More recent data on the prognostic value of the ECG have come from the LIFE study [36] in which the presence of secondary ST-T changes was associated with a 1.5-fold increase in risk of myocardial infarction or cardiovascular death over a 5-year follow-up period. Conversely, Levy and colleagues [45] found that a reduction in Cornell voltage was linked with a lower risk of cardiovascular disease. In the Heart Outcomes Prevention Evaluation Study [46], the combined endpoint of either regression of ECG LVH or prevention of progression by Sokolow Lyon voltage criteria following ramipril-based therapy was associated with a reduced risk of myocardial infarction, stroke, congestive heart failure, and death. In a study of 19,434 veterans, composite criteria were shown to be better predictors of cardiovascular mortality than voltage-only criteria [47]. In particular, a Romhilt Estes score of 5 or greater had a hazard ratio of 3.7 (95% condence interval, 3.04.4) after adjustment for age, body mass index, and heart rate. This hazard ration compares with hazard ratios of 3.1 and 2.7 for Cornell voltage and product respectively.

3 1 3 2 1 1

* Five points indicates denite left ventricular hypertrophy; 4 points indicates probable left ventricular hypertrophy. a ST-T conguration as in leads I, aVL of Fig. 3.

in V5 or V6 measured as the time from QRS onset to the peak of the R wave. Voltage- and interval-based criteria More recently Salles and colleagues [40] showed that a combination of QT-interval prolongation and Cornell product resulted in increased detection of LVH in patients who had resistant hypertension. A prolonged QTc interval greater than 440 milliseconds or prolonged QT dispersion greater than 60 milliseconds together with a Cornell product greater than 240 mVms was associated with a 5.3- to 9.3-fold higher chance of having LVH compared with individuals who did not have increased QTc or Cornell product. Eect of echocardiographic criteria for increased left ventricular mass on ECG criteria Selection of echocardiographic criteria for increased LV mass used as the reference standard can undoubtedly inuence the sensitivity of ECG criteria for LVH. Cuspidi and colleagues [41] showed in 100 untreated hypertensive patients that the sensitivity of ECG criteria ranged from 9% to 25% depending on whether the LV mass index was 126 g/m2 in men and 105 g/m2 in women or 125 g/m2 in both men and women. ECG LVH was based on either the Sokolow and Lyon or the Cornell index being present. The rst criterion for increased echocardiographic LV mass was indexed by height alone, whereas the second was indexed by body surface area. Surprisingly, the higher sensitivity was obtained in a criterion that was not sex dependent.

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ECG in heart failure Heart failure is regarded as unlikely to be present in the absence of dyspnea and an abnormal ECG or chest radiograph [48]. The ECG has a high sensitivity (94%) when used in the diagnosis of heart failure but a low specicity (61%); it has, however, an excellent negative predictive value (98%) [49]. On the other hand, when a measurement of plasma BNP or NTproBNP is available, a simple classication of the ECG into normal and abnormal was found to be of little value [50]. Future studies may clarify the role of the ECG in avoiding unnecessary referrals for echocardiography. Left ventricular hypertrophydconclusion Although clearly the echocardiogram gives information on LV volume, wall thickness, and LV function in particular, there is still much of value that can be gained from the ECG in the evaluation of LVH. The simplicity of the approach to recording the ECG, particularly in clinical trials where patients can be followed for several years, leads to the use of ECG abnormalities as markers of risk. Indeed, in the Framingham study, increased QRS voltage together with ST-T abnormalities conferred a risk similar to that of a previous myocardial infarction [51]. In many situations where a simple approach to treatment is required, such as in essential hypertension, a baseline ECG is of value in monitoring the patients condition at least on an annual basis. Such an investigation can be undertaken in the community, thereby avoiding an unnecessary visit to hospital for an echocardiogram recording.

Type B: R/S greater than 1 in V1 with R greater than 0.5 mV (clockwise inscription of the transverse plane QRS loop) Type C: Prominent S in V5 and V6 with R/S less than 1 in V5 (clockwise inscription of the transverse plane QRS loop) The rst of these criteria essentially relates to severe RVH, as in pulmonary stenosis. The second may be associated with rheumatic heart disease. On the other hand, type C is more linked with chronic obstructive pulmonary disease and sometimes mitral stenosis. Secondary ST-T changes and right ventricular hypertrophy In a fashion similar to LVH, secondary ST-T changes caused by right ventricular enlargement may be encountered. A similar pattern of ST depression with asymmetric T wave inversion is typical in V1 and V2 (Fig. 4). This pattern is encountered most frequently in patients who have congenital heart disease. Other factors An increased R/S ratio in V1 can sometimes be caused by posterior myocardial infarction. In such a case, the R-wave duration in V1 generally exceeds 40 milliseconds, and the T wave is upright. In the presence of inferoposterior myocardial infarction or even lateral myocardial infarction, an increased R/S in V1 should not be misinterpreted as being caused by RVH. Right bundle-branch block and right ventricular hypertrophy The presence of RBBB in general terms makes it dicult to report RVH. The combination of known RVH with RBBB is most often seen in congenital heart disease, but a tall R in V1 and V2 in patients who have RBBB is indeed nonspecic for RVH. Right ventricular hypertrophydconclusion The ECG criteria for RVH are so poor that an echocardiogram normally will be more valuable than an ECG in patients who have congenital heart disease or pulmonary disease. In pulmonary embolism, however, the right ventricular volume may increase, leading to ECG changes, such as T-wave inversion in V1 to V3, which are more readily followed on the ECG.

Right ventricular hypertrophy The ECG is notoriously inadequate in detecting right ventricular enlargement or hypertrophy. In an early study of Flowers and Horan [52], it was shown that criteria using V1 were very specic in detecting RVH, at 90%, but were insensitive (2%18%). The vectorcardiogram is rarely used these days, but Chou and Helm [53] described three types of RVH patterns. Essentially these patterns broadly translate to the 12-lead ECG as follows: Type A: Tall R in V1, prominent S in V6 (counterclockwise inscription of the transverse QRS loop)

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Fig. 4. An ECG showing RVH with secondary ST-T changes in a 3-year-old boy who has pulmonary valvular stenosis. Note that V4R is used to the exclusion of V3. The upright P waves in V1 and V2 have an abnormally high amplitude for age, as do the R waves in V1 and V2. T-wave inversion may be normal in V4RV4 in infants and children, but the ST depression and overall ST-T conguration in this illustration is that of a secondary ST-T change.

Biventricular hypertrophy In general terms, criteria for biventricular hypertrophy essentially are a combination of the individual criteria for LVH or RVH. There have been a number of studies linking ECGs with anatomic biventricular hypertrophy as determined at post mortem. The best of these showed a sensitivity of 20%, although the specicity was high at 94% [6]. Athletes heart With the increased advocacy of participation in sport, there has been an increase in the number of deaths associated with a variety of athletic activities. In one recent half-marathon in the northeast of England (The Great North East Run, September, 2005), four men died as a result of participating. It would seem to be prohibitive to consider undertaking an echocardiogram in all asymptomatic younger individuals with a view to detecting cardiomyopathy unless they are likely to be serious athletes. Data from Italy indicate one sudden death per year in 100,000 individuals aged 12 to 35 years in the general population, with an increase to 2.3 sudden deaths per 100,000 in those who participated in sporting activities [54]. Under these circumstances, an ECG or an echocardiogram is not likely to be cost eective in terms of the yield of abnormalities detected. The matter of screening young athletes is topical and controversial [55]. Some athletes may have

arrhythmogenic right ventricular dysplasia. This condition may rarely manifest as an epsilon wave on the ECG; additional criteria relating to dierences in the sum of QRS durations in V1 V2 V3 versus V4 V5 V6 have been suggested as being of value [56]. An MRI is more informative in skilled hands, however. On the other hand, when individuals are known to have heart disease, guidelines for advising patients wishing to take part in competitive sport have recently been issued [57,58]. Summary The echocardiogram undoubtedly is part of the cardiologists armamentarium in the diagnosis and elucidation of cardiac abnormalities. The numbers of echocardiograms recorded annually are almost certainly increasing in every hospital and private practice, but the ECG still continues to be the most frequently recorded noninvasive test in medicine. Except in extreme cases, the ECG can almost always be recorded, whereas it is generally accepted that the echocardiogram may be unsatisfactory in an admittedly diminishingly small percentage of individuals referred. For many patients, particularly those who have newly diagnosed hypertension, a 12-lead ECG recording may be the only test that is required as a baseline measure. For those who have possible heart failure, an ECG and BNP measurement may be sucient to obviate the need for an echocardiogram. On the other hand, there is no point in denying that an echocardiogram is recorded as

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part of the routine investigation of many patients, including those who have had a recent myocardial infarction, which may of course in the rst place have been diagnosed by an ECG! Thus the two techniques will continue to live side-by-side for the foreseeable future. Acknowledgments The author wishes to thank Dr. David P Macfarlane, of Glasgow Royal Inrmary, and Dr. Peter Okin, of Cornell University, New York, who provided many relevant references of interest. References
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