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BISHOP LECTURE

JACC Vol 7, No 3 March 1986 484-91

The Electrocardiogram 80 Years After Einthoven

HEIN J. J. WELLENS, MD, FACC

Maastricht, The Netherlands

For several reasons, I decided to make the electrocardiogram the subject of this Louis Bishop Lecture. First, to honor Dr. Bishop, who as a practicing cardiologist realized very early the importance of the electrocardiogram in the diagnosis and management of the cardiac patient (1), Second, as a Dutch•man, I am proud of the contributions to our understanding and use of the electrocardiogram which were made in the past 80 years by countrymen like Einthoven, Wenckebach and Durrer. The brilliant and inspiring thinking of the late Dr. Durrer logically led to my interest and activities in the field of electrocardiology.

Third, I am worried, in this age of increasing use of sophisticated (and expensive) techniques, about the decreas•ing ability of our younger colleagues to interpret the elec•trocardiogram correctly. Invasive procedures, with their di•agnostic (and financial) rewards have stolen the interest of the younger generation. This is regrettable. for as pointed out by Fisch (2), the electrocardiogram is a noninvasive technique that does not harm the patient, is inexpensive, simple and reproducible, allows serial studies and is the only practical means of recording the cardiac action potential.

Fisch (2) also stressed that the electrocardiogram: I) still serves as an independent marker of myocardial infarc•tion, 2) reflects anatomic, metabolic and hemodynamic al•terations, 3) demonstrates a variety of complex electro•physiologic concepts through deductive reasoning, 4) is a stimulus for laboratory confirmation of postulated mecha•nisms and concepts, 5) is vital for proper diagnosis and therapy, and 6) is without peer for the diagnosis of arrhyth•mias. Fourth, as will be shown, a wealth of new knowledge increasing the diagnostic value of the electrocardiogram has become available in recent years.

From the Department of Cardiology, Annadal Hospital, University of Limburg, Maastncht, The Netherlands. This review was presented by.Dr. Wellens as the Bishop Lecture at the Annual Meetmg of the Amencan College of CardIOlogy, Anaheim, California, March 1985. .

ManUSCrIpt received September 25, 1985; revised manuscnpt received October 31, 1985.

Address for reprints: Hem 1. 1. Wellens, MD, Department of Car•dIOlogy, Annadal Hospital, University of Limburg, MaastrIcht, The Netherlands.

© 1986 by the Amencan College of CardIOlogy

Einthoven It is interesting that a basic scientist, a professor of phys•

iology at Leiden University, played such an important role in the development of a technique that is nowadays used worldwide, probably more than a million times a week. Einthoven made beautiful recordings of normal and abnor•mal heart action in conditions including ventricular hyper•trophy, conduction disturbances and arrhythmias (3). His laboratory was located a few miles from the Academic Hos•pital in Leiden. but a telephone cable allowed superb reg•istrations. It is sobering that the clinicians in that hospital, feeling threatened in their clinical acumen by this connection with the physiologist, cut the cable a few years later. The lesson obviously is that close ties between clinical medicine and basic science are essential for the advancement of med•icine and should never be severed.

Role of Other Techniques in the Improvement of the Diagnostic Value

of the Electrocardiogram Reexamination of the electrocardiogram in the light of

information obtained through invasive and noninvasive techniques is essential for the expansion of our knowledge of electrocardiography. Table I gives a list (far from com•plete) of new diagnostic pointers on the electrocar~iogra~ and the techniques that played an essential role In theIr recognition (4-42). It should be stressed, however, that one should not only look for new electrocardiographic signs by using other techniques, but also critically compare the value of accepted electrocardiographic criteria with that of infor•mation from new techniques. The importance of this ap•proach was recently shown by Zoneraich (43) when he dis•cussed echocardi ographic-electrocardiographic correlates. Let us examine some new electrocardiographic findings in more detail.

1. The electrocardiogram of right ventricular infarc•tion. Infarct localization studies using 99m-technetium py•rophosphate scintigraphy showed that right ventricular in-

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JACC Vol 7. No 3 March 1986.484--91

WELLENS ELECTROCARDIOGRAM AFfER EINTHOVEN

485

Table 1. Examples of Recently Described Electrocardiographic Diagnostic Findings and the Techniques That Contributed to Their Recognition

Electrocardiogram

Localization of A V and intraventricular conduction dIsturbances

Slgmficance of site of A V and intraventricular block in myocardial infarction

DIagnosis of site of origm of wide QRS tachycardia

Diagnosis of site of origin of narrow QRS tachycardia

LocalIzation of accessory pathways

Localization of ventricular impulse formation

RIght ventncular dysplasia

Critical high LAD stenosis Right ventricular infarctIOn

QRS score, infarct size and LV function after MI QRS-T findmgs and LV wall motion DigitalIs intoxication Abnormal depolarizatIOn-induced T wave changes

Technique

Anatomic dIssection (4); electrography of the conduction system and pacing (5-9)

Electrography of the conduction system and clinical follow-up (10, II)

Intracardiac electrography using mapping and programmed stimulation (12,13)

Intracardiac electrography usmg mapping and programmed stimulation (14-17)

Programmed stimulatIOn and intracardiac and mtraoperative mappmg (18-21)

Intracardiac electrography, surgery, pacing (\2,22,23)

Intracardiac mapping, surgery , LV angiography, echocardiography (24,25)

Coronary angiography (26) Autopsy; hemodynamic, echocardiographic

and radlOnuclide studies (27-33) LV angiography (34,35) L V angiography (36) Pacing (37-39) Pacing, intracardiac electrography (40-42)

A V = atnoventricular; LAD = left anterior descending coronary artery; LV = left ventricular; MI myocardial infarctIon.

volvement is present in approximately 45% of patients with an acute inferoposterior infarction (32). By combining the radionuclide studies with right-sided chest leads it was found that ST segment elevation of 1 mm or more in lead V 4R has a high sensitivity and specificity for detecting right ven•tricular infarction. This electrocardiographic finding (Fig. 1) not only indicates a proximal occlusion of the right coro•nary artery, but also identifies a subgroup of patients having

a high chance (approximately 50%) of developing high de•gree atrioventricular (A V) block (33). The duration of ST segment elevation in lead V4R, however, is short-lived, having disappeared in half the patients 10 hours after the onset of the pain of myocardial infarction (Fig. 2). The hemodynamic picture of right ventricular infarction, char•acterized by low cardiac output and elevated right-sided pressures (28) in the presence of normal or mildly elevated

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Figure 1. Illustration of ST segment elevation as an expression of right ventricular involvement in a patient admitted because of an acute inferior myocardial infarction.

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Figure 2. Relation between electrocardiographic changes indic•ative of right ventricular involvement and time, As shown, and best seen in lead V4R, ST segment elevation, which is clearly present on admission (II AM, I hour and 30 minutes after the onset of chest pain) has disappeared 6 hours later (5 PM, 7Y2 hours after the onset of chest pain),

left-sided pressures, develops in only 5 to 10% of patients having right ventricular involvement during acute infero•posterior myocardial infarction. The long-term prognostic significance of right ventricular involvement is not known at present It is interesting, however, that recent work by Braat and Ramentol (44) suggests that both immediately after myocardial infarction and 3 months later, right ven•tricular function is better in patients in whom an occlusion

Figure 3. Electrocardiograms of a 42 year old man who had a 35 minute episode of chest pain I hour before admission, A, recorded on admission; B, 12 hours later. There were no serum enzyme changes, Coronary angiography revealed a 99% stenosis in the anterior descending branch of the left coronary artery proximal to the first septal branch,

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lACC Vol 7, No 3 March 1986 484-91

Figure 4. Electrocardiogram of a supraventricular tachycardia, During tachycardia there is a 1 : I relation between atrial and ven•tricular activity, The P waves follow the QRS complex, They have an inferosuperior and a left to right direction, Following the steps indicated in Table 3 one concludes that the patient has a circus movement tachycardia with atrioventricular (A V) conductIOn over the A V node and ventriculoatrial conduction over a septally located fast conducting accessory pathway,

high in the right coronary artery is reopened by thrombolytic therapy,

2. The electrocardiogram of a critical stenosis high in the left anterior descending coronary artery. In 1981 de Zwaan et al. (26) reported on a group of patients who were admitted with anginal pain and subsequently developed T wave changes in the precordial leads without Q waves and no or minimal cardiac serum enzyme elevation (Fig, 3), Coronary angiography in these patients (developing T wave negativity in precordial leads V 2 to V 5 or V 6) after the attack of chest pain revealed a critical stenosis high in the left anterior descending coronary artery, close to the first septal branch. Identification of these patients is of obvious im•portance. because of the risk of losing an important portion of left ventricular muscle if occlusion occurs at that site. These patients have been (and still are) classified as having suffered from a subendocardial infarction, The poor long•term prognosis of patients showing these T wave changes in the precordial leads explains why patients with a so-called subendocardial infarction were found to have a worse prog•nosis than patients with a transmural (Q wave) infarction (45,46).

3. The electrocardiogram of the patient with a wide QRS tachycardia. The introduction by Durrer et al. (I8) and Coumel et al. (47) of programmed stimulation of the heart together with the simultaneous recording of intracar•diac and extracardiac electrical activity has been of great help in understanding the electrocardiograms of patients showing either a wide or a narrow QRS tachycardia (13,16).

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487

Table 2. Steps in the Diagnosis of a Wide QRS Tachycardia

l. A V dissociatIOn? 2. QRS wIdth')

Present ~ VT >0.14 l>econd ~ VT RIO a) SVT wIth preexIsting BBB

3. Supenor frontal aXll>? b) SVT wIth anterograde conductIOn over AP

Present; favors VT (left of - 30° or nght of + 120°) RIO a) SVT with preexIstIng BBB

b) SVT with anterograde conductIOn over Kent bundle (septal or nght-sided) or Mahaim bundle

4. QRS configuratIOn? RBBB pattern V I. monophasic or blphaslc QRS ,uggestl> VT

V 6: RIS < I suggests VT LBBB pattern V I. rtachy < r" suggests SVT

r'dchy > r" suggel>ts VT V 1 to V,: slurred or notched downslope of S wave suggests VT

AP = accessory pathway: A V = atrioventricular: BBB = bundle branch block; LBBB = left bundle branch block; RBBB = right bundle branch block, RIO = rule out: SVT = supraventricular tachycardIa: VT = ventricular tachycardia.

Intracardiac electrograms make it possible to identify the site of origin and the pathway of a tachycardia. Careful correlation of this information with the configurational char•acteristics of the 12 lead electrocardiogram has resulted in a systematic approach to the analysis of the electrocardio•gram (Table 2). In our experience (48), by using this ap•proach a correct diagnosis can be made in 90% of patients showing a regular wide QRS tachycardia. The diagnosis is most difficult in patients presenting an electrocardiogram with a left bundle branch block-like QRS configuration. They tend to be overdiagnosed as having supraventricular tachycardia with left bundle branch block (49).

4. The electrocardiogram of the patient with a narrow QRS tachycardia. Using information from programmed stimulation of the heart, the most important diagnostic clues

Figure 5. Three electrocardiograms from a 23 year old man suf•fering from idiopathic paroxysmal ventricular tachycardia. The electrocardiogram on the left was recorded during tachycardIa. Subsequent tracings show negative T waves in leads showing a negative direction of QRS during tachycardia.

for the correct classification of a supraventricular tachycar•dia with a narrow QRS complex are rate, location of the P wave (in relation to the QRS complex) and configuration of atrial activity. Again. we favor a systematic approach (Table 3). This allows correct identification of the type of supraventricular tachycardia in 85% of patients (50). An example of the use of this approach in the analysis of the 12 lead electrocardiogram is given in Figure 4.

5. The electrocardiogram showing T wave changes after abnormal ventricular depolarization. In 1968 Chat•terjee et al. (40) described T wave negativity in leads re•cording electrical activity close to the site of pacing. Ro•senbaum et al. (42) recently showed that the extent and duration of T wave negativity relates to the duration of pacing. Similar postdepolarization T wave changes may occur after temporary left bundle branch block (42) and ventricular tachycardia. Figures 5 and 6 illustrate how long such T wave changes may be present after ventricular tachy•cardia. Nicolai et al. (41) reported on T wave changes that appeared after normalization of ventricular depolarization in patients with preexcitation. Typically, T wave negativity

488 WELLENS ELECTROCARDIOGRAM AFTER EINTHOVEN

Table 3. Steps in Diagnosis of Narrow QRS Tachycardia (QRS < 0,12 second)

I) 2nd degree AV block? (spontaneous or after carotid sinus massage)

~ No Yes

I Atrial rate?

/~ >25D/mm <25D/min

I /\ Atrial flutter Atrial T

2) QRS alternation?

~ No Yes

I CMTwithAP

3) P wave location?

PR > RP PmR

AVN T with 2: I block

PR < RP

I I ~ CMT withfaS! AP AVNT Atrial T CMT wuh slow AP

4a) P axis (frontal plane)

Inferior-superior

~ Atrial T

4b) P axis (horizontal plane) right ~ left

I

CMTwith AP - slow - fast (septal)

left ~ right

I

Atrial T

Other

~ CMT with fast AP (right or left)

Atrial T CMT with fast or slow AP. Atrial T

AP = accessory pathway; A V = atrioventricular; A VN = atrioventricular nodal; CMT = ClfCUS movement tachycardia; T = tachycardia,

lACC Vol 7, No 3 March 1986 484-91

is seen in the leads previously showing negative delta waves, reflecting the site of earliest onset of ventricular depolari•zation during preexcitation. In some patients with the Wolff•Parkinson-White syndrome (Fig, 7), this knowledge allows prediction of the ventricular insertion of the accessory path•way if an electrocardiogram is available during a narrow QRS circus movement tachycardia.

6. The electrocardiogram in digitalis intoxica•tion. Digitalis is still used frequently and correct dosing

therefore continues to be a challenge to the physician. It is well known that in the sick heart too much digitalis may lead to the simultaneous occurrence of abnormalities in con•duction and ectopic impulse formation, resulting in fasci•nating and complicated arrhythmias. It is less well known that ectopic activity at both the atrial and the ventricular level frequently has very typical electrocardiographic fea•tures. For example (Fig. 8), during digitalis-induced atrial tachycardia the atrium is usually activated in a superior to

JACC Vol. 7. No 3 March 1986:484-91

inferior and right to left direction, leading to P waves similar to the sinus P wave. Digitalis intoxication becomes espe•cially likely when such a P wave configuration is combined with ventriculophasic alternation in PP interval during atrial tachycardia with 2: I atrioventricular conduction (39). Ab•normal impulse formation at the ventricular level secondary

Figure 7. Electrocardiograms from a patient with the Wolff-Par•kin son-White syndrome. Deep T wave negativity is present during a circus movement tachycardia with A V conduction over the A V node (panel A) in the same leads that show negative delta waves during sinus rhythm (panel B).

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WELLENS ELECTROCARDIOGRAM AFfER EINTHOVEN

489

Figure 6. Same patient as in Figure 5, showing electrocar•diograms from subsequent days. Note that the ST -T segment normalized 10 days after tachy•cardia.

to digitalis intoxication has its origin in the Purkinje tissue leading to a relatively narrow QRS complex (0.12 to 0.14 second). As can be seen in Figure 9, changes may occur in QRS configuration during digitalis-induced ventricular tachycardia suggesting competition in impulse formation between different Purkinje fibers. Recent work by Rosen (37) and Gorgels (38) and their coworkers provides the experimental basis for this phenomenon. They showed that ectopic ventricular impulse formation can be triggered in the Purkinje fiber of the digitalis-intoxicated dog heart. In

Figure 8. The electrocardiogram on the left shows atrial tachy•cardia with 2: 1 A V conduction. During tachycardia there is ven•triculophasic behavior of the P-P interval. The P-P interval without a QRS complex is longer than the P-P interval embracing a QRS complex. Note also that the P waves during atrial tachycardia resemble the P waves during sinus rhythm (right panel). The ventriculophasic behavior and the configuration of the P waves strongly suggest that digitalis intoxication has been responsible for atrial tachycardia.

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Figure 9. Ventricular impulse formation in a patient with digitalis intoxication. Note that: 1) the QRS complex has a width of 0.12 second, 2) a slight slowing in rate is accompanied by a change in QRS configuration (best seen in the limb leads), and 3) there is 1 : I ventriculoatrial conduction.

the dog the site of impulse fonnation in the Purkinje fiber depends on the basic heart rate and the site of origin and spread of intraventricular activation (51).

Developments Threatening Advances in Knowledge of Electrocardiography

If we want to continue to expand our knowledge of electrocardivgraphy we must realize that some develop•ments may hamper these efforts. Although currently used computer programs for electrocardiographic interpretation are of great importance for screening, epidemiologic studies and storing, they tend to "freeze" our knowledge. New programs should be developed allowing recognition of new specific electrocardiographic findings in certain conditions by using both detailed electrocardiographic analysis and diagnostic infonnation from other techniques. This requires the expertise and cooperation from cardiologists active in the different noninvasive and invasive techniques.

Another problem in the advancement of electrocardiog•raphy is the increasing use of single lead monitoring in the coronary care unit. Although useful in recognizing conduc•tion disturbances and ectopic activity, single lead recordings usually do not allow detailed analysis of the site and mech•anism of abnonnal impulse formation and prevent the phy-

IACC Vol 7, No 3 March 1986 484-91

sician from gaining experience in the interpretation and un•derstanding of complex arrhythmias.

Adequate use of electrocardiography should continue to be a cornerstone in the daily management of the cardiac patient. Unfortunately, and to my surprise, I have witnessed in well known, even world famous. hospitals the proud presentation of a diagnosis reached by expensive, frequently invasive, techniques although an inexpensive multichannel electrocardiographic recording could have led to the same diagnosis.

Conclusion In recent years, several new diagnostic contributions have

been made in the field of electrocardiography. This stresses the necessity of implementing sufficient electrocardiography in the training program of the cardiologist and internist. It is important to realize that to be able to interpret the elec•trocardiogram well the physician should have all-around knowledge of cardiac anatomy, electrophysiology and hemodynamics. Electrocardiography should also be a re•current item in postgraduate teaching. To quote Fisch (2): "He who maintains that new knowledge of electrocardi•ography is no longer possible or contributive, ignores his•tory. "

The electrocardiographic examples given in the article are from work done by our group in Maastricht. Their enthUSIasm. Interest and Intelligence create the stimulatIng envIronment in whIch I am pnvlleged to work. They are, in alphabetIcal order: F. Bar, MD, S. Braat, MD. P Brugada. MD, W. Dassen, PhD, K. den Dulk. MD, H. Frank, MD, A Gorgels, MD, J. Schmitz, MD, J. Stappers, MD and C. de Zwaan, MD.

References I. Bishop LF. The BIrth of a Specialty. New York: Vantage Press, 1977.

2 Fisch C. The clinical electrocardIOgram: a classic. CIrculatIOn 1980;62(suppl 1II):III-I-4.

3. Einthoven W. Le telecardiograrnme. Arch Intern Physiol 1906;4: 132-64

4. Rosenbaum MB, Elizari MV, Lazzan JO. Los Hemibloqueos. Buenos AIres. Paldos, 1968.

5. Scherlag Bl, Lau SH, Helfant RH, BerkOWItz WD, SteIn E, Damato AN. Catheter technique for recording HIS bundle actiVIty In man. CirculatIOn 1969,39: 13-22.

6. Damato AN, Lau SH. The clInical value of the electrogram of the conducting system. Prog Cardiovasc Dis 1970; 13: 119-40.

7. Narula OS, Scherlag Bl, Samet P, Javier RP. AtrIoventrIcular block. LocalizatIon and classification by His bundle recordIngs. Am 1 Med 1971;50:146-61

8. Rosen KM. Evaluation of cardiac conductIOn In the cathetenzation laboratory. Am 1 Cardiol 1972;30:701-3.

9. Puech p, Grolleau R. L'Activite du Faisceau de Hb Normale et Path•ologlque. Paris: Ed Sandoz, 1972.

10. Lie KI, Wellens HJJ, SchUIlenburg RM. Factors InfluenCIng prognosis of bundle branch block complIcating acute myocardial Infarction. CIr•culatIOn 1974;50:935-48.

II. Tans AC, Lie KI A V nodal block In acute myocardIal infarctIOn In: Wellens HJJ, Lie KI, lanse Ml, eds. The ConductIOn System of the Heart. PhIladelphia: Lea & Febiger, 1976:655-61.

lACC Vol 7, No 3 March 1986 484.-91

12 JOi>ephson ME, Waxman HL, Marchllnskl FE, Horowitz LN, Spiel•man SR, RelatIon between site of ongIn and QRS configuratIon In ventncular rhythms In: Wellens HJJ, Kulbertus HE, eds. What's New In Electrocardiography The Hague Martinus Nljhoff, 1981.200-28.

13. Wellens HJJ, Bar FWHM, Lie KJ. The value of the electrocardiogram in the differential diagnosIs of a tachycardia With a widened QRS complex. Am J Med 1978;64:27-33

14 Wu D, Denes p, Amat-y-Leon F, et al. Clinical, electrocardIOgraphic and electrophyslOloglc observatIons In patIents With paroxysmal supra•ventncular tachycardia Am J CardlOl 1978;41: 1045-51.

15 Fafi>hldi A, Josephson ME, Horowitz LN ElectrophyslOloglc char•actenstics of concealed bypass tracts: clinical and electrocardiographic correlates Am J Cardiol 1978;41.1052-60.

16 Farre 1. Wellens HJJ. The value of the electrocardIOgram In diagnosIng site of on gIn and mechanism of supraventncular tachycardia. In. Wel•lens HJJ, Kulbertus HE, eds. What's New in Electrocardiography. The Hague: Martinus NIJhoff, 1981.l31-71.

17. Coumel P. JunctIOnal reciprocatIng tachycardia The permanent and paroxysmal forms of A V nodal reciprocating tachycardlai> J Electro•cardlOl 1975;8:79-90.

18. Durrer D, Schoo L, Schmlenburg RM, Wellens HJJ The role of premature beal> In the initiatIOn and termination of supraventricular tachycardia in the Wolff-ParkInson-White syndrome Circulation 1967.36:644-55.

19. Slama R, Coumel p, BouvraIn Y Lei> syndromes de Wolff-ParkInson•White de type A inapparents ou latents en rhytme sInusal. Arch Mal Coeur 1973;66:639-47

20. Zipes DP, Dejoseph RL, Rothbaum DA Unusual properties of ac•cessory pathwaYi> CirculatIOn 1974;49: 1200-9

21 Gallagher JJ, Pntchett ELC, Sealy WC, Kasell J, Wallace AG The pre-excitatIOn syndromei>. Prog Cardiovasc DIS 1978;20:285-327.

22. Harken AH, Josephson MF SurgICal management of ventricular tachycardia. In: Josephson ME, Wellens HJJ, eds. Tachycardla~,.

Mechanisms, DiagnOSIs. Treatment Philadelphia. Lea & Feblger. 1984:475

23. Josephson ME. Waxman HL, Cain ME. Gardner MJ. Buxton AE. Ventncular activatIOn during endocardial pacIng II. Role of pace•mapping to localize ongIn of ventncular tachycardia Am J CardlOl 1982:50.11-22.

24 FontaIne G. Gmraudon G, Frank R. StimulatIon studies and epicardial mappIng In ventrIcular tachycardia: study of mechanism and selectIon for surgery. In: Kulbertus HE, ed. Re-entrent Arrhythmias. Lancaster: MTP Press, 1977:334.

25. Marcus Fl, FontaIne G, Frank R, Grosgogeat Y Right ventncular dysplaSia. a report of 24 cases CirculatIOn 1982;69:384-92

26 De Zwaan C, Bar FWHM, Wellens HJJ Charactemtic electrocar•diographic pattern IndicatIng a cntical stenosIs high In left antenor descending coronary artery In patIents admitted because of Impending myocardial infarctIon. Am Heart J 1982.103:730-5

27. Wade WG The pathenogenesls of mfarctlOn of the nght ventncle. Br Heart J 1959;21.545-54.

28. Cohn IN, Gmha NH, Broder MI. Llmai> CJ Right ventncular In•farctIOn. Clinical and hemodynamiC features. Am J Cardlol 1974;33:209-14.

29. Candell-RleraJ, Flgureas J, Valle V, et al Right ventncular Infarction RelatIOnships between ST-segment elevatIon In V.R and hemody•namiC, scintigraphic and echocardlOgraphic findings In patIents With an acute inferior myocardial Infarction Am Heart J 1981: 10 I :281-7.

30. Erhardt LR, Sjogren A, Wahlberg j. Single nght i>lded precordial lead in the diagnosis of right ventricular involvement In mferior myocardial Infarction. Am Heart j 1976,91'571-6

31 Wackers FJ. Lie KI, Sokole EB, Res J, van der Schoot JB, Durrer D Prevalence of rIght ventricular involvement In inferIor wall In•farctIOn assessed with myocardial Imaging with thalllum-201 and tech•netium-99m pyrophosphate. Am J Cardiol 1978,42358-62.

WELLENS ELECTROCARDIOGRAM AFTER EINTHOVEN

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32. Braat SH, Brugada P, de Zwaan C, Coenegracht JM, Wellens HJJ. Value of electrocardiogram in diagnosing right ventricular involve•ment In patIents with an acute Infenor wall myocardial Infarction. Br Heart J 1983;49:368-72

33. Braat SH, de Zwaan C, Brugada P, Coenegracht JM, Wellens HJJ. Right ventricular involvement With acute Inferior wall myocardial infarction Identifies high nsk of developing atrioventricular nodal con•ductIon disturbances. Am Heart J 1984,107'1183-6.

34. Wagner GS, Freye CJ, Palmeri ST, et al. EvaluatIon of a QRS scoring system for estimating infarct size. I Specificity and observer agree•ment. Circulation 1982;65:342-9.

35. Palmeri ST, Harrison DG, Cobb FR, et al. A QRS scoring system for assessing left ventricular functIOn after myocardial infarctIon N Engl J Med 1982;306:4-8

36. Bar FW, Brugada P, Dassen WR, Van der Werf T, Wellens HJJ. PrognostIc value of Q waves, RIS ratIo, loss of R wave voltage, ST•T segment abnormalitIes, electrical axis, low voltage and notching. correlatIOn of electrocardiogram and left ventriculogram. J Am Coli Cardiol 1984;4:17-27

37. Rosen MR, Reder RF. Does triggered actIvity have a role In the genesis of cardiac arrhythmias? Ann Intern Med 1981;94:794-801.

38. Gorgels APM, Beekman HDM, Brugada P, Dassen WRM, Richards DAB, Wellens HJJ Extrastimulus related shortening of the first post•pacing Interval in digitalis-induced ventricular tachycardia. J Am Coli CardlOl 1983;1:840-57.

39 Wellens HJJ. The electrocardiogram in digitalis intoxicatIon In: Yu PN, Goodwin JF, eds. Progress in Cardiology. 5. Philadelphia: Lea & Feblger, 1976:271-90

40. Chatterjee K, Harris A, DaVies G, Leatham A. Electrocardiographic changes subsequent to artifiCial ventncu1ar depolarizatIOn Br Heart J 1969;31 :770-9.

41. Nicolai P, Medvedowsky JL, Delaage R, et al. PreexCitatlOns ven•triculaires. Diagnostic topographique des falsceaux de Kent. In: Puech P, Slama R, eds. Les Troubles du Rhythme Cardiaque. Paris. Roussel, 1978: 164-78.

42. Rosenbaum MB, Blanco HH, ElIzari MV, Lazzari 10, Vetulll HM Electrotonic modulation of ventncular repolarization and cardiac mem•ory. In: Rosenbaum MB, Elizan MV, eds. Frontiers of Cardiac Elec•trophysiology. The Hague. MartInuS Nijhoff, 1981:67-99.

43. Zoneraich S. EchocardlOgraphlc-electrocardiographic correlates. Am Heart J 1985; 110.193-6.

44. Braat SH, Ramentol M, Halders S, Wellens HJJ Effect of throm•bolysis on right and left ventricular function after Inferior wall myo•cardial infarction Circulation 1985;72:111-2.

45. Madigan NP, Rutlerford BD, Frye RL The clinical course, early prognosis and coronary anatomy of subendocardial infarclion. Am J Med 1976;60:634-44

46. Madias JE, Gorlln R. The myth of "mild" myocardial infarctIOn. Ann Intern Med 1977;86:347-55.

47 Coumel PL, Cabrol C, Fabiato A, Gourgon E, Slama R Tachycardia permanente par rhythme reciproque. Arch Mal Coeur 1967;60:1830-45.

48 Wellens HJJ, Bar FW, Vanagt EJ, Brugada P, Farre J. The differ•entiation between ventrIcular tachycardia and supraventricular tachy•cardia with aberrant conduction: the value of the 12-lead electrocar•diogram. In: Wellens HJJ, Kulbertus HE, eds. What's New in Electrocardiography. The Hague: Martinus Nljhoff, 1981: 184-99.

49. Wellens HJJ, Brugada P, Bar FW. When to use intracardiac electro•phYSIOlogical studies for diagnosing site of origin and mechanism of tachycardias. Circulation (in press)

50. Bar FW, Brugada p, Dassen WRM, Wellens HJJ. DifferentIal diag•nosis of tachycardia With narrow QRS complex (shorter than 0.12 sec). Am J Cardiol 1984;54:555-60.

51 Gorgels APM, de Wit B, Beekman HDM, Dassen WRM, Wellens HJJ. Effect of different modes of stImulatIOn on the configuratIOn of the first QRS complex after paCing during digitalis Induced ventncular tachycardia. PACE (In press).