possible role of a ventricular conduction disturbance in the electrogenesis of the ecg-vcg signs of...

J. ELECTROCARDIOLOGY 16 (4), 1983, 385-396

Possible Role of a Ventricular Conduction Disturbance in the Electrogenesis of the ECG-VCG Signs of

Myocardial Infarction BY ELIGIO PICCOLO, M.D., PIETRO DELISE, M.D., ANTONIO RAVIELE, M.D.,

DANIELE D'ESTE, M.D. , FRANCESCO LUCANGELI, M.D., PIETRO PASCOTTO, M.D., FRANCESCO DAINESE, M.D. AND FRANCESCO DI PEDE, M.D.

S U M M A R Y The typical QRS pat terns of myocardial infarction (MI-QRS) are commonly at t r ibuted

to myocardial cellular death. However, observation of a transient appearance of MI-QRS during coronary insufficiency, the disappearance of MI-QRS after coronary by-pass surgery and the appearance of MI-QRS after intracranial hemorrhage sugges t that a different electrophysioiogical mechanism may be at work.

There is not a single convincing explanation for all these observations. I t seems possible, at least theoretically, that a localized conduction disturbance can generate or con- tribute to the generation of the MI-QRS.

The results obtained in nine out of 194 cases studied by means of premature right atrial stimulation (PRAS) in our laboratory seem to confirm this hypothesis. In five of them we observed typical MI-QRS in the aberrant beats which were absent in the basal tracings. In the other four cases, MI-QRS which were present in basal tracings disappeared in the aberrant beats. In three of these a reduction in the duration of QRS was also observed, while in the fourth the duration of QRS did not change. In no case could the alterations of QRS (induction or disappearance of MI-QRS) be explained by a classical conduction disturbance, preexcitation or by a premature ventricular beat.

While the induction of MI-QRS was clearly due to an aberrant conduction in the supraventricular beats, the disappearance of basal MI-QRS changes in premature supraventricular beats is more difficult to explain. One possible electrophysiological mechanism could be a supernormal phase conduction. If this is the case, the basal MI- QRS could be due to a ventricular conduction disturbance.

In conclusion, our results suggest that MI-QRS can be generated, at least in our cases, by a localized conduction disturbance.

The typical QRS pat terns of myocardial infarction (MI-QRS) are usually long-lasting. Occa- sionally, transient MI-QRS have been reported in conditions such as experimental coronary insufficiency 1, clinical anginal a t tacks 2-4 and during open heart surgeryS.

The r e d u c t i o n or d i s a p p e a r a n c e of a pathological Q wave which occurs days or months

From the Division of Cardiology, Hospital of Mirano, Mirano- Venice, Italy. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "adver t i sement" in accordance with 18 U.S.C. w 1734 solely to indicate this fact. Reprint requests to: Prof. Eligio Piccolo, c/o Divisione Car- diologica, Ospedale Generale Provineiale, 30035 Mirano IVenezia), Italy.

after an acute myocardial infarction has also been reported6, as well as the reappearance of QRS initial forces after coronary bypass surgeryT.

I t is also well known that a pathological Q wave can be found in patients without coronary heart disease s,9 as in pr imary cardiomyopathylOa3, a f t e r i n t r a c r a n i a l hemorrhage14.15 and in metabolic or electrolyte disorders 16a8.

All these data suggest that there may be a common electrophysiological disturbance which is produced by a variety of conditions and which is responsible for MI-QRS.

The observation of rate-dependent pathological Q-waves 19 and the clinical and experimental evidence that ischemia may slow down conduction in both the working and the specific myocardium20-24, lend support to the possibility

385

3 8 6 P I C C O L O ET A L

T A B L E I

Summary of Cases Submitted to PRAS

QRS Changes Induced Disappearance VCD classical

QRS Changes Disappearance Type (Super- No QRS VCD Classi- Not Classi- MI-QRS MI-QRS Normal Phase Changes cal Type fiable Patterns Changes Conduction) Total

Angina w i t hou t infarct ion 6 11 - - 2 -- 1 20

Myocard ia l in farct ion 5 9 2 2 2 2 22

Arter ial hypertension 1 17 - - 1 -- - - 19

CCHD 26 30 - - -- - - 1 57

Primary myocard iopa thy 4 11 6 -- 1 - - 22

Rheumatic heart disease 1 11 . . . . 12 Long Q - - T syndrome -- 3 . . . . 3

No heart disease 8 28 - - -- -- 2 38

Myocard ia l bridges . . . . 1 - - 1

Tota l 51 120 8 5 4 6 194

VCD = ventr icu lar conduct ion disturbances; MI-QRS changes = QRS changes like myocardia l in farct ion; CCHD = chronic coronary heart disease.

t h a t a local conduc t ion d i s tu rbance m a y be the unde r ly ing cause for MI -QRS in some ins tances .

P r e m a t u r e r igh t a t r ia l s t imula t ion (PRAS) can induce typica l or a typ ica l QRS p a t t e r n s as a resu l t of a be r r a n t ven t r i cu la r conduc t ion a n d , therefore , r e p r e sen t s a su i tab le e x p e r i m e n t a l t e c h n i q u e fo r s t u d y i n g c o n d u c t i o n d i s t u r - bances25-29.

This pape r repor t s our resu l t s on the induc t ion and d i sappearance of MI -QRS obta ined b y P R A S in subjec t s wi th and wi thou t co rona ry hea r t disease.

MATERIALS AND METHODS 194 patients with or without cardiovascular disease

were s u b m i t t e d to PRAS dur ing an electrophysiological study in our laboratory (Table I). In nine of these patients, eight males and one female aged between 31 and 69 years {mean age -- 55 __ 10 years), we obtained induction {five cases) or disappearance {four cases) of MI-QRS. Six of these nine patients suffered from coronary heart disease: one patient had hypertrophic obstructive cardiomiopathy angiographical- ly assessed; one patient suffered from hypertensive heart disease and one patient with angina attacks had an atypical angiographic pattern {suspected myocardial bridges on the anterior descending coronary and slow flow in the right and circumflex coronaries).

All patients were under sinus rhythm at the time of the electrophysiologic study, and cardioactive drugs

were discontinued at least 48 hours before. The study was performed with patients in the resting, postab- sorptive, non-sedated state. All patients gave informed written consent.

The electrophysiological study was performed because of supraventricular tachyarrhythmias (four cases) or suspected sick sinus syndrome (four cases). In one case PRAS was performed in the subacute stage of a myocardial infarction before removing a catheter which had been positioned in the acute stage in the right ventricle owing to intermittent severe bradycardia.

Two 6F bipolar electrode catheters were passed per- cutaneously via the femoral veins into the right heart; the first was positioned in the high right atrium in order to perform PRAS and the second was advanced to the tricuspid orifice to record His bundle activity.

Single premature atrial stimuli were delivered after every eighth spontaneous beat, at progressively decreasing 10 msec coupling intervals, until the atrioven- tricular (AV) nodal or ventricular specialized conduction system effective refractory period (ERP) was reached. We used the bipolar atrial electrogram as the trigger signal. Stimuli were approximately twice the diastolic threshold, 2.5 msec in duration and elicited by a programmable digital stimulator (El Desi CD 6). PRAS was performed during spontaneous sinus rhythm. The His bundle electrogram, the surface ECG (leads I, II, III and VI), and the frontal and horizontal planes of VCG (Frank's method) were simultaneously recorded during PRAS, using an eight-channel direct writing recorder (Elema Schonander Mingograf 81) at a

J. E L E C T R O C A R D I O L O G Y 16 (4), 1983

C O N D U C T I O N IN QRS C H A N G E S OF MI 3 8 7

TABLE II Patients in W h o m MI-QRS Changes were Induced or Disappeared by PRAS

Case No. Heart Disease Basal Tracing Patterns Induced by PRAS

subacute MI with N AS MI-QRS pattern transient AS MI-QRS (82 msec) (82 msec) pattern

unstable angina N MI-QRS pattern with transient AS (110 msec) (92 msec) MI-QRS pattern

old MI AS MI-QRS pattern 1) AL MI-QRS pattern (96 msec) (88 msec)

2} EA MI-QRS pattern ( 1 O0 msec)

3) AS+I MI-QRS pattern (138 msec)

HHD LVH AS MI-QRS pattern (102 msec) i96 msec)

unstabte angina N 1 MI-QRS pattern (98 msec) (98 msec)

MI AS, I and L disappearance of MI-QRS pattern I and L MI-QRS

(98 msec) pattern (86 msec)

MI I MI-QRS disappearance of pattern + LAH I MI-QRS pattern

(118 msec) (118 msec)

myocardial bridge I + P + L normalization of on anterior inter- MI-QRS pattern QRS ventricular coronary (108 msec) (90 msec) artery and slow f low in the right and circumflex coronaries

HOM AS MI-QRS normalization of QRS pattern (78 msec)

(88 msec)

PRAS = programmed right atrial stimulation; N = normal; MI = myocardial infarction; AS = anteroseptal; AL = anterolateral; EA = extensive anterior; I = inferior; P = posterior; HHD = hypertensive heart disease; LVH = left anterior hemiblock; HOM = hypertrophic obstructive myocardiopathy.

paper speed of 50 or 100 mm]sec and an ICR 1001 In- stant VCG vectorcardiograph, respectively.

Chou and coworkers' VCG criteria30 were used for the diagnosis of myocardial infarction and of left ventricular hypertrophy. In the VCG tracings the dashes are 2 msec apart from each other.

RESULTS A:-". Induction" of MI-QRS changes.

The induction of MI-QRS changes was observed in five patients, all with arterial hypertension.

The first patient was admit ted to our hospital with a chest pain, an increase in CPK and L D H serum enzymes, and ECG evidence of acute ante-

roseptal myocardial infarction. The MI-QRS definitely disappeared four days after admission. During PRAS, which was performed 12 days later, the same MI-QRS reappeared in induced beats {Fig. 1}.

The second patient had been admit ted with unstable angina and had a transient electrocardiographic pat tern of anteroseptal MI; serum enzymes were always normal.

The electrophysiological s tudy was performed ten days later, when the patient was totally asymptomatic . The ECG showed a normal QRS pa t te rn and negative T waves in V2-V6. During PRAS, we induced an anterior myocardial infarc-


3 8 8 P ICCOLO ET AL

tion pattern. The third patient (Fig. 2), with electrocardiographic signs of an old anteroseptal MI, showed the following consecutive QRS changes during PRAS: 1) antero-lateral MI pattern, 2) extensive anterior MI with left anterior hemiblock, 3) antero-septal and inferior MI with RBBB. The fourth patient had no coronary heart disease and showed just left ventricular hypertrophy in the

basal ECG-VCG tracings. The PRAS induced a pattern of antero-septal myocardial infarction. The fifth patient was affected by unstable angina and had a normal basal ECG-VCG. PRAS induced an inferior MI pattern.

The QRS duration did not change in two cases, whilst increasing in one and decreasing in the others.

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CONDUCTION IN QRS CHANGES OF MI 389

B . " D i s a p p e a r a n c e " o f M I - Q R S .

The "disappearance" of MI-QRS was observed in four patients. In the first pat ient (Fig. 3), with ECG-VCG evidence of old antero-septal, lateral and inferior myocardial infarction, PRAS induced the disappearance of lateral and inferior MI pattern, but not of antero-septal MI pattern. In the second patient, with recent inferior MI and left anterior hemiblock, PRAS induced the disappearance of the signs of inferior MI. The third pa- t ient was a young man with atypical angina and ECG-VCG pat tern of inferior, posterior and lateral MI (Fig.4}.

Angiography showed myocardial bridge on anterior descending coronary and a slow flow in the r ight and circumflex coronaries. PRAS "conceal-

ed" the MI-QRS. In the fourth patient (Fig. 5), with hypertrophic obstructive myocardiopathy and antero-septal MI-QRS PRAS induced a QRS complex without signs of MI.

The QRS duration decreased in three cases and did not change in the other.

In all cases both the induction and the disappearance of the MI-QRS were reproducible at al- most constant H1-H2 coupling intervals.

In all cases the HV interval was normal in basal conditions and did not decrease either during PRAS or during atrial pacing.

D I S C U S S I O N

PRAS technique is able to induce, both in-normal subjects and in patients with heart disease,

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Fig. 1. Recordings from a 54-year-old female admitted to our hospital for acute myocardial infarction (typical chest pain and pathological CPK and LDH serum enzymes). The ECG on admission (panel A, to the left) is indicative of antero-septal myocardial infarction. Two days later, a left axis deviation can be observed. Four days later, (panel B) there was a reappearance of the R wave in V1-V4; the VCG was within normal limits. In panel C the effect of PI{AS performed 12 days later is shown. The basal VCG (not reported) was the same as the one of panel B. Two induced beats are shown. We can observe the progressive reproduction of antero-septal myocardial infarction signs (appearance of Q wave in V2-V4 and on the horizontal VCG an absence of anteriorly directed forces, clockwise efferent limb, 20 msec vector directed posteriorly). The QI{S duration did not change.

J. ELECTROCARDIOLOGY 16 (4), 1983

390 PICCOLO ET AL

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typ ica l (bundle b ranch block, hemiblocks) or a typ ica l p a t t e r n s owing to a b e r r a n t ven t r i cu la r conduction25-29.

The MI-QRS changes induced by P R A S in our cases are c lear ly due to a b e r r a n t conduc t ion of induced s u p r a v e n t r i c u l a r bea t s . O the r electro- phys io logica l mechan i sms which m a y ju s t i fy the induced f igures are less likely�9 Fus ion bea ts due to p r e m a t u r e ven t r i cu la r bea t s can be excluded for the following reasons: 1) the abe r r an t conduc- t ion p a t t e r n s were reproducib le a t a lmos t cons- t a n t H1-H2 coupl ing intervals ; 2) the QRS dura- t ion did no t increase in any excep t one case (case

no. 3); 3) the HV in te rva l of the induced bea t s never decreased. The presence of K en t or Mah a im fibres can be excluded because the H V in terva l was a lways normal in basal condi t ions and i t never decreased dur ing P R A S or dur ing atr ia l pacing.

In no cases were the M I - Q R S changes due to the s imula t ing effects of a conduct ion dis tur- bance such as a L B B B or an an te r io r or pos te r io r fascicular block.

Therefore , the a b e r r a n t conduc t ion induced by P R A S in our cases is p robab ly due to a de lay or b lock in one or more per iphera l conduc t ion

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Fig. 2. Recordings from a 69-year-old man who had a myocardial infarction five years later and who was admitted for unstable angina. Panel A) basal ECG-VCG; Panel B) two different induced beats: Panel C) third induced beat obtained after a pause subsequent to a spontaneous supraventricular premature beat (ex). The VCG was registered simultaneously with the induced beat (last complex to the right). The basal ECG is indicative of antero-septal myocardial infarction. The VCG shows an absence of initial anteriorly directed QRS forces: little R wave in V1 can probably be explained by the direction to the right and posteriorly of the first vectors. The duration of QRS is 96 msec. The first induced VCG (panel B, to the left) is indicative of anterolateral myocardial infarction (duration initial rightward QRS forces 24 msec, clockwise efferent limb). A slight decrease in the duration of QRS (88 msec) can be observed. The second induced VCG (panel B, to the right) shows signs of extensive-anterior myocardial infarction (absence of anteriorly directed forces, transverse plane inscribed clockwise), and left anterior hemiblock. Note the initial slowing down and the increase in the duration of QRS up to I00 msec. The third induced VCG (Panel C) shows right bundle branch block and signs of antero-septal and inferior myocardial infarction (posteriorly and leftward directed initial forces; clockwise efferent limb on the frontal plane, and superiorly directed initial forces 28 msec).


392 PICCOLO ET AL

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Fig. 3. Recordings from a 62-year-old man with an old myocardial infarction. The basal VCG (to the left) is indicative of antero-septal, inferior and probably lateral myocardial infarction {horizontal plane: absence of anteriorly directed initial QRS vectors, clockwise efferent limb, right initial forces 26 msec; frontal plane: initial superior forces 42 msec, maximum left superior force 0.65 mV). During PI{AS, we can observe (to the right) the disappearance of QI{S changes of lateral and inferior myocardial infarction. The duration of QI{S decreases from 98 to 86 msec.

pathways and perhaps in the working myocardial tissues31-35.

The MI-QRS were induced only in patients with coronary heart disease or hypertensive heart disease and never in normal cases or in patients with other heart diseases. It is known that an increase of myocardial refractoriness can be found in the myocardial tissue surrounding a gross or microscopic scar 36-3s. Since the MI-QRS which we observed appeared only in patients with coronary heart disease or hypertensive heart disease and never in patients with other cardiac conditions or in normal subjects, we hypothesize a conduction disturbance in localized areas, with abnormally prolonged refractoriness.

We cannot establish whether the conduction impairment was in the specific or in the working tissues. Many experimental electrophysiological data have shown that premature aberrant beats are generally the result of a delay or block of the stimulus in the specific pathways. Nevertheless it cannot be excluded that in some conditions the site of the block can be in the common myocardium.

In case no. 3 we think that the site of the block was in the working tissues. In fact this pat ient showed both the appearance of MI-QRS and an initial delayed QRS like the "intrainfarction block"39.

We did not find any increase in the duration of QRS in our patients. This was probably due to an involvement of only the first part of the ventricular activation as demonstrated by the impor- tant changes of the initial forces with slight changes in the middle and terminal forces.

The reduction or disappearance of MI-QRS changes observed in the other four cases is more difficult to explain. In none of these cases did we induce a typical conduction disturbance (branch or fascicular blocks) which could conceal MI- QRS. Only in patient no. 1 (Fig. 3) is the induced VCG morphologically similar to an incomplete left bundle branch block, but the simultaneous reduction of the duration of QRS is in contrast with this interpretation. Two other possible ex- planations are more likely. Firstly, the induction of a conduction disturbance generating electrical forces opposite to the vectors of the "necrosis"



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Fig. 4. Recordings from a 31-year-old man�9 The basal VCG (to the left) is indicative of posterior, inferior and lateral myocardial infarction (horizontal plane: initial rightward forces 30 msec and 0.2mV, maximum QI{S vector directed to +23 ~ duration of anterior QRS forces 62 msec; frontal plane: initial superior QRS forces 36 msec, maximum left superior force = 0.42 mV). During PRAS, we can observe (to the right) the disappearance of MI-QI{S changes�9 The duration of QRS decreases from 108 to 90 msec.

with reorientation of the first vector with or without the phenomenon of cancellation. This may particularly hold for patient no. 7 in whom we observed a delayed initial QRS limb without changes of the QRS duration. Secondly, a supernormal phase conduction 40-43 may be suggested by a significant reduction of the duration of QRS {8, 18, and 10 msec, respectively) in the three re- maining cases. This second electrophysiological interpretation implies that the MI-QRS present in the basal tracings of these pat ients were due to a conduction disturbance.

In conclusion, our results show that a conduction disturbance can partially or totally generate MI-QRS patterns, at least in some cases. Some authors thought that a conduction disturbance in the septal fascicle of the left bundle could explain transient anteroseptal pseudoinfarction patterns. However, it has never been shown that conduc-

tion disturbance can mimic inferior or extensive anterior MI patterns.

This observation could be of some clinical im- portance. In fact, there are many clinical observations which until now have been difficult to explain, such as the disappearance of QRS signs of myocardial infarction over a period of days or months after the acute episode6.9, the transient appearance of MI-QRS during coronary insuffi- ciency2,3, 4, the disappearance of MI-QRS after bypass surgery~, the lack of a close relationship between anatomical and electrocardiographic exten- sion at autopsy despite the presence of MI-QRS changes1.44-46 and the appearance of MI-QRS changes in some nonischemic heart disease.

These findings cannot be explained with the c l a s s i ca l i n t e r p r e t a t i o n of ce l lu la r d e a t h . Histological myocitolisis unrecognized at autop- sy47, cellular edema 4s, cellular metabolic stress 1,


394 PICCOLO ET AL

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Fig. 5. Recordings from a 52-year-old man with hypertrophic obstructive myocardiopathy. The basal VCG (panel A, to the left) is indicative of localized anterior myocardial infarction {initial anterior septal forces are present, and the 20 msec QRS vector is directed posteriorly). During PRAS {panel A to the right and panel B), we can observe the progressive disappearance of M]- QRS changes. The duration of QI{S decreases from 88 to 78 msec.



cellular e lect rophysiological inertness2, 49 and conduc t ion impa i rmen t in the septa l fascicle of the lef t bundle b ranch 19 have all been p u t fo rward as possible explanat ions .

I t is l ikely t h a t more than one mechan i sm is a t work in these d i f ferent condit ions. Our work sugges t s t h a t one of t hem could be a local conduc t ion d i s tu rbance gene ra t ing or con t r ibu t ing to the genera t ion of the MI -QRS changes . However , fur- the r exper imenta l and clinical work is needed in order to conf i rm this hypothes is .

R E F E R E N C E S 1. Gauss, H, RUBIN, I L, LAUFER, H, BLOOMBERG, A

E, Buinoso, L AND DELMAN, A J: Transient abnormal Q waves in the dog without myocardial infarction. Am J Cardiol 14:669, 1964

2. RUBIN, I L, Gauss, H AND VIGLIANO, E hi: Tran- sient abnormal Q waves during coronary insufficiency. Am J Cardiol 71:254, 1966

3. MELLER, J, CONDE, C A, DONOSO, E AND DACK, S: Transient Q waves in Prinzmetal's angina. Am J Cardiol 35:691, 1975

4. HELFANT, R H: Q waves in coronary heart disease: New understanding of their clinical implications. Am J Cardiol 38:662, 1976

5. KLEIN, H O, GRoss, H AND RUBIN, I L: Transient electrocardiographic changes simulating myocardial infarction during open heart surgery. Am J Cardiol 79:463, 1970

6. KALBFLEISCII, J M, SIIADAKSIIARAPPA, K S, CON- I~AD, L L ANn SARKAR, N K: Disappearance of the Q deflection following myocardial infarction. Am Heart J 76:193, 1968

7. ZEFT, H J, FRIEDBERG, H D, KING, J F, MANLEY, J C, HUSTON, J H AND JOHNSON, W D: Reappearance of anterior QRS forces after coronary bypass surgery. An electrovectorcardiographic study. Am J Cardiol 36:163, 1975

8. KILPATRICK, D: Exercise vectorcardiography in the diagnosis of ischemic heart disease. Lancet 2:332, 1964

9. HORAN, L G, FLOWERS, N C AND JOIINSON, J: Significance of the diagnostic Q wave of myocardial infarction. Circulation 43:428, 1971

10. ESTES, H, WIIALEN, R, ROBERTS, S AND MCINToSII, H: Electrocardiographic and vectorcardiographic findings in idiopathic hypertrophic subaortic stenosis. Am Heart J 65:155, 1963

II. PRESCOTT, R, QUINN, J, LITTMANN, D AND Rox" BURY, W: Electrocardiographic changes in hypertrophic subaortic stenosis which simulate myocardial infarction. Am Heart J 66:42, 1963

12. CONE, J: New concepts of intramural myocardial conduction in hypertrophic obstructive car- diomyopathy. Br Heart J 30:546, 1968

13. VAN DAM R, Ross, J AND DURRER, D: Electrical ac-

tivation of ventricles and interventricular septum in hypertrophic obstructive cardiomyopathies. Br Heart J 34:100, 1972

14. PFISTER, C W ANI) DE PANDO, B: Cerebral hemorrhage simulating acute myocardial infarction. Dis Chest 42:206, 1967

15. OFFERIIAUS, L AND VAN GOOL, J: Electrocar- diographic changes and tissue catecholamines in experimental subarachnoid hemorrhage. Car- diovasc. Res. 3:433, 1969

16. KOI.IN, A AND DWASNICKA, J: Pseudo infarction pattern of the QRS complex in experimental cardiac hypoxia induced by noradrenalin. Electrocar- diographical and histochemical study. Cardiologia 43:362, 1962

17. NORA, J R AND PILZ, C G: Pseudoinfarction pattern associated with electrolyte disturbance. Arch In- tern Med 104:300, 1959

18. SIIUGOLL, G I: Transient QRS changes simulating myocardial infarction associated with shock and severe metabolic stress. Am Heart J 74:402, 1967

19. GAMBETTA, hi G AND CHII.DERS, R W: Rate- dependent right precordial Q waves: 32:196, 1973

20. HAML1N, R L, PIPERS, F S, HELLERSTEIN, H K AND SMITH, C R: QRS alterations immediately following production of left ventricular free wall ischemia in dogs. Am J Physiol 215:1032, 1968

21. HAMLIN, R L, PIPERS, F S, HELLERSTEIN, H K AND SMITll, C R: Alterations in QRS during ischemia of the left ventricular free wall in goats. J Electrocar- diol 2:223, 1969

22. HOLLAND, R P ANn BROOKS, H: The QRS complex during myocardial ischemia. An experimental analysis in the porcine heart. J Clin Invest 57:541, 1976

23. DURRER, D, VAN LIER, A A W AND BULLER, J: Epicardial and intramural excitation in chronic myocardial infarction. Am Heart J 68:765, 1964

24. SCllICK, T D, DERSIIAM, G H, JONES, S A ANn HAN, J: Nonuniform epicardial depolarizations during coronary occlusion in dogs. J Electrocardial 13:37, 1980

25. COIIEN, S E, LAU, S H, STEIN, E, YOUNG, M W AND DAMATO, A N: Variations of aberrant ventricular conduction in man; Evidence of isolated and com- bined block within the specialized conduction system. An electrocardiographic and vectorcardiographic study. Circulation 38:899, 1968

26. KULBERTUS, H E, DE LEVAL-RuTTEN, F AND CASTERS, P: Vectorcardiographic study of aberrant conduction. Anterior displacement of QRS: Another form of intraventricular block. Br Heart J 38:549, 1976

27. PICCOLO, E, DELISE, P, ARTUSI, L, TOTARO, G, RAVIELE, A AND DE PICCOLI, B: Evaluacion de la conduccion intrahisiana a traves de la elec- trostimulacion auricular asociada a la vectorcar- diografia. Im A BAYES Y J COSlN, eds. Dyagnostico y tratamiento de las arritmias cardiacas, Ediciones Doyma, Barcelona, 1978, p 374


396 PICCOLO ET AL

28. PiccoLo, E, RAVIELE, A, DELISE, P, DAINESE, F, PAscovro, P, TOTMtO, G, SAItTOIU, F ANn D'EsTE, D: The role of left ventricular conduction in the electrogenesis of left ventricular hypertrophy. An electrophysiologic s tudy in man. Circulation 59:1044, 1979

29. Piccot.o, E, DELISE, P, RAVIELE, A, D'EsTE, D, TOTARO, G, DE PICCOLI, B, ARTUSI, L AND CAZZIN, R: The anterior displacement of the QRS loop as a right ventricular conduction disturbance. Elec- trophysiologic and vectorcardiographic study in man. J Electrocardiol 13:267, 1980

30. Cllou, S I, LAU, S H, STEIN, E, YOUNG, M W AND DAMATO, A N: Variations of aberrant ventricular conduction in man: Evidence of isolated and com- bined block within the specialized conduction system. An electrocardiographic and vectorcardiographic study. Circulation 38:899, 1968

31 VAN DAM, R, HOFFMANN, B ANn STUCKEY, J: Recovery of excitability and of impulse propaga- tion in the situ canine conduction system. Am J Cardiol 14:184, 1964

32. MOE, G, MENDEZ, C AND HAN, J: Aberrant AV impulse propogation in dog heart: Study of functional bundle branch block. Circulation Research 16:261, 1965

33. MYERBURG, R J, CASTELLANOS, A, BASSETT, A AND GELBAND, H: Functional properties of the distal AV conduction system. Adv Cardiol 14:94, 1975

34. ZIPES, D P, KNOPE, R R, MENDEZ, C AND MOE, G K: The site of functional right bundle branch block in the intact canine heart. Adv Cardiol 14:105, 1975

35. ELIZARI, M V, GREENSPAN, K AND FincH, C: Elec- trophysiological studies on intraventricular aberrant conduction. Adv Cardiol 14:115, 1975

36. MANDEL, W J, BURGESS, M J, NEVILLE, J AND AnII,DSKOV, J A: Analysis of T wave abnormalities associated with myocardial infarction using a theoretic model. Circulation 38:178, 1968

37. WILSON, F N, JOHNSTON, F D AND HILL, U G W: Form of the electrocardiogram in experimental myocardial infarction: IV. Additional observations on the later effects produced by ligation of the anterior descending branch of the left coronary artery. Am Heart J 10:1025, 1935

38. ~{YERBURG, R J, EPSTEIN, K, GAIDE,M S, WONG, S S, CASTELLANOS, A, GEl.BAND, H AND BASSETT, A L: Electrophysiologic consequences of experimental acute ischemia superimposed on healed myocardial infarction in cats. Am J Cardiol 49:323, 1982

39. CARRERA, E, COSTA RoCIIA, J AND FLORES, G: El vectorcardiolograma de los infartos miocardicos con trastorno de conduceion intraventriclar. Arch Inst Cardo Mex., Arch Inst Cardiol Mex 29:625, 1959

40. SARACIIEK, N S: Bradycardia-dependent bundle branch block. Relation to supernormal conduction and phase 4 depolarization. Am J Cardiol 25:727, 1970

41. SINGER, D H AND TEN EICK, R E: Aberrancy: Elec- trophysiologic aspects. Am J Cardiol 28:381, 1971

42. EL-SIIERIF, N: Tachycardia-dependent versus bradycardia dependent intermittent bundle branch block. Br Heart J 34:167, 1972

43. ROSEN, M R: Electrophysiology of the cardiac specialized conduction system. In: His Bundle E l e c t r o c a r d i o g r a p h y and Cl in ica l Elec- trophysiology, O S NARULA, Ed. P. A. Davis Com- pany, Philadelphia, 1975, p 19

44. BAROLDI, G: Different types of myocardial necrosis in coronary heart disease, A pathophysiologic review of their functional significance. Am Heart J 89:742, 1975

45. Cnou, T C: Pseudoinfarction {non infarction Q waves). Cardiovasc Clin 5:190, 1973

46. DUREN, D R ANn BECKER, A E: Focal myocytolysis mimicking the electrocardiographic pattern of transmural anteroseptal myocardial infarction. Chest 69:506, 1976

47. HASSETT, M A, WILLIAMS, R R AND WAGNER, G S: Transient QRS changes simulating acute myocardial infarction. Circulation 62:975, 1980

48. HACKEL, D B, WAGNER, G S, RATLIFF, N B, CIES, A ANn ESTES, E H: Anatomic studies of the cardiac conducting system in acute myocardial infarction. Am Heart J 83:77, 1972

49. DE PASQUALE, N P, BURCH, G E AND PUILIPS, J H: Electrocardiographic alterations associated with electrically "silent" areas of myocardium. Am Heart J 68:697, 1964


possible role of a ventricular conduction disturbance in the electrogenesis of the ecg-vcg signs of...

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