electrophysiologic findings in long-term asymptomatic chagasic individuals

Electrophysiologic findings in long-term asymptomatic chagasic individuals

Under electrophysiologic studies, 44 asymptomatic chagasic individuals were studied. The mean age was 39.9 years, with 26 being male. The surface ECG showed normal tracings in 12 patients, left anterior fascicular block in three, incomplete right bundle branch block in two, and right bundle branch block in 27 (isolated in six, associated with left anterior fascicular block in 19 and with left posterior fascicular block in two). Sinus nodal dysfunction was found in eight (18.1%), and 29 (66%) presented with some form of abnormal AV nodal behavior during atrial stimulation. Repetitive ventricular beats were recorded in 17 (41.4%) patients. Finally, in 19 (43.1%), patterns of dysfunction at two or more levels of the cardiac conducting system were found. It is concluded that the chagasic cardiomyopathy produces diffuse lesions in the conducting tissue of the human heart in the stages when the disease is detected, and that the individuals are still asymptomatic. (AM HEART J 106:374, 1983.)

Jo50 Pimenta, M.D., Manoel Miranda, M.D., and Carlos Britto Pereira, M.D. SCo Paulo, Brazil

Despite the fact that the disease was described in 1909 by Brazilian physician Carlos Chagas,’ the South American trypanosomiasis has several still unexplained aspects, although new techniques in the assessment of this disease, mainly in the cardiac involvement, have been used recently. It is known that the chagasic cardiomyopathy is an endemic disease in some areas of South America, including Brazil, transmitted by an insect, and a long time after the insect bite the disease presents itself in two forms: the myogenic form, affecting predominantly the ordinary myocardium, with evolution to congestive heart failure; and the neurogenic form, affecting the conducting system of the heart, leading to bundle branch block (commonly right bundle branch block) and atrioventricular (AV) block. However, positive serologic tests with no overt organic involvement can be considered as “indeter- minate form.” Thus the disorders of the exciting and conducting tissue have been poorly investigated, mainly in the initial stages of the illness when the individuals are still asymptomatic. This report presents the findings in asymptomatic long-term

From the Cardiology Service, Hospital do Servidor Ptihlico Estadual.

Supported in part hy a Grant from the “Fundo de Aperfei$oamento P I’esquisa em Cardiologia” (FAPEC) of the Sociedade Brasileira de Cardi- ologia.

Keceived for publication July 27, 1981; revision received Jan. 4, lY82; accepted Feb. 17, 1982.

Keprint requests: Dr. Jodo Pimenta, Hospital do Servidor Plihlico Estad- ual. Servipo de Cardiologia. 8’ andar, Caixa Postal 8570, Sk Paula Brazil.

chagasic individuals submitted to intracardiac potential recordings and heart stimulation, demonstrating the high frequency of excitation and conducting abnormalities when the disease is detected.

METHODS

Patients. Forty-four asymptomatic volunteers with positive serologic tests for Chagas’ disease, detected during selection for blood donors or during periodic checkup, were submitted to electrophysiologic examination for complementation studies of cardiac evaluation. The individuals with PR interval shorter than 0.12 and longer than 0.20 second, with tracings suggestive of preexcitation, clinical or documented tachyarrhythmias, and with any degree of congestive heart failure or cardiomegaly, were not included in the protocol. No patient had cardiac murmurs or extraneous heart sound on physical examination and none were taking any cardioactive drug.

EPS techniques. After the procedure had been careful- ly explained to all volunteers and consent had been obtained, the subjects were submitted to electrophysiologic studies (EPS) with the use of techniques described previously.“, ’ Then intracardiac potentials from the high right atrium and His bundle region, simultaneously with standard ECG leads I, II, and V,, were recorded. The right atrium was paced with incremental heart rate, a minimum of five different cycle lengths (CL), during at least 60 seconds for AV conduction and sinus node recovery time evaluation. The same technique was used in the right ventricle. Afterwards, the right atrium and right ventricle were scanned by programmed stimulation with extrasti- muli 6,) coupled with regular atria1 or ventricular pacing (S,), with fixed rates at approximately 100 bpm, with a progressively shortened S, -S? coupling interval until the

374

Volume 106 Number 2 Electrophysiologic study of asymptomatic Chagas’ disease 375

Table I. Data from 44 chagasic patients

Surface ECG

Sinus rhythm Repetitive

SN Prolonged AV block Prolonged LD VA uentricu- Ptlsexlage Dysf AH or HV CL > 460 ERP AVN cond lar beats

-

l/M/47 2/M/41 3/F/37 4/M/41 5/F/27 6/F/36

l/F/48 8/M/33 9/M/42

10/F/29 11/F/47 12/F/51

LAH

IRBBB

RBBB

RBBB +LAH

RBBB +LPH

13/M/47 14/F/37 15/F/51 16/M/45 17/M/32 18/M/57 19/F/33 20/M/38

21/M/23 22/M/35 23/M/53 24/F/50 25/F/44 26/M/46 27/F/26 28/M/36 29/F/47 30/M/33 31/M/49 32/F/50 33/M/29 34/F/31 35/F/43 36/M/38 37/M/51 38/M/49 39/M/32 40/M/30 41/M/55 42/M/25 43/M/28 44/F/36

- - - - - - - - - + - +

- + + - - - - -

- -

+ + - - + -

+ - -

-

- - - - - - -

- - - - - - - - - + - - - - - - - - - - +

i

+ AV node - -

- - - - - -

With intraventricular conduction defects - - - - + AV node - - - - - - - -

- - - - - - AV node + H-P

-

* * - IV-Re - HPS-Re - HPS-Re - HPS-Re + - - - - HPS-Re * * - -

+ AVN-Re - -

- - - -

HV - - - - -

HV -

AH -

H-P -

AV node - -

- -

AV node - -

- -

AH HV

-

II -

HV HV

- -

+ AV node - -

+ AV node + AV node + AV node + AV node + AV node - - - -

- - + + + 1 - - - - + -

- - + - + - - - - - + - + - - - +

- - - + - -

$ 1 - + - - - -

+ HPS-Re - -

+ AVN-Re - HPS-Re - HPS-Re + IV-Re - - - IV-Re + -

+ -

+ - * *

- - - - - -

t IV-Re - -

-

t - - - - -

+ AVN-Re + - - IV-Re + -

+ HPS-Re - -

t - - IV-Re - f -

Abbreviations: AVN-Re = AV nodal reentry; CL = cycle length; ERP = effective refractory period; F = female; H-P = His-Purkinje system; HPS- Re = His-Purkinje system reentry; IRBBB = incomplete right bundle branch block; IV-Re = intraventricular reentry; LAH = left anterior fascicular block; LPH = left posterior fascicular block; LD AVN = longitudinal dissociation in AV node; M = male; RBBB = right bundle branch block; SN dysf = sinus node dysfunction; VA cond = ventriculoatrial conduction. Symbols: + = present; - = not obtained; * = not performed; t = retrograde conduction until; 1 = discontinuous AV nodal curves with induction of reciprocating supraventricular tachycardia; 8 = type II AV block with atria1 pacing CL of 390 msec; I/ = His bundle potential was not recorded.

effective refractory period (ERP) of the paced site was reached. The atrial, His bundle, and ventricular activation during sinus rhythm are A, H, and V, respectively. The same potentials elicited by S, and S, are A,, H,, and V,, and AZ, Hz, and V,, respectively; A’, H’, and V’ are the

same potentials during reciprocating supraventricular tachycardia (RSVT) or atrial fibrillation. The maximum sinus node recovery time was evaluated according to Mandel et a1.4 and Ferrer6 (normal up to 1400 msec) and the maximum corrected sinus node recovery time was

376 Pimenta, Miranda, and Pereira August. 1983

American Heart Journal

Fig. 1. Illustrative tracings from patient No. 26, in whom diffuse conducting system disease was observed. From top to bottom, standard ECG leads I, II, and V,, high right atria1 (RA), and His bundle (HBE) electrograms. A, H. and V are atrial, His, and ventricular activations during sinus rhythm. A, is the atria1 deflection produced by extrastimulus S,. H’ and V’ are His bundle and ventricular activations produced during atria1 fibrillation. All measurements are in milliseconds. Time line distance equals 1 second. During sinus rhythm with CL of 1020 msec, premature atria1 stimulus S, with A-A, coupling interval of 320 msec induced a short run of atria1 fibrillation with spontaneous reversion to sinus rhythm, with pause of 3990 msec and electrophysiologic pattern of induced bradycardia-tachycardia syndrome. On other occasions, atria1 fibrillation lasted longer, but this example was chosen for illustrative purposes.

assessed according to Narula et al.” (normal up to 525 msec), but the sinus nodal dysfunction was only diagnosed when both parameters were prolonged. The antegrade AV nodal function curves were analyzed according to Denes et al.; and Rosen et al.H by plotting H,-H, responses against A,-A, coupling intervals, and continuous curves were considered to be a normal response. The AV nodal response to regular atria1 pacing with progressively shorter CL was considered normal response when type I second-degree AV block was obtained with atria1 pacing CL shorter than 460 msec (approximately above 130 atria1 bpm).” The induction of two distinct PR intervals at the same atria1 pacing CL, discontinuous antegrade AV nodal function curves with induction of RSVT, type I second- degree AV block with atria1 pacing CL longer than 460 msec, or AV nodal ERP longer than 360 msecl” were considered to be abnormal AV nodal response to atria1 pacing. The recognition of the repetitive ventricular beats induced by single premature ventricular stimulation (S) coupled with regular ventricular pacing was based on the conclusions of Akhtar et al.,” and the ERP and its respective normal values were analyzed according to the method of Wu et al.“’

RESULTS

The essential findings from 44 patients are sum- marized in Table I. The surface ECG showed normal

patterns in 12 patients and intraventricular conduction defects in 32, with the following breakdown: left anterior fascicular block in three, incomplete right bundle branch block in two, right bundle branch block in six, right bundle branch block plus left anterior fascicular block in 19, and right bundle branch block plus left posterior fascicular block in two. None of them had serious complications such as asystole, advanced AV block, or ventricular fibrillation, and after the study the patients left the hospital walking with no complications. Only patient No. 26 showed atria1 fibrillation at the end of the study, induced by atria1 pacing which was converted to sinus rhythm after oral quinidine sul- fate. In two patients the His bundle potential was not recorded because of technical problems, and in no case was the splitting of the His bundle recorded.

Sinus nodal function. In the entire group sinus nodal dysfunction was found in eight (18.1% ) patients, two with normal ECG, two with left anterior fascicular block, and four with right bundle branch block plus left anterior fascicular block. One patient showed characteristic electrophysiologic patterns of brady-tachycardia syndrome, with

Volume 106 Number 2 Electrophysiologic study of asymptomatic Chagas’ disease 377

induction of paroxysmal atria1 fibrillation on several occasions with a single atrial premature stimulus. Thus in Fig. 1, during sinus rhythm with atrial CL of 1020 msec, the single atria1 premature stimulus (bipolar pacing) with a coupling interval of 320 msec induced a short run of atria1 fibrillation, converted spontaneously to sinus rhythm, with a sinus pause of 3990 msec. On other occasions, the atria1 fibrillation lasted for several minutes and at the end of the study the conversion occurred only after quinidine therapy. On other hand, only five patients with some degree of sinus nodal dysfunction had a basic sinus CL longer than 1000 msec (sinus rate below 60 b-4.

AH interval. AH interval was prolonged in two patients, both with advanced intraventricular conduction disturbances, although with normal PR intervals.

HV interval. HV interval was prolonged in five patients, all of them with advanced intraventricular blocks such as right bundle branch block with left anterior fascicular block (3 of 19) and right bundle branch block with left posterior fascicular block (two patients). However, it was observed that in two patients, the recording of the His potential was not obtained, and the AH and HV intervals were not able to be determined.

AV block. In all patients but one (No. 24), type I second-degree AV block was obtained. However, AV nodal Wenckebach phenomenon with CL longer than 460 msec was observed in 11 patients, in spite of the fact that three patients had normal resting ECG tracings. The higher frequency of type I second-degree AV nodal block was observed in patients with right bundle branch block with left anterior fascicular block (7 of 19), suggesting simultaneous alteration of the AV node and bundle branches. Patient No, 6 always ended a Wenckebach cycle, with CL of 310 msec with reciprocal atrial beats and RSVT. Patient No. 24 had an HV interval of 100 msec during sinus rhythm and showed type II infra-His second-degree AV block, with an atria1 CL of 390 msec.

AV nodal function curves. These findings were in part reported previously elsewhere.3 Thus during programmed atria1 stimulation, abnormal AV nodal response patterns in 14 patients were found, five with normal resting ECG and nine with intraventricular blocks. Thirteen had discontinuous antegrade AV nodal function curves and one patient (No. 6) showed normal antegrade AV nodal curves but had two distinct PR intervals during regular atrial pacing. This patient and the other two with discontinuous antegrade AV nodal function curves had induced RSVT. Fig. 2 shows an example of atypical

Fig. 2. Tracings from patient No. 37, with atypical induction of reciprocating supraventricular tachycardia (RSVT) during programmed atria1 stimulation, coupled with regular atria1 pacing (SJ with CL of 620 msec. A,, H,, and V, and AZ, Hz, and V, are activations of the high right atrium, His bundle, and right ventricle, induced by S, and Ss, respectively. A ‘, H’ , and V’ are atrial, His bundle, and ventricular activations during RSVT. All measurements are in milliseconds and the time lines are 1 second apart. Panel A shows an atria1 premature beat with a coupling interval of 320 msec, with an H,-H, interval of 380 msec, AZ-Hz of 150 msec, and Hz-V, of 50 msec. In panel B, there is a “jump” of the H,-H, interval to 650 msec, after a single premature atria1 beat, with an AZ-H, of 440 msec, a characteristic electrophysiologic pattern of longitudinal dissociation on the AV node although without atria1 reciprocal beats or RSVT. Panel C, however, shows an A,-A, of 290 msec (S,-S, of 260 msec), H,-H, interval of 340 with A,-H, of 120 msec, with an H, duration of 40 and an Hz-V, of 90 msec, eliciting an atria1 reciprocal beat and RSVT, after a “jump” of the Hz-H’ interval to 570 msec with an A’-H’ interval of 380 msec. This mode of initiation of RSVT is atypical but it was common in this patient.

induced RSVT in an asymptomatic patient (No. 37) with a discontinuous antegrade AV nodal curve. With A,-A, coupling intervals between 320 and 300 msec (Fig. 2, A and B), there is a “jump” of the H,-H, interval from 380 to 650 msec, due to length- ening of the A,-H, interval from 150 to 440 msec, without induction of an atria1 echo beat or RSVT.

378 Pine&a, Miranda, and Pereira August. 1983


However, with A,-A, of 290 msec (Fig. 2, C, with S,-S, of 260 msec), there is an H,-H, interval of 340 msec; with conduction delay in the His bundle with H duration of 40 msec and HZ-V, of 90 msec with reciprocal atria1 beat A’, there is a developing RSVT with an A’H’ of 380 msec. On all occasions the beginning of RSVT in this patient occurred with a short HI-H2 interval and prolonged HZ-H’, and the break of tachycardia occurred with single, paired, or bursts of atria1 stimuli. Another patient with antegrade abnormal AV nodal response patterns showed RSVT during an attempt at His bundle pacing. During atria1 or ventricular pacing, the induction of RSVT was not obtained, perhaps due to the single premature stimulus used in this study.

Retrograde conduction. Sixteen out of 41 patients had retrograde conduction through the His bundle; in 13 of 16 conduction continued to the atrium, but in 3 of 16 it was blocked in the AV node. Patients with advanced intraventricular conduction defects showed a higher frequency of blockage of retrograde conduction. The analysis of the retrograde AV nodal function curves revealed discontinuous curves in two patients (No. 11 and 37).

Repetitive ventricular responses. Seventeen out of 41 patients in whom ventricular stimulation was performed showed repetitive ventricular responses due to a single ventricular extrastimulus. Eight patients showed repetitive beats with patterns of His-Purkinje system reentry, six with patterns of intraventricular reentry, and three exhibited AV nodal reentry. The occurrence of intraventricular reentry was more frequent in patients with right bundle branch disturbances.

Refractory periods. Atria1 and ventricular ERPs were within normal limits. The evaluation of the AV nodal ERP was possible in only 26 patients due to atria1 limitations, and was prolonged (longer than 360 msec) in 11 patients. It is interesting to observe that the majority of the individuals with AV nodal dysfunction detected by regular atria1 pacing (second-degree AV block with an atria1 pacing CL longer than 460 msec) also had AV nodal ERP prolongation. His-Purkinje system ERP could be determined in only two patients. However, the relative refractory period of the left bundle branch could be determined in three patients and the relative refractory period of the right bundle branch was determined in one. Another patient presented HZ-V, prolongation from an H,-H, interval of 440 msec. There was no relationship between HV interval prolongation and the possibility of determining the His-Purkinje system refractory periods. Only patient No. 24 presented HV interval prolongation and a His-Purkinje system ERP of 435 msec.

Simultaneous damage at different levels. Six patients had alterations of the sinus node associated with AV nodal abnormalities, although six had sinus nodal dysfunction and intraventricular blocks. On the other hand, AV nodal disturbances and intraventricular blocks in 17 patients were simultaneously observed, while in six patients functional abnormalities of the sinus and AV nodes and intraventricular conduction defects were found. Only two patients were electrophysiologically normal (No, 1 and 7). These data suggest that the Chagas’ disease may produce diffuse lesions of the cardiac conducting system.

DISCUSSION

After careful searching of the literature, we believe this study to be the first report about EPS in asymptomatic long-term chagasic individuals without cardiomegaly and with intact AV conduction during the resting ECG. Former reports described some electrophysiologic aspects of the chagasic cardiomyopathy,‘21 I3 but a study of a global population to determine inapparant conduction or excitability abnormalities was not performed until now. In the past, classic studies carried out by Rosenbaum et a1.,14 by Laranja et a1.,15 and by Pinto Lima et alI6 analyzed the frequency of bundle branch block in chagasic cardiomyopathy, ranging from 48 5% to 61% of the studied chagasic patients. The present population showed an incidence of 65.9 % of right bundle branch disturbances in 44 chagasic patients, but it is possible that this percentage is not representative because in this investigation, patients with cardiomegaly, prolonged PR interval, paroxysmal tachycardia, and congestive heart failure were not studied, probably patients with bundle branch blocks. For a better analysis the population of a general hospital or of a small community should have been studied, but that was not the main purpose of this investigation.

Sinus node. Although the atria1 ERP was normal in all studied patients, sinus nodal dysfunction was detected in 18.1% , demonstrating the high frequency of this disorder in individuals considered healthy until now, although this abnormality had been reported recently in symptomatic patients.17 Brasill and Amorim et a1.‘g-21 had investigated these aspects and postulated the alteration of the innervation supply of the sinus node; this was confirmed by Koberle,“” who found a decrease in the number of the parasympathetic ganglia in the sinus nodal region. On the other hand, Andrade et a1.23 also observed lesions in the sinus node as sclerosis of the cells. As a result of our findings, it may be concluded that electrophysiologically it is still impossible to

Volume 106 Number 2 Etectrophysiologic study of asymptomatic Chagas’ disease 379

prove if the sinus nodal dysfunction is due to lack of autonomic nervous supply or to lesions in the sinus node or in the perinodal region. As far as we know, the bradycardia-tachycardia syndrome is described for the first time in this disease. It is important to note that the existence of sinus bradycardia does not really represent sinus nodal dysfunction, because in seven long-term chagasic patients with a basic CL longer than 1000 msec (sinus rate less than 60 bpm), only three presented electrophysiologic patterns of sinus nodal dysfunction.

Atrioventricular junctional system. The marked conduction abnormality found in Chagas’ disease is the AV block. In this study only two patients had prolonged AV nodal conduction (increased AH interval) and five had prolonged HV interval, perhaps because patients with prolonged PR interval were not included in the protocol. However, during incremental or programmed atrial pacing, 14 patients with AV nodal conduction disturbances were considered as having type I second-degree AV block, with an atria1 CL longer than 460 msec or an AV nodal ERP longer than 360 msec. These five patients with a prolonged HV interval identify trifascicular block as occurring in this disease in approximately 11% of the chagasic patients studied, in 24% (5 of 21) of the chagasic individuals with bifascicular blocks, or in every patient with right bundle branch block with left posterior fascicular block (two patients). Although reported previously 3, l2 it is important to observe the high frequency of abnormal AV nodal response to programmed atrial pacing when the AV nodal function curves are analyzed. Thus 29.5% of patients presented discontinuous antegrade AV nodal function curves suggesting dual AV nodal pathways; one patient presented with two different PR intervals at the same atria1 CL, and there was induction of RSVT in three patients. Then 56.8% (25 of 44) of patients presented abnormal antegrade AV nodal response under different analyzed parameters, as well as 11% (5 of 44) who had alterations in the His-Purkinje system, demonstrating the high frequency of AV junctional system disorders in the chagasic patients still asymptomatic.

Ventricles. A high frequency of repetitive ventricular responses to single ventricular premature beats was observed, in spite of the normal ventricular ERP in all patients. The repetitive beats with patterns of intraventricular reentry had a higher frequency in patients with right bundle branch block. The clinical implications of these beats remain unknown. Recently, Greene et a1.24 corre- lated the repetitive ventricular responses to sudden death by comparing patients with ventricular tachy-

cardia and postmyocardial infarction to normal individuals, concluding that the presence of repetitive ventricular beats may be a predictor of sudden death. In this study the presence in 41.4% of patients of repetitive ventricular responses has to be emphasized, because ventricular tachycardia, ventricular fibrillation, and sudden death are very common in chagasic patients. Future observations of this population will be useful to reach a definite conclusion.

Diffuse damage of the conducting system. This aspect was reported years ago by Rosenbaum,25 who called the lesions of the conducting system and ordinary myocardium “pan-myocarditis.” However, only patients in advanced stages of the disease were analyzed, and these were probably all symptomatic. The present study demonstrates that 19 (43.1% ) out of 44 long-term asymptomatic chagasic patients showed abnormalities in two or more levels of the conducting system, and only two patients were electrophysiologically normal. These findings suggest that there are severe lesions, chiefly in the conducting system, in the stage at which the disease is detected, even in the asymptomatic individuals. It is interesting to note that patient No. 26 presented electrophysiologic abnormalities in all levels evaluated by this technique such as sinus node, AV node, His-Purkinje system, and bundle branches, except that he did not exhibit repetitive ventricular beats under programmed ventricular pacing.

Conclusions. These data lead to the conclusion that chagasic cardiomyopathy presents diffuse lesions in the cardiac conducting system even when the disease is detected and the individuals are still asymptomatic.

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electrophysiologic findings in long-term asymptomatic chagasic individuals

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