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Accelerated A-V conduction associated with complete A-V block
Accelerated A-V conduction complete A-V block
associated
with
Venkatraman Krishnaswami, M.D.* Anthony R. Geraci, M.D., F.C.C.P.** Toledo, Ohio
Localization of sites of A-V block and the identification of accelerated pathways of conduction have become clinically applicable with the advent of His-bundle recordings. Identification of the anatomic site of block or the type of pathway in accelerated conduction produces a clearer understanding of the pathogenesis of clinical findings and enables treatment to be more rationally selected in type, be this drugs or permanent pacing. Routine His-bundle electrograms (HBE) are not generally obtained in patients with heart block who require permanent demand pacemakers. In our institution, however, an effort is made to obtain HBE in most patients selected for permanent pacing. The information is clinically useful in the follow-up of pacemaker patients in an effort to determine the persistance or resolution of varying types of A-V block. In addition, atria1 pacing at the time of HBE recording will uncover rate-dependent A-V blocks, display evidence of accelerated conduction if present, and estimate sinus node function. In the course of evaluation of a patient with complete heart block associated with a narrow QRS, HBE and atria1 pacing revealed an intraHis-bundle block and confirmed an accessory atrial-to-proximal His-bundle pathway. Cast3 report A 75-year-old white female presented with complaints of dizzy spells, weakness, and fatigue for three months. These From The Department of Medicine and Cardiology, The Toledo Hospital and The Medical College of Ohio at Toledo. Received for publication June 11, 1973. Reprint requests to: Dr. A. R. Geraci, Cardiovascular Laboratory, The Toledo Hospital, 2142 N. Cove Blvd., Toledo, Ohio 43696. “Fellow in Cardiology, The Medical College of Ohio at Toledo, Toledo, Ohio. **Associate Clinical Rofeesor Ohio at Toledo, Toledo, Ohio.
of Medicine,
The
Medical
October, 1974, Vol. 88, No. 4, pp. 463-466
College
of
symptoms were insidious in onset and related to effort. Syncope or seizures had not occurred. In the past, she had been treated for hypertension and also experienced recurrent episodes of rapid heart action characterized by abrupt onset and termination. She was treated with digitalis for presumed paroxysmal supraventricnlar tachycardia. An electrocardiogram obtained in sinus mechanism revealed a P-R of 0.14 sec. and a normal QRS. There were no delta waves. Physical examination revealed a regular heart rate of 40 per minute. Irregular “cannon” waves were seen in the neck veins. Neurologic examination and a routine cheat x-ray were normal. The electrocardiogram (Fig. 1) showed complete heart block with a ventricular rate of 38 per minute and QRS complexes, 0.08 second in duration. No evidence of infarction or ischemia was noted. The atria1 rate was 74 per minute with no capture beats present.
Electrophysiologic
studies
HBE’s were recorded on a multiple channel oscilloscope photographic recorder (Electronics for Medicine, White Plains, N. Y.1 using a No. 7 tripolar electrode (USC& Billerica, Mass.1 introduced from the femoral vein. Recordings were made at paper speeds of 150 msec. with time lines at 0.1 second intervals. Atria1 pacing was performed using a bipolar pacing catheter (Medtronic No. 5942) positioned against the right atrial wall. The resting HBE demonstrated two His-bundle potentials (Fig. 2). Hl was recorded following the atria1 electrogram (Al and H2 preceding the ventricular electrogram (vl with independent A-H1 and H2-V activity (Fig. 31. The AHl interval measured 80 msec. and the H2-Q interval 37 msec. The atria were paced at increasing rates up to 130 per minute and A-H1 intervals recorded. Fig. 4 demonstrates the absence of an increase in the A-H1 interval which remained at 80 msec. These findings suggest an A-V nodal bypass and an A-V block above H2. A permanent bipolar demand pacemaker was then inserted in the usual fashion.
American Heart Journal
463
Kriehnaswami
and Geraci
Fig. 1. Twelve lead electrocardiogram ventricular rate of 38 per minute.
&
showing No capture
complete is noted
3”
Fig. 2. His-bundle recording demonstrating Hl following the atria1 electrogram (A) with an A-H1 interval of 80 msec. The second His-bundle spike (H2) preceding ventricular potential (V) with an H2-Q interval of 37 msec. Time lines are at 0.1 second intervals with recording speed of 150 mm. per second.
464
heart block with an atria1 rate and the QRS width is normal.
of 74 per minute
and a
Discussion
Many different sites of A-V block have been documented with the utilization of His-bundle recordings.‘v2Block may occur proximal to the AV node, within the A-V node (A-H), within the His bundle (Hl-H2), or distal to the His bundle (H-V). The first three types of block are generally associated with a narrow QRS on the surface electrocardiogram in the absence of bundle branch block. The electrocardiogram of the patient reported demonstrated a narrow QRS suggesting that an A-H block would be found. The demonstration of a His-bundle spike following each atria1 complex is evidence that a pathway of conduction from the atria1 to the proximal His bundle is intact. A consistent H2 was found preceding the ventricular electrogram and the onset of the QRS on the electrocardiogram. These data suggest an intra-His block between sites Hl and H2.3Conduction through the A-V node was not demonstrated as the atria1 pacing did not produce an increase in the A-H1 interval. This finding is consistent with complete bypass of the A-V node and is defined as a Type III response.4 Whether an anatomic A-V node is present or not cannot be documented. It is possible that block of the A-V nodal conduction was present at the time of the recording permitting conduction
October,
1974, Vol. 88, No. 4
Accelerated
A-V conduction
with A-V
block
Fig. 3. Resting HBE demonstrates Hl potential following the atria1 electrogram with an A-H1 interval of 80 msec. The HZ spike precedes the ventricular potential (V) at H2-Q interval of 37 msec. The Hl -H2 potentials display independent activity.
only via the bypass fiber, although both pathways may have functioned intermittently in the past. This hypothesis is consistent with the clinical history of intermittent tachycardia previously mentioned. It was because of the history of tachycardia that atria1 pacing was performed. The H2Q interval was constant and unrelated to A-H1 activity at rest or during the atria1 pacing. The narrow QRS is thus consistent with the usual pattern of His-bundle rhythms in patients with A-H block. The finding of intact A-H1 conduction and unrelated H2-V conduction suggests that intra-His block is present. The failure of A-H1 to increase with atria1 pacing confirms an alternate atrial-to-proximal His-bundle pathway but does not determine the presence of, or block within, the A-V node as no evidence of conduction through this structure could be demonstrated. Atria1 pacing at faster rates or with coupled premature stimulation may have been of value if the refractory period of the accelerated pathway exceeded that of the A-V node.4 The development of complete A-V block with the history of supraventricular tachycardia would suggest that if an accelerated pathway is
American
Heart Journal
present, this can only be of the James fiber type when the QRS complex is narrow and not deformed. A Kent fiber would be expected to conduct the atria1 impulses to the ventricle at the sinus rate and conceal the A-V block, although deforming the QRS. The development of A-V block with a Mahiam fiber would result in atrioventricular dissociation with the initial part of the QRS deformed. A-V block in this situation could be A-H or Hl-H2. The spontaneous development of A-V block in this patient successfully terminated the effects of recurring supraventricular tachycardia by abolishing the conduction of an increased number of impulses to the ventricle. The resultant slow ventricular rate following the block was associated with symptoms of decreased cardiac output for which the patient finally sought medical attention. The value of the present information regarding the accelerated pathway and the site of A-V regarding the durablock lies in the uncertainty tion or permanency of this type of block. Block distal to the His bundle (H-V) is usually permanent and the presence of an accessory A-V nodal bypass would not be of great concern. A-H blocks,
465
Krishnaswami
and Geraci
Fig. 4. His-bundle recording with atrial pacing. The A-H1 interval remained constant as the atria1 pacing rate was increased (80 msec.). The H2-V interval and ventricular rate remained unchanged.
however, may not be fixed conduction defects and should the patient recover A-H conduction, the tachycardia may recur. Pharmacologic treatment in cases with an accessory pathway is generally unsuccessful and creation of a surgical block could theoretically be required as has been the case in several instances of intractable tachyarrhythmias with accelerated pathways.5 The spontaneous interruption of A-H conduction has, for the present, successfully treated this aspect of the patient’s problem. The value of recording HBE’s in patients with A-V block may reveal other examples of intra-His block or accelerated pathways which will increase our understanding of these complex problems. Summary
HBE’s were recorded in a 70-year-old female patient with complete heart block, narrow QRS, and past episodes of supraventricular tachycardia. The HBE revealed split His potentials with intra-His block. Atria1 pacing at increased
466
rates failed to increase the AH1 interval, suggesting an accelerated pathway between the atria and the proximal His bundle bypassing the A-V node. Below the site of block, the ventricles were paced by a distal His bundle (H2) with a resultant normal QRS interval.
REFERENCES
1. Narula, 0. S., Scherlag, B. J., Javier, R. P., et al.: Analysis of A-V conduction defect in complete heart block utilizing His-bundle electrograms, Circulation 41:437, 1970. 2. Narula, 0. S., Scherlag, B. J., Samet, P., et al.: Atrioventricular block, Am. J. Med. 50:146, 1970. 3. Narula, 0. S., Scherlag, B. J., and Samet, P.: His-bundle blocks and His-bundle rhythms, Dis. Chest 56:238, 1969. (Abetr.) 4. Caracta, A. R., Damato, A. N., Gallagher, J. J., et al.: Electrophysiologic studies in the syndrome of short PR interval, normal QRS complex, Am. J. Cardiol. 31:245, 1973. 5. Burchell, H. B.: Surgical approach to the treatment of ventricular pre-excitation, In: Advances in Internal Medicine, Stollerman, G. H., editor. Chicago, 1970, Yearbook, vol. 26.
October,
1974, Vol. 88, No. 4
associated
with
Venkatraman Krishnaswami, M.D.* Anthony R. Geraci, M.D., F.C.C.P.** Toledo, Ohio
Localization of sites of A-V block and the identification of accelerated pathways of conduction have become clinically applicable with the advent of His-bundle recordings. Identification of the anatomic site of block or the type of pathway in accelerated conduction produces a clearer understanding of the pathogenesis of clinical findings and enables treatment to be more rationally selected in type, be this drugs or permanent pacing. Routine His-bundle electrograms (HBE) are not generally obtained in patients with heart block who require permanent demand pacemakers. In our institution, however, an effort is made to obtain HBE in most patients selected for permanent pacing. The information is clinically useful in the follow-up of pacemaker patients in an effort to determine the persistance or resolution of varying types of A-V block. In addition, atria1 pacing at the time of HBE recording will uncover rate-dependent A-V blocks, display evidence of accelerated conduction if present, and estimate sinus node function. In the course of evaluation of a patient with complete heart block associated with a narrow QRS, HBE and atria1 pacing revealed an intraHis-bundle block and confirmed an accessory atrial-to-proximal His-bundle pathway. Cast3 report A 75-year-old white female presented with complaints of dizzy spells, weakness, and fatigue for three months. These From The Department of Medicine and Cardiology, The Toledo Hospital and The Medical College of Ohio at Toledo. Received for publication June 11, 1973. Reprint requests to: Dr. A. R. Geraci, Cardiovascular Laboratory, The Toledo Hospital, 2142 N. Cove Blvd., Toledo, Ohio 43696. “Fellow in Cardiology, The Medical College of Ohio at Toledo, Toledo, Ohio. **Associate Clinical Rofeesor Ohio at Toledo, Toledo, Ohio.
of Medicine,
The
Medical
October, 1974, Vol. 88, No. 4, pp. 463-466
College
of
symptoms were insidious in onset and related to effort. Syncope or seizures had not occurred. In the past, she had been treated for hypertension and also experienced recurrent episodes of rapid heart action characterized by abrupt onset and termination. She was treated with digitalis for presumed paroxysmal supraventricnlar tachycardia. An electrocardiogram obtained in sinus mechanism revealed a P-R of 0.14 sec. and a normal QRS. There were no delta waves. Physical examination revealed a regular heart rate of 40 per minute. Irregular “cannon” waves were seen in the neck veins. Neurologic examination and a routine cheat x-ray were normal. The electrocardiogram (Fig. 1) showed complete heart block with a ventricular rate of 38 per minute and QRS complexes, 0.08 second in duration. No evidence of infarction or ischemia was noted. The atria1 rate was 74 per minute with no capture beats present.
Electrophysiologic
studies
HBE’s were recorded on a multiple channel oscilloscope photographic recorder (Electronics for Medicine, White Plains, N. Y.1 using a No. 7 tripolar electrode (USC& Billerica, Mass.1 introduced from the femoral vein. Recordings were made at paper speeds of 150 msec. with time lines at 0.1 second intervals. Atria1 pacing was performed using a bipolar pacing catheter (Medtronic No. 5942) positioned against the right atrial wall. The resting HBE demonstrated two His-bundle potentials (Fig. 2). Hl was recorded following the atria1 electrogram (Al and H2 preceding the ventricular electrogram (vl with independent A-H1 and H2-V activity (Fig. 31. The AHl interval measured 80 msec. and the H2-Q interval 37 msec. The atria were paced at increasing rates up to 130 per minute and A-H1 intervals recorded. Fig. 4 demonstrates the absence of an increase in the A-H1 interval which remained at 80 msec. These findings suggest an A-V nodal bypass and an A-V block above H2. A permanent bipolar demand pacemaker was then inserted in the usual fashion.
American Heart Journal
463
Kriehnaswami
and Geraci
Fig. 1. Twelve lead electrocardiogram ventricular rate of 38 per minute.
&
showing No capture
complete is noted
3”
Fig. 2. His-bundle recording demonstrating Hl following the atria1 electrogram (A) with an A-H1 interval of 80 msec. The second His-bundle spike (H2) preceding ventricular potential (V) with an H2-Q interval of 37 msec. Time lines are at 0.1 second intervals with recording speed of 150 mm. per second.
464
heart block with an atria1 rate and the QRS width is normal.
of 74 per minute
and a
Discussion
Many different sites of A-V block have been documented with the utilization of His-bundle recordings.‘v2Block may occur proximal to the AV node, within the A-V node (A-H), within the His bundle (Hl-H2), or distal to the His bundle (H-V). The first three types of block are generally associated with a narrow QRS on the surface electrocardiogram in the absence of bundle branch block. The electrocardiogram of the patient reported demonstrated a narrow QRS suggesting that an A-H block would be found. The demonstration of a His-bundle spike following each atria1 complex is evidence that a pathway of conduction from the atria1 to the proximal His bundle is intact. A consistent H2 was found preceding the ventricular electrogram and the onset of the QRS on the electrocardiogram. These data suggest an intra-His block between sites Hl and H2.3Conduction through the A-V node was not demonstrated as the atria1 pacing did not produce an increase in the A-H1 interval. This finding is consistent with complete bypass of the A-V node and is defined as a Type III response.4 Whether an anatomic A-V node is present or not cannot be documented. It is possible that block of the A-V nodal conduction was present at the time of the recording permitting conduction
October,
1974, Vol. 88, No. 4
Accelerated
A-V conduction
with A-V
block
Fig. 3. Resting HBE demonstrates Hl potential following the atria1 electrogram with an A-H1 interval of 80 msec. The HZ spike precedes the ventricular potential (V) at H2-Q interval of 37 msec. The Hl -H2 potentials display independent activity.
only via the bypass fiber, although both pathways may have functioned intermittently in the past. This hypothesis is consistent with the clinical history of intermittent tachycardia previously mentioned. It was because of the history of tachycardia that atria1 pacing was performed. The H2Q interval was constant and unrelated to A-H1 activity at rest or during the atria1 pacing. The narrow QRS is thus consistent with the usual pattern of His-bundle rhythms in patients with A-H block. The finding of intact A-H1 conduction and unrelated H2-V conduction suggests that intra-His block is present. The failure of A-H1 to increase with atria1 pacing confirms an alternate atrial-to-proximal His-bundle pathway but does not determine the presence of, or block within, the A-V node as no evidence of conduction through this structure could be demonstrated. Atria1 pacing at faster rates or with coupled premature stimulation may have been of value if the refractory period of the accelerated pathway exceeded that of the A-V node.4 The development of complete A-V block with the history of supraventricular tachycardia would suggest that if an accelerated pathway is
American
Heart Journal
present, this can only be of the James fiber type when the QRS complex is narrow and not deformed. A Kent fiber would be expected to conduct the atria1 impulses to the ventricle at the sinus rate and conceal the A-V block, although deforming the QRS. The development of A-V block with a Mahiam fiber would result in atrioventricular dissociation with the initial part of the QRS deformed. A-V block in this situation could be A-H or Hl-H2. The spontaneous development of A-V block in this patient successfully terminated the effects of recurring supraventricular tachycardia by abolishing the conduction of an increased number of impulses to the ventricle. The resultant slow ventricular rate following the block was associated with symptoms of decreased cardiac output for which the patient finally sought medical attention. The value of the present information regarding the accelerated pathway and the site of A-V regarding the durablock lies in the uncertainty tion or permanency of this type of block. Block distal to the His bundle (H-V) is usually permanent and the presence of an accessory A-V nodal bypass would not be of great concern. A-H blocks,
465
Krishnaswami
and Geraci
Fig. 4. His-bundle recording with atrial pacing. The A-H1 interval remained constant as the atria1 pacing rate was increased (80 msec.). The H2-V interval and ventricular rate remained unchanged.
however, may not be fixed conduction defects and should the patient recover A-H conduction, the tachycardia may recur. Pharmacologic treatment in cases with an accessory pathway is generally unsuccessful and creation of a surgical block could theoretically be required as has been the case in several instances of intractable tachyarrhythmias with accelerated pathways.5 The spontaneous interruption of A-H conduction has, for the present, successfully treated this aspect of the patient’s problem. The value of recording HBE’s in patients with A-V block may reveal other examples of intra-His block or accelerated pathways which will increase our understanding of these complex problems. Summary
HBE’s were recorded in a 70-year-old female patient with complete heart block, narrow QRS, and past episodes of supraventricular tachycardia. The HBE revealed split His potentials with intra-His block. Atria1 pacing at increased
466
rates failed to increase the AH1 interval, suggesting an accelerated pathway between the atria and the proximal His bundle bypassing the A-V node. Below the site of block, the ventricles were paced by a distal His bundle (H2) with a resultant normal QRS interval.
REFERENCES
1. Narula, 0. S., Scherlag, B. J., Javier, R. P., et al.: Analysis of A-V conduction defect in complete heart block utilizing His-bundle electrograms, Circulation 41:437, 1970. 2. Narula, 0. S., Scherlag, B. J., Samet, P., et al.: Atrioventricular block, Am. J. Med. 50:146, 1970. 3. Narula, 0. S., Scherlag, B. J., and Samet, P.: His-bundle blocks and His-bundle rhythms, Dis. Chest 56:238, 1969. (Abetr.) 4. Caracta, A. R., Damato, A. N., Gallagher, J. J., et al.: Electrophysiologic studies in the syndrome of short PR interval, normal QRS complex, Am. J. Cardiol. 31:245, 1973. 5. Burchell, H. B.: Surgical approach to the treatment of ventricular pre-excitation, In: Advances in Internal Medicine, Stollerman, G. H., editor. Chicago, 1970, Yearbook, vol. 26.
October,
1974, Vol. 88, No. 4