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Intermittent Left Bundle Branch Block in the Athletic Heart Syndrome
Austrian and Willis. 6 They found acute exudative consolidation could be induced by intratracheal injection of acid-fast organisms into rabbits. Larson and Long 7 confirmed the importance of a hypersensitivity reaction associated with tuberculoproteins by intratracheal injections of tuberculin into normal and tuberculous guinea pigs. In human tuberculosis, Rich4 found areas of fresh pneumonic exudate surrounding caseous foci in which few or no acid-fast bacilli were seen and attributed this peripheral reaction to a hypersensitivity response to tuberculoprotein. Acute tuberculous pneumonia probably represents an exudative hypersensitivity reaction to tuberculoprotein, rather than actual inflammation caused by the Mycobacterium tuberculosis organism per se. These infiltrates can appear within a matter of days and can clinically simulate acute bacterial pneumonia. Tuberculosis should be considered in the differential diagnosis of acute pneumonic infiltrates.
REFERENCES 1 Calix AA, Ziskind MM, Leonard AJ, et al: Acute tuberculous pneumonia in the Negro. Am Rev Tuberc 68:382-392, 1953 2 Schwartz WS, Moyer EE : The management of massive tuberculous pneumonia. Am Rev Tuberc 64:41-49, 1951 3 Pinner M: Pulmonary Tuberculosis in the Adult. Springfield, Ill, Charles C Thomas, 1946, p 241 4 Rich AR: The Pathogenesis of Tuberculosis. Springfield, Ill, Charles C Thomas, 1944, pp 828-830 5 Schwartz P: The role of the lymphatics in the development of bronchogenic tuberculosis. Am Rev Tuberc ff1 :440, 1953 6 Austrian CH, Willis HS : The pulmonary effects of intratracheal injections of tubercle bacilli and blood in rabbits. Am Rev Tuberc 14:306, 1926 7 Larson A, Long ER: Experimental tuberculin pneumonia. Am Rev Tuberc 23:41-44, 1931
Intermittent Left Bundle Branch Block in the Athletic Heart Syndrome* Autonomic Influence on Intraventricular Conduction John H . Chapman, M.D.
A 30-year-old man with typical findings of the athletic heart syndrome is presented because of the unique feature of intermittent left bundle branch block. Observations during right atrial pacing and exercise support the concept of autonomic control of intraventricular conduction, both adrenergic and cholinergic.
T
rained athletes often have an increase in left ventricular mass, which is considered an adaptive
°From the Department of Cardiovascular Medicine, Geisinger Medical Center, Danville, Pa. Reprint requests: Dr. Chapman, Geisinger Medical Center, Danville, Pennsylvania 17821
176 JOHN H. CHAPMAN
change necessary for maintenance of optimal cardiac performance during maximum exercise.l-3 This increase in heart size may persist into middle age, even in former athletes no longer in active training.4 Electrocardiographic abnormalities are often found in these individuals, the most common findings being QRS complexes with large amplitude, suggesting ventricular hypertrophy; incomplete right bundle branch block and other nonspecific defects of intraventricular conduction; junctional ST-segment elevation and T waves of large amplitude, frequently biphasic or inverted in the precordial leads; and sinus bradycardia, atrioventricular block, and other arrhythmias. 5 • 8 This complex of findings, termed the "athletic heart syndrome," is important to recognize, in order to avoid mislabeling a supernormal heart as abnormal. In this report a case of "athletic heart syndrome" with the unique feature of intermittent left bundle branch block is presented. Some implications regarding autonomic influence on intraventricular conduction are discussed.
CASE REPoRT A 30-year-old maintenance man involved daily in heavy lifting had consulted his family physician because of chest pain. II). high school the patient had participated in basketball and track, where his best event was the 440-yard run. This had kept him in active training for at least nine months of every year. Since graduation, he had continued to keep in shape by running a mile daily, which he accomplished in approximately five minutes, by daily weight lifting, and by frequent pickup games of basketball. The patient was asymptomatic except for musculoskeletal pain in the left pectoral region which had come on suddenly when he helped lift a 500-lb oven-top. An electrocardiogram showed striking STsegment elevation with biphasic T waves in the precordial leads and intermittent complete left bundle-branch block. Based on this study, a tentative diagnosis of myocarditis was made, and the patient was referred for cardiac evaluation. There was no history of exercise intolerance, dyspnea, palpitation, preceding viral illness, or trauma to the chest On physical examination the blood pressure was 130/80 mm Hg in both arms, and there was a resting bradycardia of 50 beats per minute. The patient was tall and mU.scular, appearing healthy. The carotid pulses were full and bounding, suggesting a large stroke volume. The jugular venous pulse was normal, aild the lungs were clear to percussion and auscultation. The left ventricular impulse was slightly prominent but not sustained. The second heart sound split physiologically, and there were no murmurs or gallops. Findings from the remainder of the physical examination were normal. The results of urinalysis, a complete blood cell count, and blood chemistry screening were normal. The ECG showed ST-segment elevation, biphasic T waves in the precordial leads, and increased voltage, suggesting left ventricular hypertrophy ( Fig 1 ) . Intermittent complete left bundle branch block was demonstrated, with minor increases in heart rate brought about by assuming the upright posture, walking, or gentle handgrip. The defect in conduction was clearly dependent on heart rate, appearing at a critical rate of 78 beats per minute ( Fig 2A) . The transition from normal conduction to left bundle-branch block was usually abrupt; but, occasionally, intermediate forms appeared in a Wenckebach-like pattern as the critical heart rate was approached ( Fig 2B).
CHEST, 71: 6, JUNE, 1977
hospitalize d for complete cardiovasc ular evaluation . Normal hemodyna mics were demonstra ted at cardiac catheteriza tion. The cardiac output measured by the Fick method was 7.6 L / min, the cardiac index being 3.7 L/ min/ sq m, with a stroke volume of 95 ml/beat. All intracardia o pressures were normal, including the left ventricula r enddiastolic pressure of 7 mm Hg. The left ventriculo gram demonstra ted a large end-diasto lic volume with uniform excellent contractili ty and a calculated ejection fraction of 71 percent, using the length-are a method of Sandler and Dodge.s Coronary angiogram s were normal. His bundle electrographic studies and right atrial pacing demonstra ted normal atrioventri cular conduction with 1 : 1 pacing through a range of 90 to 170 impulses per minute. His-ventri cle conduction was normal throughou t. Rate-relate d left bundle-bra nch block was easily reproducib le at all pacing rates, starting as low as 85 impulses per minute (Fig 3). An echocardio gram also demonstra ted a large left ventricular end-diasto lic dimension of 53 mm and a normal ejection fraction of 76 percent calculated by the cube method.9 Echocardi ographic measurem ents of septal thickness ( 16 mm ) and left ventricula r free wall thickness ( 12 mm ) were slightly above the reported normal values. A treadmill exercise test was performed using the Bruce protocol. The patient easily accomplis hed a workload of 18 METs without symptoms and was clearly still performing submaxim ally when the test was terminated . The maximum heart rate achieved was 184 beats per minute, which was 96 percent of his predicted maximum. Interesting ly, his rate-relate d left bundle-bra nch block did not appear until a rate of 180 beats per minute was achieved during exercise, whereas with right atrial pacing the block appeared at a rate of 85 beats per minute (Fig 4). FIGURE 1. 12-lead ECG taken at rest during normal intraventricula r conduction , showing abnormali ties of repolarization typical of "athletic heart syndrome. " Normal conduction could be reestablish ed by simple maneuvers, such as carotid massage or assuming the supine position, always associated with a return of the heart rate to below the critical level. The chest x-ray film showed a generous but normal heart size and configurati on. Because the question of organic heart disease had been raised and the patient's ability to return to his strenuous job was in question; he was
DISCUSSI ON
Intermitte nt left bundle branch block is nearly always seen in associatio n with organic heart disease, most often ischemic or hypertens ive in origin, but there have been isolated reports of this finding in patients with apparently normal hearts. 10 - 14 Although one cannot entirely exclude the possibility of a previous myocardit is, the data in the case presented here suggest the absence of any organic heart disease. It is possible that the dis-
A
FIGURE 2. Rhythm strips demonstra ting ratedependent bundle branch block. A, Appearance of left bundle branch block at critical heart rate of 78 beats per minute. B, Intermediate QRS complexes with Wenckeba chlike progressio n to complete left bundle branch block as critical heart rate is approached.
CHEST, 71: 6, JUNE, 1977
INTERMITTENT LEFT BUNDLE BRANCH BLOCK 777
FiGURE 3. His-bundle electrogram ( HBE) with simultaneous leads 1 and V1 during right atrial pacing at 85 impulses per minute, showing rate-dependent left bundle branch block. With cessation of pacing, normal intraventricular conduction is restored. A, Atrial depolarization; H, Hisspike potential; and P, pacing spike.
turbances in conduction seen in the athletic heart syndrome are in some way related to the "physiologic hypertrophy" now known to be present in these supernormal individuals. 15 Many reports have stressed the importance of a critical heart rate at which fatigue of the conduction system occurs and bundle branch block appears. 18• 1 8 Maneuvers which accelerate the heart rate, such as exercise, the upright posture, and the adminiStration of atropine and of amyl nitrite, repeatedly reproduce the block at a critical rate. Pharmaeologic agents that slow intraventricular conduction, such as procaine amide hydrochloride and potassium, can r~produce the block without necessarily causing a change in rate. 19 Normalization of conduction has been demonstrated with maneuvers that slow the heart below the ~ritical rate, such as deep inspiration, the recumbent posture, carotid sinus massage, and the administration of reserpine.U There are conHicting data regarding the effect of carotid sinus stimulation, with the weight of earlier evidence pointing to a negative influence of vagal discharge on intraventricular conduction. Carotid sinus massage has long been known to normalize the conduction pattern, almost always by slowing the heart rate, but rarely without producing a change in rate. Previous studies have, for the most part, been performed in pa-
Rate 175
na
JOHN H. CHAPMAN
tients with known organic heart disease, arid the possibility of a coronary vasodilator effect of carotid massage has been suggested as the mechanism in those without a change in rate. 20 In one carefully studied patient with coronary heart disease, light carotid massage produced normalization of conduction, with slowing of the heart rate, whereas forceful massage actually induced conversion from a normal pattern to left bundle-branch block, despite associated bradycardia.19 In that same patient, acceleration of the heart rate to 180 beats per minute by infusion of isoproterenol did not induce left bundlebranch block, whereas block had consistently appeared at rates of 120 to 140 beats per minute with mild exercise. Other reports have also demonstrated the association of transient bundle branch block with increased vagal tone. 21 - 25 In the normal individual with athletic heart syndrome presented here, observations during right atrial pacing and exercise suggest that intraventricular conduction is affected by autonomic influences, with parasympathetic tone slowing conduction and sympathetic tone augmenting conduction. The critical rate at which left bundle branch block appeared was between 78 and 85 beats per minute, both at rest and with right atrial pacing; however, with treadmill exercise the block did not appear until a rate of 180 beats per minute was reached. This is
Rate 180
FiGURE 4. Modified lead VG during submaximal treadmill exercise. At rate of 175 beats per minute, normal conduction is still present. Left bundle branch block appears at rate of 180 beats per minute.
CHEST, 71: 6, JUNE, 1977
analogous to the appearance of atrio-His block in normal individuals during atrial pacing at rest, dependent upon parasympathetic tone, and to the absence of block in normal subjects when the heart rate is increased by exercise at a time when sympathetic discharge is present. Recently, there has been a renewed interest in the possibility of vagal innervation of the ventricles. Ventricular tachycardia has been converted to normal sinus rhythm with administration of phenylephrine, presumably through a vagal reflex. 28 Premature ventricular contractions can be suppressed by administration of phenylephrine, both in animals and man. 27 Numerous cholinergic nerve fibers have been demonstrated in human ventricular conductive tissue, and vagal tone mediated through these fibers increases the threshold of ventricular fibrillation under both ischemic and nonischemic conditions. 28 The case reported herein suggests autonomic inlluence on intraventricular conduction in intermittent left bundle branch block and further supports the concept of both adrenergic and cholinergic innervation of the ventricular conduction system. In addition, this case adds still another electrocardiographic "abnormality.. to the list of those that can be found in the trained athlete. ACKNOWLEDGMENTS: I wish to t:bault the following persons for their helpful review of the manuscript: Frederick L. Jo~s, Jr., M.D.; Charles A. Laubach.,. Jr., M.D.; William J. Kimber, M.D.; V. F. Pytko, M.D.; ana John B. Garvey, M.O.
REFERENCES 1 Gott PH, Roselle HA, Crampton RS: The athletic heart syndrome. Arch Intern Med 122:340-344, 1968 2 Morganroth J, Maron BJ, Henry WL, et al: Comparative left ventricular dimensions in trained athletes. Ann Intern Med 82:521-524, 1975 3 Badeer HS: The genesis of cardiomegaly in strenuous athletic training: A new loolc. J Swrt;s Med Phys Fitness 15:57-67, 1975 4 Saltin B, Grimby G: Physiological analysis of middle-aged and old former athletes. Circulation 38:1104-1115, 1968 5 Lichbnan J, O'Rourke RA, Klein A, et al : ElectrocardiOgram of the athlete. Arch Intern Med 132:763-770, 1973 6 Van Ganse W, Versee L, Eylenbosch W, et al: The electrocardiogram of athletes. Br Heart J 32:160-164, 1970 7 Venerando A, Rulli V: Frequency morphology and meaning of the electrocardiographic anomalies found in olympic marathon runners and walkers. J Sports Med Phys Fitness 4:135-141, 1964 8 Sandler H, Dodge HT: The use of single plane angiocardiograms for the calculation of left ventricular volume in man. Am Heart J 75:325-334, 1968 9 Feigenbaum H: Echocardiography. Philadelphia, Lea and Febiger, 1972, pp 109-114 10 Comeau WJ, Hamilton JGM, White PD: Paroxysmal bundle-branch bloclc associated with heart disease. Am Heart J 15:276-316, 1938 11 Sandberg AA, Wener J, Master AM, et al: Intermittent and transient bundle branch bloclc: Aclinical and electrocardiographic study. Ann Intern Med 35:1085-1109, 1951 12 Eichert H: Transient bundle branch bloclc associated with tachycardia. Am Heart J 31:511-518, 1946
CHEST, 71: 6, JUNE, 1977
13 Herrmann G, Ashman R: Partial bundle-branch bloclc: A theoretical consideration of transient normal intraventricular conduction in the presence of apparently complete bundle-branch bloclc. Am Heart J 6 :375-403, 1931 14 Baragan J, Femandez-Caamano F, Coblence B, et al: Intermittent complete left bundle-branch block: Phonocardiographic and mecha.nocardiographic study oE one case. Br Heart J 29:5 0-5 :a, 1967 15 Roeske WR, O'Rourlce RA, Klein A, et al: Non-invasive evaluation of ventricular hypertrophy in professional athletes. Circulation 53:286-292, 1976 16 Shearn MA, Rytand DA: Intermittent bundle-branch block. Arch Intern Med 91:448-463, 1953 17 Bauer GE: Bundle-branch bloclc under voluntary control. Br Heart J 26:167-179, 1964 18 Hein GE, Sanazaro PJ: Intermittent bundle-branch bloclc of long duration. Arch Intern Med ff1 :694-706, 1951 19 Wallace AG, Laszlo J: Mechanisms influencing conduction in a case of intermittent bundle-branch block. Am Heart J 61:548-555, 1961 20 Harrington JF: Reversion of left bundle-branch bloclc to normal conduction by carotid sinus pressure. N Engl J Med 277:37-38, 1967 21 Wilson FN: A case in which the vagus influenced the form of the ventricular complex of the electrocardiogram. Arch Intern Med 16:1008-1027, 1915 22 Ritchie WT: The action of the vagus on the human heart. Q J Med 6:47, 1912 23 Dressler W: Transient bundle-branch bloclc occurring during slowing of the heart beat and following gagging. Am Heart J 58:760-764, 1959 24 Purks WK: Further evidence in regard to functional bundle-branch bloclc. Ann Intern Med 12:1105-1112, 1939 25 Vesell H: Critical rates in ventricular conduction: Unstable bundle-branch block. Am J Med Sci 202:198-207, 1941 26 Waxman MB, Downar E, Berman ND, et al: Phenylephrine ( Neosynephrine) terminated ventricular tachycardia. Circulation 50:656-664, 1974 27 Weiss T, Lattin GM, Engleman K.: Vagally mediated suppression of premature ventricular contractions in man. Am Heart J 89:700-707, 1975 28 Kent KM, Epstein SE; Cooper T, et al: Cholinergic innervation of the canine and human ventricular conducting system. Circulatioo 50:948-955, 1974
Regional Pulmonary Function m Scimitar Syndrome* M . Khalil Ali, M .D., F .C.C.P.;•• M. El-Guindy, M.D.;t and C. C.Shullenbergef', M.D.t
AD8Iysls of regloaal palmoaary fmctlon cUstrlbatlon usina ndfoac:tive 133xenon ps ucl eight ldntlllation de•From The University of Texas System Cancer Center; the Department of Medicine, M. D. Anderson Hospital and Tumor Institute; and the Texas Heart Institute, Houston. • • Associate Professor of Medicine and Chief, Cardiopulmonary Section, Department of Medicine. tFellow in Cardiology, St. Lulce's Hospital and Texas Heart Institute. tProfessor of Medicine and Acting Head, Department of Medicine. Reprint requem: Dr. AU, Uraioersfttl of Te%68 Sf/Item Cancer Center, 6723 Bertner, Howton 77030
PULMONARY FUNCTION IN SCIMITAR SYNDROME 779
REFERENCES 1 Calix AA, Ziskind MM, Leonard AJ, et al: Acute tuberculous pneumonia in the Negro. Am Rev Tuberc 68:382-392, 1953 2 Schwartz WS, Moyer EE : The management of massive tuberculous pneumonia. Am Rev Tuberc 64:41-49, 1951 3 Pinner M: Pulmonary Tuberculosis in the Adult. Springfield, Ill, Charles C Thomas, 1946, p 241 4 Rich AR: The Pathogenesis of Tuberculosis. Springfield, Ill, Charles C Thomas, 1944, pp 828-830 5 Schwartz P: The role of the lymphatics in the development of bronchogenic tuberculosis. Am Rev Tuberc ff1 :440, 1953 6 Austrian CH, Willis HS : The pulmonary effects of intratracheal injections of tubercle bacilli and blood in rabbits. Am Rev Tuberc 14:306, 1926 7 Larson A, Long ER: Experimental tuberculin pneumonia. Am Rev Tuberc 23:41-44, 1931
Intermittent Left Bundle Branch Block in the Athletic Heart Syndrome* Autonomic Influence on Intraventricular Conduction John H . Chapman, M.D.
A 30-year-old man with typical findings of the athletic heart syndrome is presented because of the unique feature of intermittent left bundle branch block. Observations during right atrial pacing and exercise support the concept of autonomic control of intraventricular conduction, both adrenergic and cholinergic.
T
rained athletes often have an increase in left ventricular mass, which is considered an adaptive
°From the Department of Cardiovascular Medicine, Geisinger Medical Center, Danville, Pa. Reprint requests: Dr. Chapman, Geisinger Medical Center, Danville, Pennsylvania 17821
176 JOHN H. CHAPMAN
change necessary for maintenance of optimal cardiac performance during maximum exercise.l-3 This increase in heart size may persist into middle age, even in former athletes no longer in active training.4 Electrocardiographic abnormalities are often found in these individuals, the most common findings being QRS complexes with large amplitude, suggesting ventricular hypertrophy; incomplete right bundle branch block and other nonspecific defects of intraventricular conduction; junctional ST-segment elevation and T waves of large amplitude, frequently biphasic or inverted in the precordial leads; and sinus bradycardia, atrioventricular block, and other arrhythmias. 5 • 8 This complex of findings, termed the "athletic heart syndrome," is important to recognize, in order to avoid mislabeling a supernormal heart as abnormal. In this report a case of "athletic heart syndrome" with the unique feature of intermittent left bundle branch block is presented. Some implications regarding autonomic influence on intraventricular conduction are discussed.
CASE REPoRT A 30-year-old maintenance man involved daily in heavy lifting had consulted his family physician because of chest pain. II). high school the patient had participated in basketball and track, where his best event was the 440-yard run. This had kept him in active training for at least nine months of every year. Since graduation, he had continued to keep in shape by running a mile daily, which he accomplished in approximately five minutes, by daily weight lifting, and by frequent pickup games of basketball. The patient was asymptomatic except for musculoskeletal pain in the left pectoral region which had come on suddenly when he helped lift a 500-lb oven-top. An electrocardiogram showed striking STsegment elevation with biphasic T waves in the precordial leads and intermittent complete left bundle-branch block. Based on this study, a tentative diagnosis of myocarditis was made, and the patient was referred for cardiac evaluation. There was no history of exercise intolerance, dyspnea, palpitation, preceding viral illness, or trauma to the chest On physical examination the blood pressure was 130/80 mm Hg in both arms, and there was a resting bradycardia of 50 beats per minute. The patient was tall and mU.scular, appearing healthy. The carotid pulses were full and bounding, suggesting a large stroke volume. The jugular venous pulse was normal, aild the lungs were clear to percussion and auscultation. The left ventricular impulse was slightly prominent but not sustained. The second heart sound split physiologically, and there were no murmurs or gallops. Findings from the remainder of the physical examination were normal. The results of urinalysis, a complete blood cell count, and blood chemistry screening were normal. The ECG showed ST-segment elevation, biphasic T waves in the precordial leads, and increased voltage, suggesting left ventricular hypertrophy ( Fig 1 ) . Intermittent complete left bundle branch block was demonstrated, with minor increases in heart rate brought about by assuming the upright posture, walking, or gentle handgrip. The defect in conduction was clearly dependent on heart rate, appearing at a critical rate of 78 beats per minute ( Fig 2A) . The transition from normal conduction to left bundle-branch block was usually abrupt; but, occasionally, intermediate forms appeared in a Wenckebach-like pattern as the critical heart rate was approached ( Fig 2B).
CHEST, 71: 6, JUNE, 1977
hospitalize d for complete cardiovasc ular evaluation . Normal hemodyna mics were demonstra ted at cardiac catheteriza tion. The cardiac output measured by the Fick method was 7.6 L / min, the cardiac index being 3.7 L/ min/ sq m, with a stroke volume of 95 ml/beat. All intracardia o pressures were normal, including the left ventricula r enddiastolic pressure of 7 mm Hg. The left ventriculo gram demonstra ted a large end-diasto lic volume with uniform excellent contractili ty and a calculated ejection fraction of 71 percent, using the length-are a method of Sandler and Dodge.s Coronary angiogram s were normal. His bundle electrographic studies and right atrial pacing demonstra ted normal atrioventri cular conduction with 1 : 1 pacing through a range of 90 to 170 impulses per minute. His-ventri cle conduction was normal throughou t. Rate-relate d left bundle-bra nch block was easily reproducib le at all pacing rates, starting as low as 85 impulses per minute (Fig 3). An echocardio gram also demonstra ted a large left ventricular end-diasto lic dimension of 53 mm and a normal ejection fraction of 76 percent calculated by the cube method.9 Echocardi ographic measurem ents of septal thickness ( 16 mm ) and left ventricula r free wall thickness ( 12 mm ) were slightly above the reported normal values. A treadmill exercise test was performed using the Bruce protocol. The patient easily accomplis hed a workload of 18 METs without symptoms and was clearly still performing submaxim ally when the test was terminated . The maximum heart rate achieved was 184 beats per minute, which was 96 percent of his predicted maximum. Interesting ly, his rate-relate d left bundle-bra nch block did not appear until a rate of 180 beats per minute was achieved during exercise, whereas with right atrial pacing the block appeared at a rate of 85 beats per minute (Fig 4). FIGURE 1. 12-lead ECG taken at rest during normal intraventricula r conduction , showing abnormali ties of repolarization typical of "athletic heart syndrome. " Normal conduction could be reestablish ed by simple maneuvers, such as carotid massage or assuming the supine position, always associated with a return of the heart rate to below the critical level. The chest x-ray film showed a generous but normal heart size and configurati on. Because the question of organic heart disease had been raised and the patient's ability to return to his strenuous job was in question; he was
DISCUSSI ON
Intermitte nt left bundle branch block is nearly always seen in associatio n with organic heart disease, most often ischemic or hypertens ive in origin, but there have been isolated reports of this finding in patients with apparently normal hearts. 10 - 14 Although one cannot entirely exclude the possibility of a previous myocardit is, the data in the case presented here suggest the absence of any organic heart disease. It is possible that the dis-
A
FIGURE 2. Rhythm strips demonstra ting ratedependent bundle branch block. A, Appearance of left bundle branch block at critical heart rate of 78 beats per minute. B, Intermediate QRS complexes with Wenckeba chlike progressio n to complete left bundle branch block as critical heart rate is approached.
CHEST, 71: 6, JUNE, 1977
INTERMITTENT LEFT BUNDLE BRANCH BLOCK 777
FiGURE 3. His-bundle electrogram ( HBE) with simultaneous leads 1 and V1 during right atrial pacing at 85 impulses per minute, showing rate-dependent left bundle branch block. With cessation of pacing, normal intraventricular conduction is restored. A, Atrial depolarization; H, Hisspike potential; and P, pacing spike.
turbances in conduction seen in the athletic heart syndrome are in some way related to the "physiologic hypertrophy" now known to be present in these supernormal individuals. 15 Many reports have stressed the importance of a critical heart rate at which fatigue of the conduction system occurs and bundle branch block appears. 18• 1 8 Maneuvers which accelerate the heart rate, such as exercise, the upright posture, and the adminiStration of atropine and of amyl nitrite, repeatedly reproduce the block at a critical rate. Pharmaeologic agents that slow intraventricular conduction, such as procaine amide hydrochloride and potassium, can r~produce the block without necessarily causing a change in rate. 19 Normalization of conduction has been demonstrated with maneuvers that slow the heart below the ~ritical rate, such as deep inspiration, the recumbent posture, carotid sinus massage, and the administration of reserpine.U There are conHicting data regarding the effect of carotid sinus stimulation, with the weight of earlier evidence pointing to a negative influence of vagal discharge on intraventricular conduction. Carotid sinus massage has long been known to normalize the conduction pattern, almost always by slowing the heart rate, but rarely without producing a change in rate. Previous studies have, for the most part, been performed in pa-
Rate 175
na
JOHN H. CHAPMAN
tients with known organic heart disease, arid the possibility of a coronary vasodilator effect of carotid massage has been suggested as the mechanism in those without a change in rate. 20 In one carefully studied patient with coronary heart disease, light carotid massage produced normalization of conduction, with slowing of the heart rate, whereas forceful massage actually induced conversion from a normal pattern to left bundle-branch block, despite associated bradycardia.19 In that same patient, acceleration of the heart rate to 180 beats per minute by infusion of isoproterenol did not induce left bundlebranch block, whereas block had consistently appeared at rates of 120 to 140 beats per minute with mild exercise. Other reports have also demonstrated the association of transient bundle branch block with increased vagal tone. 21 - 25 In the normal individual with athletic heart syndrome presented here, observations during right atrial pacing and exercise suggest that intraventricular conduction is affected by autonomic influences, with parasympathetic tone slowing conduction and sympathetic tone augmenting conduction. The critical rate at which left bundle branch block appeared was between 78 and 85 beats per minute, both at rest and with right atrial pacing; however, with treadmill exercise the block did not appear until a rate of 180 beats per minute was reached. This is
Rate 180
FiGURE 4. Modified lead VG during submaximal treadmill exercise. At rate of 175 beats per minute, normal conduction is still present. Left bundle branch block appears at rate of 180 beats per minute.
CHEST, 71: 6, JUNE, 1977
analogous to the appearance of atrio-His block in normal individuals during atrial pacing at rest, dependent upon parasympathetic tone, and to the absence of block in normal subjects when the heart rate is increased by exercise at a time when sympathetic discharge is present. Recently, there has been a renewed interest in the possibility of vagal innervation of the ventricles. Ventricular tachycardia has been converted to normal sinus rhythm with administration of phenylephrine, presumably through a vagal reflex. 28 Premature ventricular contractions can be suppressed by administration of phenylephrine, both in animals and man. 27 Numerous cholinergic nerve fibers have been demonstrated in human ventricular conductive tissue, and vagal tone mediated through these fibers increases the threshold of ventricular fibrillation under both ischemic and nonischemic conditions. 28 The case reported herein suggests autonomic inlluence on intraventricular conduction in intermittent left bundle branch block and further supports the concept of both adrenergic and cholinergic innervation of the ventricular conduction system. In addition, this case adds still another electrocardiographic "abnormality.. to the list of those that can be found in the trained athlete. ACKNOWLEDGMENTS: I wish to t:bault the following persons for their helpful review of the manuscript: Frederick L. Jo~s, Jr., M.D.; Charles A. Laubach.,. Jr., M.D.; William J. Kimber, M.D.; V. F. Pytko, M.D.; ana John B. Garvey, M.O.
REFERENCES 1 Gott PH, Roselle HA, Crampton RS: The athletic heart syndrome. Arch Intern Med 122:340-344, 1968 2 Morganroth J, Maron BJ, Henry WL, et al: Comparative left ventricular dimensions in trained athletes. Ann Intern Med 82:521-524, 1975 3 Badeer HS: The genesis of cardiomegaly in strenuous athletic training: A new loolc. J Swrt;s Med Phys Fitness 15:57-67, 1975 4 Saltin B, Grimby G: Physiological analysis of middle-aged and old former athletes. Circulation 38:1104-1115, 1968 5 Lichbnan J, O'Rourke RA, Klein A, et al : ElectrocardiOgram of the athlete. Arch Intern Med 132:763-770, 1973 6 Van Ganse W, Versee L, Eylenbosch W, et al: The electrocardiogram of athletes. Br Heart J 32:160-164, 1970 7 Venerando A, Rulli V: Frequency morphology and meaning of the electrocardiographic anomalies found in olympic marathon runners and walkers. J Sports Med Phys Fitness 4:135-141, 1964 8 Sandler H, Dodge HT: The use of single plane angiocardiograms for the calculation of left ventricular volume in man. Am Heart J 75:325-334, 1968 9 Feigenbaum H: Echocardiography. Philadelphia, Lea and Febiger, 1972, pp 109-114 10 Comeau WJ, Hamilton JGM, White PD: Paroxysmal bundle-branch bloclc associated with heart disease. Am Heart J 15:276-316, 1938 11 Sandberg AA, Wener J, Master AM, et al: Intermittent and transient bundle branch bloclc: Aclinical and electrocardiographic study. Ann Intern Med 35:1085-1109, 1951 12 Eichert H: Transient bundle branch bloclc associated with tachycardia. Am Heart J 31:511-518, 1946
CHEST, 71: 6, JUNE, 1977
13 Herrmann G, Ashman R: Partial bundle-branch bloclc: A theoretical consideration of transient normal intraventricular conduction in the presence of apparently complete bundle-branch bloclc. Am Heart J 6 :375-403, 1931 14 Baragan J, Femandez-Caamano F, Coblence B, et al: Intermittent complete left bundle-branch block: Phonocardiographic and mecha.nocardiographic study oE one case. Br Heart J 29:5 0-5 :a, 1967 15 Roeske WR, O'Rourlce RA, Klein A, et al: Non-invasive evaluation of ventricular hypertrophy in professional athletes. Circulation 53:286-292, 1976 16 Shearn MA, Rytand DA: Intermittent bundle-branch block. Arch Intern Med 91:448-463, 1953 17 Bauer GE: Bundle-branch bloclc under voluntary control. Br Heart J 26:167-179, 1964 18 Hein GE, Sanazaro PJ: Intermittent bundle-branch bloclc of long duration. Arch Intern Med ff1 :694-706, 1951 19 Wallace AG, Laszlo J: Mechanisms influencing conduction in a case of intermittent bundle-branch block. Am Heart J 61:548-555, 1961 20 Harrington JF: Reversion of left bundle-branch bloclc to normal conduction by carotid sinus pressure. N Engl J Med 277:37-38, 1967 21 Wilson FN: A case in which the vagus influenced the form of the ventricular complex of the electrocardiogram. Arch Intern Med 16:1008-1027, 1915 22 Ritchie WT: The action of the vagus on the human heart. Q J Med 6:47, 1912 23 Dressler W: Transient bundle-branch bloclc occurring during slowing of the heart beat and following gagging. Am Heart J 58:760-764, 1959 24 Purks WK: Further evidence in regard to functional bundle-branch bloclc. Ann Intern Med 12:1105-1112, 1939 25 Vesell H: Critical rates in ventricular conduction: Unstable bundle-branch block. Am J Med Sci 202:198-207, 1941 26 Waxman MB, Downar E, Berman ND, et al: Phenylephrine ( Neosynephrine) terminated ventricular tachycardia. Circulation 50:656-664, 1974 27 Weiss T, Lattin GM, Engleman K.: Vagally mediated suppression of premature ventricular contractions in man. Am Heart J 89:700-707, 1975 28 Kent KM, Epstein SE; Cooper T, et al: Cholinergic innervation of the canine and human ventricular conducting system. Circulatioo 50:948-955, 1974
Regional Pulmonary Function m Scimitar Syndrome* M . Khalil Ali, M .D., F .C.C.P.;•• M. El-Guindy, M.D.;t and C. C.Shullenbergef', M.D.t
AD8Iysls of regloaal palmoaary fmctlon cUstrlbatlon usina ndfoac:tive 133xenon ps ucl eight ldntlllation de•From The University of Texas System Cancer Center; the Department of Medicine, M. D. Anderson Hospital and Tumor Institute; and the Texas Heart Institute, Houston. • • Associate Professor of Medicine and Chief, Cardiopulmonary Section, Department of Medicine. tFellow in Cardiology, St. Lulce's Hospital and Texas Heart Institute. tProfessor of Medicine and Acting Head, Department of Medicine. Reprint requem: Dr. AU, Uraioersfttl of Te%68 Sf/Item Cancer Center, 6723 Bertner, Howton 77030
PULMONARY FUNCTION IN SCIMITAR SYNDROME 779