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Reversibility and benign recurrence of complete heart block in athletes
Introduction The prognosis of athletes with complete heart block is uncertain. We report two patients who had symptomatic bradyarrhythmias after vigorous physical training. Symptoms persisted in one patient who nevertheless had a favourable long-term outcome. Case 1 highly-trained competitive sportsman lost consciousness for 30 seconds whilst shaving. In the preceding 2 weeks he had had 5 cpisodcs of near syncopc. Physical examination was normal, his resting pulse being 48 beats/minute. The chest radiograph, and precordial echocardiography were normal (ventricular septal thickness 0.9 cm). His
electrocardiogram showed sinus bradycardia (Fig. 1). He exercised to stage 6 of the Bruce protocol, achieving a maximal heart rate of 166 beats/minute which slowed to 83 beats/minute within 7 minutes of recovery. Ambulatory monitoring recorded 7 cpisodcs of asymptomatic complete heart block during the afternoon. each lasting approximately 10 seconds (Fig. 1). After stopping exercise for one week his resting heart rate was 70 beats/minute. Over the next 6 months hc exercised recreationally and remained asymptomatic. Repeat ambulatory monitoring was normal.
A ‘I-year-old
(> IO hours/week),
Fig. I. Upper
panel:
IL-lead
electrocardiogram of patient rhythm strip from patient
Case 2 A 19-year-old physical education student fainted 6 times in 6 months. She performed strenuous cxcrcisc daily in the hockey and basketball teams. Physical
1. SV, + RV, = il.2 cm. Lower panel: ambulatory 1, demonstrating complete heart block.
electrocardiographic
Discussion
07.49 -
------t-,-n
07.50 --..a-
a-__
^ ._.-. .-.-
Fig. 2. Ambulatory electrocardiographic rhythm strip from patient 2 demonstrating first-, second- and third-degree heart block at different times of the day.
examination and the chest radiograph were normal. She had a resting bradycardia of 50 beats/minute. Precordial echocardiography was normal (septal thickness 1.0 cm). She completed stage 4 of a Bruce protocol exercise test normally, but 2 minutes later the PR interval increased abruptly to 0.26 seconds. It returned to normal after 5 minutes. Ambulatory electrocardiographic recordings showed asymptomatic intermittent first-, second- (Wenkebach and Mobitz 2), and thirddegree heart block (Fig. 2), the latter occurring predominantly during sleep but also once on waking. Sinus pauses (I 2.5 seconds) were also present. An intracardiac electrophysiological study revealed supra-Hisian atrioventricular delay (AH interval at rest 200 mseconds; normal < 120 mseconds). Atrial pacing (llO/minute) caused intermittent Mobitz type II and Wenkebach second-degree heart block. After 0.6 mg atropine intravenously, the AH interval became normal (80 mseconds). The HV interval was always normal (35-4.5 mseconds). Tilting to 45” head-up for 1 hour, after 30 minutes lying flat, induced no symptoms. After stopping exercise her symptoms resolved, but on resuming strenuous exercise, they rccurrcd. In 4 years she has had 5 further syncopal attacks. Serial electrocardiograms have shown intermittent first-degree heart block, and ambulatory monitoring demonstrates asymptomatic second- and third-degree heart block during sleep, and first-degree block when awake.
First and Wenkebach second-degree heart block may occur as a consequence of extreme fitness, but in athletes Mobitz type 2 and complete heart block are so rare that irrefutable evidence of an association is lacking [I]. There were only 2 casts of complete heart block on the resting electrocardiograms of 12.000 athletes, and both subjects were asymptomatic [2]. The mechanism is probably high vagal tone, as suggested in our second patient by supra-Hisian block reversed by atropine. Athletes with complete heart block and syncope may be managed by deconditioning [3,4], which also reverses lesser degrees of heart block [4,5]. Thus, our first patient benefited from strict rest. The prognosis of athletes with complete heart block is uncertain. One athlete who reduced exercising rcmaincd asymptomatic for 5 years [3] and another had no symptoms over one year [2]. To our knowledge, ours is the first report of an athlete with symptomatic heart block who continued training. Since no ECG has been recorded during syncope, and she has normal infra-Hisian conduction. WC arc reluctant to insert a paccmaker. Prolonged deconditioning is difficult for this patient as her carter involves playing competitive sport. Her symptoms recur, albeit infrequently, whenever she resumes strenuous training, but after 4 years she rcmains well. This suggests that patients with fitncss-induced heart block can continue to train and be managed conservatively. References Huston TP. Puffer JC. MacMillan RW, The athletic heart syndrome. N Engl J Med 19X5:313:24-31. Fenici R, Caselli G. Zeppilli P, Piovano G. High degree A-V block in I7 well-trained endurance athletes. In: Lubich T. Venerando A, eds. Sports cardiology. Bologna: Auto Gaggi. 1981);523-537. Di Nardo-Ekery D, Abedin Z. High degree A-V block in a marathoner with a S-year follow-up. Am Heart J IYX7:l 13:X34~x37. Ector H, Verlinden M, Vanden Eynde E. De Geelrt H. Bourgois J, Hermans L. Bradycardia, ventricular pauses, syncope, and sports. Lancet 19X4:2:591-594. Zeppilli P, Fenici R. Sassara M. Pirrami MM, Caselli G. Wenkebach second-degree A-V block in top-ranking athletes: an old problem revisited. Am Heart J 19X0:100:2X1294.
electrocardiogram showed sinus bradycardia (Fig. 1). He exercised to stage 6 of the Bruce protocol, achieving a maximal heart rate of 166 beats/minute which slowed to 83 beats/minute within 7 minutes of recovery. Ambulatory monitoring recorded 7 cpisodcs of asymptomatic complete heart block during the afternoon. each lasting approximately 10 seconds (Fig. 1). After stopping exercise for one week his resting heart rate was 70 beats/minute. Over the next 6 months hc exercised recreationally and remained asymptomatic. Repeat ambulatory monitoring was normal.
A ‘I-year-old
(> IO hours/week),
Fig. I. Upper
panel:
IL-lead
electrocardiogram of patient rhythm strip from patient
Case 2 A 19-year-old physical education student fainted 6 times in 6 months. She performed strenuous cxcrcisc daily in the hockey and basketball teams. Physical
1. SV, + RV, = il.2 cm. Lower panel: ambulatory 1, demonstrating complete heart block.
electrocardiographic
Discussion
07.49 -
------t-,-n
07.50 --..a-
a-__
^ ._.-. .-.-
Fig. 2. Ambulatory electrocardiographic rhythm strip from patient 2 demonstrating first-, second- and third-degree heart block at different times of the day.
examination and the chest radiograph were normal. She had a resting bradycardia of 50 beats/minute. Precordial echocardiography was normal (septal thickness 1.0 cm). She completed stage 4 of a Bruce protocol exercise test normally, but 2 minutes later the PR interval increased abruptly to 0.26 seconds. It returned to normal after 5 minutes. Ambulatory electrocardiographic recordings showed asymptomatic intermittent first-, second- (Wenkebach and Mobitz 2), and thirddegree heart block (Fig. 2), the latter occurring predominantly during sleep but also once on waking. Sinus pauses (I 2.5 seconds) were also present. An intracardiac electrophysiological study revealed supra-Hisian atrioventricular delay (AH interval at rest 200 mseconds; normal < 120 mseconds). Atrial pacing (llO/minute) caused intermittent Mobitz type II and Wenkebach second-degree heart block. After 0.6 mg atropine intravenously, the AH interval became normal (80 mseconds). The HV interval was always normal (35-4.5 mseconds). Tilting to 45” head-up for 1 hour, after 30 minutes lying flat, induced no symptoms. After stopping exercise her symptoms resolved, but on resuming strenuous exercise, they rccurrcd. In 4 years she has had 5 further syncopal attacks. Serial electrocardiograms have shown intermittent first-degree heart block, and ambulatory monitoring demonstrates asymptomatic second- and third-degree heart block during sleep, and first-degree block when awake.
First and Wenkebach second-degree heart block may occur as a consequence of extreme fitness, but in athletes Mobitz type 2 and complete heart block are so rare that irrefutable evidence of an association is lacking [I]. There were only 2 casts of complete heart block on the resting electrocardiograms of 12.000 athletes, and both subjects were asymptomatic [2]. The mechanism is probably high vagal tone, as suggested in our second patient by supra-Hisian block reversed by atropine. Athletes with complete heart block and syncope may be managed by deconditioning [3,4], which also reverses lesser degrees of heart block [4,5]. Thus, our first patient benefited from strict rest. The prognosis of athletes with complete heart block is uncertain. One athlete who reduced exercising rcmaincd asymptomatic for 5 years [3] and another had no symptoms over one year [2]. To our knowledge, ours is the first report of an athlete with symptomatic heart block who continued training. Since no ECG has been recorded during syncope, and she has normal infra-Hisian conduction. WC arc reluctant to insert a paccmaker. Prolonged deconditioning is difficult for this patient as her carter involves playing competitive sport. Her symptoms recur, albeit infrequently, whenever she resumes strenuous training, but after 4 years she rcmains well. This suggests that patients with fitncss-induced heart block can continue to train and be managed conservatively. References Huston TP. Puffer JC. MacMillan RW, The athletic heart syndrome. N Engl J Med 19X5:313:24-31. Fenici R, Caselli G. Zeppilli P, Piovano G. High degree A-V block in I7 well-trained endurance athletes. In: Lubich T. Venerando A, eds. Sports cardiology. Bologna: Auto Gaggi. 1981);523-537. Di Nardo-Ekery D, Abedin Z. High degree A-V block in a marathoner with a S-year follow-up. Am Heart J IYX7:l 13:X34~x37. Ector H, Verlinden M, Vanden Eynde E. De Geelrt H. Bourgois J, Hermans L. Bradycardia, ventricular pauses, syncope, and sports. Lancet 19X4:2:591-594. Zeppilli P, Fenici R. Sassara M. Pirrami MM, Caselli G. Wenkebach second-degree A-V block in top-ranking athletes: an old problem revisited. Am Heart J 19X0:100:2X1294.