A number of electrocardiographic abnormalities have been described in athletes.1 Among these are sinus bradycardia and varying degrees of atrioventricular (AV) block. These findings have been attributed to the "athlete's heart," and are felt to be due to enhanced vagal tone seen with excellent physical conditioning. Secondarily it has also been suggested that there are intrinsic changes within the sinoatrial and AV nodes themselves, including prolonged sinus node recovery time and AV nodal Wenckebach, and these abnormalities persist following autonomic blockade.
A 46-year-old exercise physiologist presented with abdominal pain and hallucinations after a 4-day alcohol-drinking binge that averaged more than 2 L of hard liquor per day. Initial emergency department workup revealed a diagnosis of acute alcoholic pancreatitis with serum amylase and lipase of 218 U/L and 524 U/L, respectively. Baseline electrocardiogram revealed normal sinus rhythm at 78 beats per minute (bpm). The patient was admitted to a monitored bed for potential complications of alcohol withdrawal. The patient’s clinical status improved rapidly, and by the next day, he was pain free and tolerating a diet with normalizing pancreatic enzymes. Telemetry, however, revealed that overnight, the patient experienced multiple episodes of sinus bradycardia at 40 bpm along with episodes of atrioventricular (AV) nodal block and no ventricular activity lasting as long as 6.95 seconds (Figure 1). The patient was asleep during these episodes and asymptomatic. The patient revealed that he had been diagnosed with first-degree heart block a year ago, but no further work-up was performed. The patient denied ever having symptoms of presyncope, syncope, lightheadedness, or generalized weakness. The patient was an extremely well-conditioned individual who averaged 2 hours of aerobic exercise 6 days per week.
Figure 1. Telemetry rhythm strip demonstrating a 7-second episode of AV block with continued
sinus nodal activity with sinus rate at 42-48 beats per minute.
Evaluation and Diagnosis
The patient was monitored on telemetry during his 3-day admission and, in addition, had a 48-hour Holter monitoring performed. He was found to have episodes of AV nodal block only during sleep. A thorough history of the patient’s dietary supplements was obtained, none of which were known to cause bradycardia. During this period, a two-dimensional transthoracic echocardiogram was performed, which did not reveal any evidence of structural heart disease. Specifically, left ventricular chamber size and wall thickness were normal. Electrophysiology consultation was obtained; after reviewing the tracings, the impression was that the patient exhibited effects of increased vagal tone during sleep. Because the patient refused any further testing, the electrophysiologist referred to the phenomena of sinus node slowing prior to AV block (evidenced by increased P-P intervals) and P-R interval variation after AV block documented on Holter monitoring (Figure 2) as support that the block was indeed at the level of the AV node. This vagal sensitivity was likely secondary to the patient’s remarkable level of physical fitness.
Figure 2. Continuous tracing of AV block on Holter monitoring. Note progressive increase in P-P
interval (horizontal black lines) with minimal change in P-R interval prior to episode of AV block,
and also varying P-R interval (arrows) after episode of AV block.
Although these episodes did not result in adverse clinical events, due to the prolonged length of the pauses in a patient with no clinical evidence of obstructive sleep apnea (OSA), permanent pacemaker implantation was recommended for rhythm protection during these episodes.
The patient refused pacemaker implantation. He was concerned that his active lifestyle and acting career would be hindered by the device, and accepted the potential associated risks, which included sudden cardiac death. The patient did agree, however, to ambulatory Holter monitoring that revealed recurrent nocturnal episodes of ventricular asystole, with the longest ventricular pause lasting 5.18 seconds (Figure 3). All events occurred during sleep and were not associated with events in the patient’s symptom diary. The patient failed to present for his follow-up appointment.
Figure 3. Rhythm strip obtained during outpatient Holter monitoring demonstrating a 5.18-
second episode of AV block during sleep at 9:30 AM.
It has been well documented that bradyarrhythmias are a common finding in highly trained athletes, resulting in resting heart rates as low as 25 bpm.1 First-, second-, and third-degree heart block as well as sinus pauses have been recognized to occur in athletes.2 Sinus pauses lasting more than 2 seconds occurred in greater than one third of athletes evaluated in 1 study.3 In the absence of organic heart disease, these changes appear to be reversible with the cessation of high-performance sports4 and are thought to be due to elevated vagal tone common in athletes.5 Less has been written about sustained ventricular pauses in a patient in sinus rhythm. While prolonged ventricular pauses as long as 16 seconds have been documented during episodes of OSA,6 they are of uncertain significance, because they occur in a patient population which is typically obese with significant comorbidity. Less has been studied about the significance of ventricular pauses in seemingly healthy, athletic individuals. One prospective study found that highly trained athletes with ventricular pauses as long as 3 seconds failed to show evidence of increased clinical risk compared with age-matched controls with regards to syncope, near syncope, or death at long-term follow-up, despite continued training.7 Our patient in the above case is unique in that the length of ventricular pauses were significantly longer than those found in the literature with regard to athletes. Our patient did not have sinus pauses, as he maintained sinus rhythm throughout each event. His sinus node activity became relatively slowed during these ventricular pauses, again suggesting excessive vagal effect on the sinus node. Vagal inhibition of AV nodal activity and slowing of ventricular rhythm have been demonstrated,8,9 which would explain the lack of junctional or ventricular escape rhythm in our patient. Interestingly, bradycardia and asystole were observed during direct vagal nerve stimulation in the treatment of epilepsy, further demonstrating the susceptibility of the AV node to vagal stimulation.10,11 The prognostic significance of this patient’s clinical presentation is unknown, although the literature suggests that sinus bradycardia in athletes is usually not concerning unless it is symptomatic or produces ventricular pauses exceeding 4 seconds.12
The clinical significance of ventricular pauses greater than 4 seconds remains to be seen or studied. While shorter pauses have been documented in athletic individuals, in the absence of organic heart disease, they appear to be of little clinical or prognostic significance. Nevertheless, patients demonstrating sustained ventricular pauses should be evaluated for OSA, as the bradyarrhythmias associated with it tend to resolve with continuous positive airway pressure treatment,13 obviating the need for permanent pacemaker implantation.