Download ECG Findings in Active Patients

ECG Findings in Active Patients
Differentiating the Benign From the Serious
N. A. Mark Estes III, MD; Mark S. Link, MD; Munther Homoud, MD; Paul J. Wang, MD
Exercise and Sports Cardiology Series
Editor: Paul D. Thompson, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 29 - NO. 3 - MARCH 2001
This article was adapted from the recently published book: Thompson PD (ed): Exercise and Sports
Cardiology, New York City, McGraw-Hill Medical Publishing, 2000 (to order: 1-800-262-4729 [ISBN:0-07-1347739]).
In Brief: ECGs and cardiac rhythms of normal athletes can vary widely. The heightened vagal tone from
athletic conditioning can result in variant ECG findings that may mimic serious disorders. ECG patterns of long-QT
syndrome, arrhythmogenic right ventricular dysplasia, Wolff-Parkinson-White syndrome, and hypertrophic
cardiomyopathy signal the need for further evaluation, therapy, and possible participation restriction.
Radiofrequency ablation may be appropriate when symptomatic supraventricular arrhythmias or Wolff-ParkinsonWhite syndrome is present. Further research is needed to effectively distinguish normal ECG changes in the
athlete from changes that underlie cardiac disease. Improvements in identifying athletes at risk of serious or lifethreatening arrhythmias are also needed.
Changes in the surface electrocardiogram (ECG) are common in the athlete and reflect physiologic
changes occurring in myocardial conduction, repolarization, and impulse formation from athletic conditioning and
changes in autonomic tone. Because these changes can be interpreted as underlying cardiac disease,
distinguishing normal from abnormal ECGs in the athlete can represent a challenge to the physician (table 1). The
athlete may be subject to diagnostic evaluations (stress test, ambulatory monitoring) or invasive tests
(electrophysiologic evaluation or cardiac catheterization) because of ECG abnormalities (1-40). In some
instances, unnecessary restriction from exercise or unwarranted therapy may be recommended (41). In contrast,
the ECG may manifest changes that indicate the potential for a life-threatening arrhythmia.
TABLE 1. Common ECG Findings in Athletes
Sinus bradycardia
Sinus arrhythmia
First-degree AV block
Second-degree Wenckebach AV block
Incomplete right bundle branch block
Notched P waves
Right ventricular hypertrophy (by voltage criteria)
Left ventricular hypertrophy (by voltage criteria)
Repolarization abnormalities (including ST-segment elevation and depression)
Corrected QT interval at the upper limit of normal
Tall, peaked, and inverted T wave
Based on these considerations, it is particularly important to appreciate the ECG changes that can
accompany athletic conditioning and those that signal underlying structural heart disease or vulnerability to
cardiac arrhythmias. It is important to remember that an interpretation of an ECG or arrhythmia should always be
evaluated in light of the patient's medical and family history, symptoms, physical examination, and, when
appropriate, studies evaluating the presence of underlying structural heart disease (1-40).
Sinus Bradycardia and Sinus Arrhythmia
A broad spectrum of normal bradyarrhythmias exists in the conditioned athlete due to physical
conditioning (1-19).
Sinus bradycardia
Among the most common findings in the athlete's ECG is sinus bradycardia or a heart rate less than
60/min (figure 1). Generally, unless symptoms of sinus bradycardia are present, evaluation and therapy are not
warranted.
Up to 91% of athletes will have sinus bradycardia at rest depending on the sport (1-12). In endurance
sports such as long-distance running, bicycling, and swimming, the resting heart rates become lower as the level
of conditioning increases (20). One study (21) of athletes documented average resting heart rates of 56/min in
runners, 57/min in cyclists, 62/min in swimmers, and 51/min in wrestlers. Other studies showed that elite longdistance runners had a mean resting heart rate of 47/min (7), and one runner had an asymptomatic resting rate as
low as 25/min (9), Sinus pauses longer than 2 seconds without symptoms are common in athletes (1). In runners,
pauses have been observed up to 2.55 seconds while awake and 2.8 seconds while asleep (17).
Physicians may wish to assess the adequacy of sinus node function with an exercise stress test or an
ambulatory monitor during exercise in those athletes with or without structural heart disease and resting heart
rates less than 30/min. In the absence of symptoms from sinus bradycardia, the athlete need not be restricted
from sports unless restriction is required based on underlying structural heart disease (41,42).
Sinus arrhythmia
This is common in the athlete and is defined as respiratory variation in heart rate with an increased heart
rate during inspiration. The condition normally disappears with exercise (9,21,31-35).
Conduction Abnormalities
In 10% to 33% of athletes, ECGs reveal a delay in conduction through the atrioventricular (AV) node with
first-degree AV block (defined as a PR interval >0.20) (2,14,15). Similar to sinus bradycardia, this phenomenon is
generally attributed to enhanced vagal tone. First-degree AV and Wenckebach-type blocks in the athlete typically
normalize with exercise or atropine as vagal tone is withdrawn (3,7,12,15,18). Review of 122,043 ECGs of healthy
men in the military showed that 0.65% had first-degree AV block (17).
Mobitz type 1. Ambulatory monitoring has shown that up to 40% of athletes with first-degree AV block will
also demonstrate Mobitz type 1 (Wenckebach-type) block with progressive PR prolongation before a
nonconducted P wave followed by a PR-interval shortening (1,12). Among nonathletes, the prevalence of Mobitz
type 1 block was 0.003% (17). This conduction disappears with exercise and with deconditioning.
Mobitz type 2. Among athletes, the frequency of Mobitz type 2 block and advanced AV block with more
than one consecutive, nonconducted P wave is unknown, but it is rare compared with first-degree or
Wenckebach-type block. Generally, Mobitz type 2 block should be considered a potential marker of underlying
heart disease and an indication for further evaluation. Advanced AV block and concomitant structural heart
disease or significant conduction system disease below the level of the AV node may be a marker of higher risk of
progression to higher-degree AV block and often warrants permanent pacemaker implantation.
Complete heart block. This condition is extremely rare in athletes. Not uncommonly with congenital
complete heart block, the junctional rhythm will accelerate to rates that allow athletic participation without
symptoms.
Congenital complete heart block is most commonly asymptomatic and may be associated with certain
types of structural heart disease. In individuals with symptoms such as presyncope or syncope, athletic
participation should be restricted until they have undergone 3 to 6 months of definitive therapy for the bradycardia
(41,42). Athletes who require a permanent pacemaker should not participate in contact sports (41,42).
In the absence of symptoms, worsening of the AV block with exercise, or underlying structural heart disease,
there is no need to restrict participation of athletes with first-degree AV block or Wenckebach block.
Intraventricular Conduction Delays
Incomplete right bundle branch block (RBBB) is the most common form of prolongation of intraventricular
conduction and has been noted in up to 51% of athletes in some series (2,12,15,20). Prolongation of QRS
conduction greater that 0.12 sec from a complete RBBB or left bundle branch block is extremely rare (1,16) and
would prompt evaluation for underlying structural heart disease.
QRS Axis
Generally, the QRS frontal axis is between 0° and 90° (12,20). Left-axis deviation with an axis less than 0°
is very uncommon and when present should be considered as a possible marker of underlying structural heart
disease, particularly when accompanied by a bundle branch block.
P Wave
Multiple studies (2,3,7) have noted that the P-wave amplitude is greater in athletes than in age-matched
nonathletes. The basis is unknown but may stem from atrial hypertrophy.
Ventricular Hypertrophy
It is common to find electrocardiographic criteria for either left ventricular hypertrophy (LVH) or right
ventricular hypertrophy (RVH) in athletes (12,20). ECG evidence of LVH has been studied extensively in athletes
and correlated with echocardiographic measurements of left ventricular wall thickness (12). LVH is seen in up to
76% of athletes by standard ECG criteria (2,3,5-7,13,15,25).
Sequential increases in voltage criteria occur with progressive training and regress with training cessation (20).
When endurance athletes and sprinters are compared, endurance athletes have a significantly higher incidence
of LVH than sprinters (44% vs 32%) (6). Both groups exhibit similar dimensions of left ventricle cavity dilatation,
but the endurance athletes have greater wall thickness. No meaningful research has been done on what
relationship exists between chest wall musculature and meeting the criteria for ventricular hypertrophy, but the
general impression is that the thinner chest wall in endurance athletes is associated with ECG evidence of LVH.
Nonetheless, athletes commonly meet the criteria for LVH, and the condition can be considered physiologic and
within the normal spectrum for them.
Repolarization Changes in the Athlete
J-point elevation. J-point elevation, ST-segment elevation, and T-wave changes are reported with high
frequency in athletes (figure 2) (1,12,18,43). It has been reported that these elevations normalize with exercise. Jpoint elevations may be difficult to distinguish from changes seen in ECGs of acute pericarditis because the
elevation is commonly accompanied by ST-segment elevation. However, the clinical setting and the localization of
the J-point changes to the inferior and anterior leads, in contrast to the global nature of the changes in
pericarditis, can help differentiate the two.
ST depression and T waves. ST-segment depression is unusual in the athlete. Only one series (14)
noted this finding in athletes; 3% of bicyclists had 0.1 mm J-point and ST-segment depression. In contrast, Twave changes with inversions in the precordial or limb leads have been seen in up to 30% of endurance athletes
(1,2,4,7,15,27,29). The T waves may also be peaked and tall (20), biphasic, or isoelectric. These T-wave changes
have been observed to normalize with exercise or with isoproterenol infusion (18). Distinguishing such T-wave
changes from metabolic or ischemic causes is based on the clinical setting.
Supraventricular Arrhythmias
Premature atrial contractions. Noted in a high percentage of long-distance runners (36,42), premature
atrial contractions are generally asymptomatic but may be symptomatic or detected by the physician.
When symptoms such as frequent or severe palpitations or light-headedness are present, beta-blockers are the
first-line therapy. Because premature atrial contractions are frequently episodic, a reasonable approach is a few
weeks' therapy with a long-acting beta-blocker such as atenolol (25 to 50 mg daily). If the patient remains highly
symptomatic, larger dosages can be given, or a long-acting calcium channel blocker such as verapamil
(controlled-release, 120 to 240 mg daily) can be substituted. Without any significant cardiac disease, athletes with
premature atrial contractions are not restricted from any sports (40-42).
Sustained supraventricular tachycardia and treatment. Sustained supraventricular tachycardia (SVT) in
athletes generally stems from AV nodal reentry (AV nodal reentry tachycardia or AVNRT) (42). Typically, SVT
starts and terminates abruptly. Triggers may include physical or emotional stress, caffeine, and alcohol. Valsalva
maneuvers or intravenous (IV) adenosine or verapamil are commonly used to terminate the acute episode. IV
adenosine (6 mg) is given as a rapid bolus over 1 to 2 seconds, followed by a fluid bolus. If the arrhythmia is not
terminated within 1 to 2 minutes, a 12-mg bolus can be given and repeated a second time if needed. Doses
higher than 12 mg are not recommended.
IV verapamil may be given over 1 to 2 minutes. Second doses may be given later if no response is seen.
A backup defibrillator should always be available. Verapamil is a vasodilator and may decrease blood pressure.
During exercise, athletes may experience symptoms ranging from mild palpitations to syncope, depending on
several factors, including the rate of the tachycardia and the blood pressure. Evaluation should include a history,
physical examination, and invasive electrophysiologic evaluation to define the tachycardia mechanism.
Occasionally, stress testing will provoke the arrhythmia or an episode can be documented with ambulatory or
loop monitoring.
A curative approach with radiofrequency ablation is the preferred initial treatment (42-45), because it has
a success rate greater than 95% and a low complication rate (<1%). Individuals electing pharmacologic therapy
should have no episodes for 6 months before they resume competitive, low-intensity athletics (41-44). Drug
therapy for patients who have recurrent SVT secondary to AVNRT includes beta-blockers, calcium channel
blockers, digoxin, and, rarely, class 1A (quinidine, procainamide, disopyramide) or 1C (flecainide, propafenone)
antiarrhythmic agents.
Rarely do physicians need to resort to therapy with class 1A antiarrhythmic or with class 1C
antiarrhythmic agents, especially given these drugs' potential for stimulating proarrhythmia. If used, 1A agents
should be administered in the hospital with continuous ECG monitoring. A stress test to assess for arrhythmia
recurrence or proarrhythmia is reasonable for individuals on pharmacologic therapy, though no prospective data
have documented the approach's predictive value. For athletes undergoing successful catheter ablation,
competitive athletics may be resumed after 3 months (41-44). Radiofrequency catheter ablation is preferred for
those with more severe arrhythmia-related symptoms or for athletes involved in high-intensity competitive sports.
Wolff-Parkinson-White Syndrome
Wolff-Parkinson-White (WPW) syndrome is found in approximately 3 in 1,000 individuals. This condition
manifests on the surface ECG with a short PR interval (<0.12 sec) and a delta wave appearing as a slurred
upstroke on the QRS complex from early ventricular myocardium activation (figure 3). The evaluation of the athlete
who has asymptomatic WPW remains controversial, but many experts recommend observation without restriction
of athletics since the risk of sudden death is very low (41-44).
Characteristics. The risk of sudden cardiac death in WPW syndrome is about 1 in 1,000 patient-years
(40-42). The mechanism is considered to be atrial fibrillation with rapid conduction down the accessory pathway
resulting in ventricular fibrillation. Symptomatic WPW patients should have an electrophysiologic study to establish
the potential for the bypass tract to conduct rapidly to the ventricle. Attempts at determining noninvasive indices
of the accessory bypass tracts' potential for rapid antegrade conduction have not been conclusive. A history of
syncope, the presence of multiple bypass tracts, and an interval of 250 msec or less (equivalent to a heart rate
<240/min) between two maximally preexcited QRS complexes during atrial fibrillation are considered markers for
increased risk of sudden death. Intermittent preexcitation (abrupt loss of preexcitation and the lengthening of the
PR interval) during a continuous ECG recording with minimal variation in the underlying sinus rate is considered a
sign that the accessory bypass tract has a prolonged effective refractory period (41-43). Radiofrequency ablation
is reasonable therapy if conduction to the ventricle exceeds 240/min (41-44).
Causes. Symptomatic arrhythmias from WPW may be due to AV reciprocating tachycardia, atrial
fibrillation, or, rarely, ventricular fibrillation. Typically, the SVT in WPW is a narrow complex rhythm with P waves
visible with a short RP interval during the tachycardia. Less commonly, the tachycardia proceeds antegrade
through the bypass tract and retrograde via the AV node, resulting in a wide-complex preexcited tachycardia that
can mimic ventricular tachycardia.
Manifest preexcitation may not be present on the surface ECG with a short PR interval and delta wave,
but a retrograde bypass tract may still be identified at the time of electrophysiologic evaluation. This "concealed"
bypass tract allows retrograde conduction from the ventricle to the atrium during the tachycardia and serves as
the substrate for the reentrant circuit. Radiofrequency ablation is the preferred approach. All athletic activities can
be resumed 3 months after successful ablation; however, with drug therapy, resumption is allowed only after 6
months without recurrence (41-44).
The commonest arrhythmia associated with WPW syndrome is orthodromic atrioventricular reentrant
tachycardia (AVRT). This manifests as a narrow-complex tachycardia and can be distinguished from AVNRT
associated with dual AV pathways by the presence of retrograde P waves inscribed in either the ST segment or T
waves of the tachycardia. Acute treatment of acute orthodromic AVRT is the same as for AV nodal tachycardia: IV
adenosine, IV beta-blockers, or calcium channel blockers. If these agents fail or the patient is hemodynamically
compromised, synchronized DC cardioversion should be employed.
Treatment. First-line drugs used in preventing recurrences are the class 1C antiarrhythmic agents
flecainide acetate or propafenone. These drugs prolong the accessory bypass tract's refractory period and
reduce the incidence of atrial and ventricular premature beats (SVT triggers). Although propafenone has not been
approved for use in SVT, its beta-blocking effect may help limit recurrences. In patients with underlying structural
heart disease, both drugs have the potential to exacerbate preexisting arrhythmias. Great care should be
exercised in excluding underlying cardiac disease before initiating these agents in a monitored hospital setting.
Although beta-blockers can be used in WPW patients, digoxin and calcium channel blockers are best avoided as
chronic therapy. This limits their use to patients who have had electrophysiologic studies to confirm drug safety.
Atrial Fibrillation and Atrial Flutter
Atrial fibrillation or atrial flutter in the athlete may be more common than in age-matched nonathletes (45).
One form of atrial fibrillation has been described in young patients without underlying structural heart disease but
with paroxysmal atrial fibrillation. This proclivity to start during sleep and after meals may implicate a
parasympathetic origin. Digoxin, a common treatment for atrial fibrillation, is not effective for this type and may
make the condition worse. Self-limited atrial fibrillation in young individuals often occurs after heavy alcoholic
beverage consumption.
The incidence of atrial fibrillation increases with age and with underlying heart disease. Patients younger
than 65 with no underlying cardiovascular disease or hyperthyroidism are classified as having "lone atrial
fibrillation." They have a relatively low risk of thromboembolism and constitute a distinct minority of patients.
However, young athletes with atrial fibrillation are likely to be in this group. Management of recently diagnosed
young patients should routinely include an ECG and an echocardiogram.
Cardioversion. Most cases of acute atrial fibrillation convert spontaneously within 24 hours of onset.
However, cardioversion should not be delayed beyond the first 48 hours of onset because of the increased risk of
developing left atrial thrombus. If atrial fibrillation exceeds 48 hours or the time of onset cannot be reliably
determined, conversion to sinus rhythm should be deferred until after administration of 3 weeks of anticoagulation
therapy.
Other tests and therapies. Athletes may be predisposed to atrial fibrillation due to the high vagal tone
from training. A history, physical examination, ECG, echocardiogram, thyroid function tests, and tests for illicit
drug use should be completed. The maximal exertional rate of the atrial fibrillation or flutter should be assessed
with an exercise tolerance test. An ambulatory monitor to assess maximal and minimal rates and the presence of
any ventricular arrhythmias should also be performed. Options for therapy include rhythm control by
reestablishing and maintaining normal sinus rhythm or rate control during atrial fibrillation. Rhythm control has the
advantage of avoiding anticoagulation but the potential disadvantage of risks and cost of the antiarrhythmic drug
therapy (45,46). Athletes with structural heart disease or other risk factors for embolic events may require chronic
anticoagulation with warfarin sodium, and would then be prohibited from any sport having a risk of body collision.
Ventricular Arrhythmias
Premature ventricular contractions. These are common in athletes. Fortunately, premature ventricular
contractions rarely cause symptoms that necessitate therapy. Without congenital or acquired structural heart
disease, there is no increased risk of life-threatening cardiac arrhythmias. Athletes with premature ventricular
contractions should have a history, physical examination, ECG, and echocardiogram. Further evaluation is
needed for those with congenital heart disease such as long-QT syndrome, hypertrophic cardiomyopathy,
arrhythmogenic right ventricular dysplasia, or anomalous origin of the coronary arteries--or with acquired heart
disease such as coronary artery disease or dilated cardiomyopathy (46-57).
In the absence of heart disease, therapy with beta-blockers may decrease symptoms with or without
reducing premature ventricular contraction. Other antiarrhythmic agents are not recommended unless the
symptoms are severe and persist despite beta-blocker therapy. When the premature ventricular contractions do
not cause symptoms with exertion or worsen with exercise, no athletic restrictions are needed in the absence of
structural heart disease (41,42).
Nonsustained ventricular tachycardia. This is defined as ventricular tachycardia less than 30 seconds in
duration and, unless structural heart disease is present, carries no additional risk of sudden cardiac death (42,5658). Management is similar to that for premature ventricular contractions. However, athletes with nonsustained
polymorphic ventricular tachycardia may be at higher risk for life-threatening ventricular arrhythmias, and therapy
with beta-blockers should be considered (58).
Sustained ventricular tachycardia. This condition or prior episodes of ventricular fibrillation require a
comprehensive evaluation of cardiac status including selective use of the stress test, cardiac magnetic
resonance imaging, cardiac catheterization, and electrophysiologic evaluation (41,42,46,47). In the absence of
any identifiable structural heart disease, sustained ventricular tachycardia can originate from the right ventricular
outflow tract or other regions of the right or left ventricle (idiopathic ventricular tachycardia). Programmed
ventricular stimulation supplemented by isoproterenol infusion can usually induce the arrhythmia for mapping.
When cured by radiofrequency ablation, these athletes can return to competition in 3 months (41,42).
Sustained ventricular tachycardia or ventricular fibrillation usually occurs in patients who have structural heart
disease. In athletes younger than 35, congenital abnormalities like hypertrophic cardiomyopathy most commonly
predispose them to sudden cardiac death (47-58). Since a risk of arrhythmia recurrence exists, antiarrhythmic
therapy or an implantable cardioverter defibrillator (ICD) should be used. In patients with an anomalous coronary
artery, competitive athletics can be resumed 6 months after bypass surgery (41). In athletes older than 35,
coronary artery disease is the most common cause of sudden cardiac death. An ICD confers superior protection
over drug therapy against sudden death in this group. Patients with ICDs are generally prohibited by current
guidelines from competitive athletics.
Exercise. In many cardiovascular conditions that predispose to sudden death, exercise may trigger the
arrhythmia (42,56,57). In both right ventricular outflow tract ventricular tachycardia and in the sustained
monomorphic ventricular tachycardia associated with right ventricular dysplasia, arrhythmias are commonly
exercise induced (42). Exercise can also trigger sudden death in patients with congenital coronary artery
abnormalities (56). Approximately 15% of those with idiopathic ventricular fibrillation have cardiac arrest during
exercise (46,59,60). In hypertrophic cardiomyopathy--the most common underlying structural heart disease
associated with sudden cardiac death in the young--arrhythmias are exertionally induced in most patients.
Restriction of athletic activity for these patients has been a successful strategy for preventing sudden death (61).
Sudden death in patients with long-QT syndrome is generally exertional or immediately postexertional
(62). Beta-blockers have been shown to decrease the frequency of syncope and sudden death in this group,
though ICDs provide better protection against sudden cardiac death. Restriction from athletic activities is
recommended alongside therapy (41).
Implantable cardioverter defibrillators. No one knows how well ICDs can terminate lethal arrhythmias precipitated
by vigorous competitive athletics (41). ICDs should not be placed to allow continued sports participation in
patients at risk. Generally, for those with ICDs, all moderate- and high-intensity sports are contraindicated (41,42),
and low-intensity competitive sports without a significant risk to the ICD should be restricted for at least 6 months
after the last episode requiring intervention.
Parting Comments
Changes in autonomic tone and chamber hypertrophy that accompany athletic conditioning can cause
normal physiologic changes that resemble ECG abnormalities. It is especially important for physicians to
recognize on the ECG the specific abnormalities associated with the risk of serious or life-threatening arrhythmias.
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