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Electrocardiographic Findings in Sports Medicine: Normal Variants and the Ones That Should Not Be Missed

Kane, Shawn F. MD*; Oriscello, Ralph G. MD; Wenzel, Robert B. MD

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Current Sports Medicine Reports: April 2005 - Volume 4 - Issue 2 - p 68-75
doi: 10.1097/01.CSMR.0000306076.90192.87
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The sudden and unexpected deaths of previously healthy and presumably asymptomatic athletes, whether young or old, have a considerable emotional and social impact on the lay and medical communities in which they occur. These events draw significant amounts of media exposure and generate considerable public interest and debate. In a recently published study, Maron [1••] found that the etiology of 74% of the cases of sudden death in an athlete were found to be from a cardiac abnormality followed by trauma, drugs, and heat exposure. In the young athlete (< 35 years) congenital and structural abnormalities, of which 26% were hypertrophic cardiomyopathy (HCM), are the common causes of cardiac death. Acquired coronary artery disease is the most common cause of cardiac death in the older athlete (> 35 years).

Although the exact frequency of sudden and unexpected cardiovascular deaths is unknown, currently it is believed that one sudden cardiac death (SCD) will occur per 200,000 to 300,000 student athletes per year. This may seem high, but in comparison the sudden death rate in previously asymptomatic joggers and marathon runners is one in 15,000 and one in 50,000, respectively [2].

The athletic and medical communities attempt to screen individuals who are participating in some form of exercise and risk stratify them according to their chances of having an SCD. Unfortunately, most of the conditions that cause SCD are silent and asymptomatic until they present as a fatal event. When compared with the total numbers of people who are participating in some form of physical activity these events are very rare. We are looking for the proverbial “needle in a haystack” [3,4].

The preparticipation examination may be the only patient encounter that will give us the opportunity, albeit small, to identify an athlete with a potentially fatal condition and intervene prior to a possibly fatal event. Identifying who should be screened and how thoroughly are questions that do not appear to have a clear answer at this point. Italian law mandates that every competitive athlete undergo rigorous annual cardiovascular screening to include an electrocardiogram (ECG), graded exercise test, echocardiogram, and more when needed. Despite this intense screening program in a very homogenous population there are still cases of SCD in Italian athletes [5]. This type of comprehensive program is not feasible, even at the elite or professional level, in the United States due to population differences and the prohibitive cost.

In 1996, The American Heart Association (AHA) issued a consensus statement on Cardiovascular Preparticipation Screening of Competitive Athletes. The AHA recommendation that some form of cardiovascular preparticipation screening for high school and college athletes occur is both justifiable and compelling. Individuals who are found to be potentially at risk for a SCD based on their screening history and physical examination, would warrant further evaluation prior to participation in competitive athletics (Table 1) [6••].

Table 1
Table 1:
“Red flag” cardiac history and physical examination findings that warrant further evaluation

The ECG is usually the first test ordered when there is the suspicion of cardiac disease in an athlete. Interpreting ECGs accurately is a vital skill for the primary care sports medicine physician or any physician who is helping in the care of athletes. Physicians must be able to identify the normal variants of a healthy athletic heart verses the subtle findings of a potentially serious pathologic heart. The obvious and most important reason to identify these potentially serious conditions is to attempt to prevent the sudden death of an athlete and, at the same time, minimize the time he or she is out of competition while being put through exhaustive, expensive, and sometimes unnecessary cardiac evaluations.

The purpose of this article is twofold: 1) to identify the normal variants found in the ECG of athletes, and 2) to identify and review some findings that should alert the provider to the possibility of an undiagnosed, underlying, and potentially fatal heart condition. We focus on the structural abnormalities of HCM and arrhythmogenic right ventricular dysplasia, and the conduction abnormalities of long QT syndrome, Brugada syndrome, Wolff-Parkinson-White syndrome, and short QT syndrome. All of these conditions are associated with a high risk of sudden death. Many of the ECG abnormalities are very subtle and can be easily missed if one is not careful or is not comfortable with reading ECGs. It is our recommendation that physicians who care for athletes establish a relationship with a cardiologist to discuss and review challenging situations prior to determining a treatment plan.

Resting Electrocardiogram of An Athlete's Heart

Cardiac muscle responds and adapts to athletic training in order to improve cardiovascular function and to meet the demands placed on it during competition. Athletic training results in heightened vagal tone, changes in myocardial conduction, repolarization, and impulse formation that result in changes to the ECG that can be interpreted as abnormal. These adaptations cause ECG changes that an inexperienced physician may interpret as abnormal. The challenge for the physician is to identify those abnormalities that may be the first and only sign to a potentially fatal underlying condition and at the same time identify normal variants and prevent the athlete from being subjected to numerous invasive, expensive, and unnecessary tests (Table 2) [7••].

Table 2
Table 2:
Common ECG findings in athletes

Up to 91% of athletes, especially those that participate in endurance sports, will have sinus bradycardia (heart rate of less than 60 beats/min) at rest. It is also not abnormal for highly trained athletes to have sinus pauses of up to 2.5 seconds. Sinus arrhythmia (respiratory variation in heart rate) is another normal finding on the resting ECG. All three of these conditions usually disappear with exercise and, in the absence of symptoms, should not preclude athletic participation.

Conduction delay through the atrioventricular (AV) node leading to first-degree AV block (PR interval > 0.20) is a common finding in up to 30% of athletes. Up to 40% of athletes with frist-degree AV block will also be found to have Mobitz type 1 (Wenckebach) second-degree heart block (progressive prolongation on the PR interval prior to the nonconduction of a P wave followed by PR-interval shortening) [7••]. Interventricular conduction delays (QRS between 0.10–0.12 sec), usually of a right bundle branch block variety can be found in up to 51% of athletes. Treatment of these normal conduction variants is similar to that of the rate abnormalities. Unless the athlete is symptomatic with exertion or has a concomitant heart abnormality, there is no need for any further work-up of conduction variants and no reason to limit an athletes training and competition.

Electrocardiographic voltage criteria for ventricular hypertrophy are a common finding in athletes. Up to 80% of conditioned athletes with ECG criteria for left ventricular hypertrophy (LVH) will have echocardiographic measurements that confirm the findings [8••]. LVH in and of itself is not a disqualifying condition, but is one that should prompt an evaluation to rule out potentially significant causes before giving it the “athlete's heart” diagnosis. Repolarization abnormalities such as J-point elevation, ST-segment elevation, and T-wave changes (inversions, peaked, tall, or biphasic) are found in up to 50% of athletes. ST-segment depression or down sloping ST segments are a rare finding in athletes and their presence requires evaluation to rule out an underlying condition.

Most abnormal findings on the resting ECG are secondary to the increased vagal tone commonly found in athletes. Therefore, exercising the patient and obtaining an exercise ECG should resolve many of the abnormalities found at rest and can be a source of reassurance for the physician.

Electrocardiographic Abnormalities That Can't Be Missed

It is essential to focus on some of the more significant ECG findings in an athlete. The two main abnormal groups are those with structural abnormalities and those with abnormalities predominantly confined to the conduction system. These findings in the right clinical setting should concern the clinician enough to recommend abstinence from further athletic participation until after a more thorough evaluation [9•]. It is generally recommended that athletes who have significantly abnormal resting ECGs or significant findings on their history and physical examination be followed-up with at least an echocardiogram and a graded exercise test. The primary care sports medicine physician or any physician caring for an athlete with a cardiovascular condition should not hesitate to reference the AHA/American Academy of Pediatrics guidelines for cardiovascular screening [10••], the National Association for Sport & Physical Education Consensus Statement on arrhythmias and the athlete [11••], the consensus panel guidelines of the 26th Bethesda Conference [12••], or refer the athlete to a trusted cardiologist for another opinion.

Structural Abnormalities

Hypertrophic cardiomyopathy

As mentioned previously, HCM is the most common cause of SCD in the young American athlete. Up to 95% of the ECGs of patients with HCM are abnormal and therefore should help in the identification of at-risk patients. The caveat to this is most patients are asymptomatic and in the United States routine screening of athletes does not include an ECG.

The ECG of a patient with HCM will usually be markedly abnormal with prominent Q waves, deep, negative T waves, increased precordial R and S wave voltages, axis deviations, and repolarization abnormalities (Fig. 1). Physicians should recommend that athletes with an abnormal ECG and concerning findings on history or physical examination should be withheld from athletic participation until the completion of a reassuring echocardiogram. The ECG, history, and physical are sensitive tests but lack specificity as the data in most studies show that of all patients referred for echocardiography with the presumptive diagnosis of HCM less than 1% to a maximum of 3% will actually have the disease [5,13].

Figure 1
Figure 1:
Electrocardiogram demonstrating the typical findings associated with hypertrophic obstructive cardiomyopathy. Note 1) the pseudo-infarct pattern inferiorly with Q waves in leads II, III, and aVF, 2) the large R wave in V1, and 3) the deep Q waves in leads V5 and V6.

After the diagnosis is confirmed, the physician should recommend that all first-degree family members undergo periodic screening with echocardiography. Adolescent family members should undergo annual screening and the screening for all family members will be for life as HCM may not present until the sixth or seventh decade. Treatment of this condition is challenging and beyond the scope of this article, but it will require the input of many people to allow the patient, the family, and the institution to make an informed decision [14].

Arrhythmogenic right ventricular dysplasia (cardiomyopathy)

Arrhythmogenic right ventricular dysplasia (ARVD) is a cardiomyopathy characterized by regional or full thickness replacement of myocardium of the right free ventricular wall by fat and fibrous tissue that leads to electrical instability. ARVD predominately impacts the right ventricle, although it has been associated with fibrous infiltration of the left ventricle in younger patients [15]. This condition is thought to cause approximately 17% of sudden deaths in the United States, although the exact true incidence in unknown because of difficulties with establishing the diagnosis. In the Veneto region of Northern Italy, ARVD is the primary cause of sudden death in young athletes, probably from a genetic predisposition and better awareness of the diagnosis [16].

Electrocardiograms in patients with ARVD will likely have 1) a ventricular arrhythmia consisting of single or multiple ventricular premature contractions with a left bundle branch block appearance (due to the origin of the arrhythmia in the right ventricle), 2) T-wave inversions in leads V1 to V4, and 3) normal to slightly widened QRS complexes. An epsilon wave (a late positive deflection in the terminal portion of the QRS-ST wave complex) on the ECG although not present in every case, is pathognomonic of this condition [8••] (Fig. 2). Echocardiography is recommended to evaluate right ventricular dilation and dysfunction in the light of a concerning ECG. An MRI looking for fatty infiltration of the myocardium is another possible option that is less invasive than the gold standard endomyocardial biopsy.

Figure 2
Figure 2:
Electrocardiogram demonstrating findings consistent with the diagnosis of arrhythmogenic right ventricular dysplasia. Note 1) ventricular premature contractions with a left bundle branch block (LBB) appearance, 2) the epsilon wave in the ST segment of V1 and V2 (when present pathognomonic for the condition), and 3) inverted T waves in V1 to V3.

Arrhythmogenic RVD is a progressive condition with a mortality rate of around 20%. Therapeutic regimens tend to be nonsustaining as currently helpful regimens may cease to be therapeutic 1 or 2 years later. β-Blockers and antiarrhythmic drugs have been used and result in an 85% to 89% survival rate at 3 years. Patients fitted with an implantable cardioverter defibrillator (ICD) had a 100% survival rate at 3 years in one published study [15,16].

Cardiac Conduction Abnormalities


Wolff-Parkinson-White (WPW) is a rare abnormality that occurs in approximately 0.15% to 0.30% of the general population; it is caused by an accessory (extranodal) electrical pathway in the cardiac conduction system. This conduction abnormality can lead to symptomatic tachyarrhythmias, and occasionally (0.1%) sudden death [8••,17]. The ECG of an athlete with WPW will have the classic electrocardiographic triad: a short PR interval (< 0.12 sec), a prolonged QRS complex, and an initial slurring of the upstroke on the QRS complex (delta wave) (Fig. 3).

Figure 3
Figure 3:
Example of the typical findings in an individual with Wolff-Parkinson-White. Note 1) the shortened PR interval (normal usually 200 msec), 2) the delta wave in all the limb leads and most prominently in leads V4 to V6, 3) the widened QRS (normal usually around 120 msec), and 4) the reciprocal ST-T wave changes.

Athletes with the above ECG abnormalities and symptoms such as palpitations, lightheadedness, and syncope are at a higher risk of sudden death from ventricular fibrillation. Athletes with symptomatic WPW should be evaluated with an exercise test, 24-hour arrhythmia monitoring, and possibly an electrophysiology study (EPS) for confirmation of the diagnosis and treatment via ablation of the accessory pathway. The evaluation and treatment of the asymptomatic WPW patient is a controversial topic. Estes et al. [7••] and Pappone et al. [18] recommend risk stratifying asymptomatic patients as either high- or low-risk for an arrhythmia based on the inducibility of an AV reciprocating tachycardia or atrial fibrillation during electrophysiologic testing. High-risk asymptomatic patients should be treated the same as symptomatic ones with accessory pathway ablation, whereas the low-risk asymptomatic group may be treated conservatively. The risk of sudden death is so low in the latter group that no restriction on athletic participation is necessary.

Long QT syndrome

Long QT syndrome (LQTS), an infrequently occurring disorder estimated to occur in approximately one in 5000 people, is defined as a corrected QT interval (QTc) of greater than 450 msec in men or 460 msec in children and women with stress-induced syncope [19]. The QT interval should be measured from the onset of the Q wave to the end of the T wave in the ECG lead in which the amplitude of the T wave is large enough to accurately identify the termination of the T wave (usually lead II). Additionally, Moss [20] found a distinctive T-wave pattern of either notched or bifid T waves in the precordial leads V2 through V4 in some patients with LQTS.

Patients affected with LQTS will usually present with syncope following emotional stress or physical activity, in particular swimming [21•]. LQTS may also be discovered on an incidental ECG in an asymptomatic athlete, or unfortunately as a cause of SCD. Boys typically are at a higher risk of SCD before puberty and women during adulthood. Pregnancy confers a small additional risk to women and there is a significant increase risk for cardiac events in the 9-month postpartum period.

Long QT syndrome places the athlete at risk for an “R on T” phenomenon, a premature ventricular complex firing during the vulnerable phase of the repolarization interval that can initiate a rapid, polymorphic ventricular tachycardia (torsades de pointes) that can deteriorate into ventricular fibrillation [22]. Acquired QT interval prolongation may be secondary to reactions to numerous drugs, electrolyte abnormalities, and other medical conditions. Patients with congenital prolonged QT syndrome should be excluded from competitive athletics permanently due to their increased risk of sudden death or at least until they are asymptomatic with the appropriate medical therapy. Athletes with acquired prolonged QT syndrome should be withheld from competition until the etiology of the syndrome is found and corrected, and their ECG has returned to normal.

Brugada syndrome

A relatively recent clinical entity, first described in 1992, that is associated with a high risk of SCD. Brugada syndrome is an autosomal dominant, paternally transmitted disease that has incomplete penetrance and results in mutations of the sodium channels in the heart. The exact incidence is unclear but it is thought to have an incidence somewhere between five and 66 per 10,000. Brugada syndrome is believed to be responsible for 4% to 12% of all sudden deaths and approximately 20% of deaths in patients with structurally normal hearts [23,24]. It is endemic in Southeast Asia and in people of Southeast Asian descent and predominately affects men in their 30s to 40s, but can also occur in children.

Electrocardiographic abnormalities, the hallmark of Brugada syndrome, may be intermittent and often concealed. The abnormalities include 1) depolarization and repolarization abnormalities that include multiple types of ST-segment elevation and T-wave inversions in the right precordial leads, 2) complete or incomplete right bundle branch block, 3) slightly prolonged QRS, 4) normal QTc, 5) pronounced broad S waves in leads I, II, and III, and axis deviation, and 6) a slightly prolonged PR interval [23].

The diagnosis of Brugada syndrome will be challenging and will likely involve numerous members of the sports medicine team and the patients' family. Intravenous procainamide, a sodium channel blocker, can be used during EPS to induce the classic ECG changes of Brugada syndrome. The prognosis for patients with Brugada syndrome can be poor, with a substantial mortality rate regardless of the degree of symptoms. When compared in trials that include no therapy, β-blocker therapy, and other antiarrhythmic therapy, the prevention of sudden death by ICDs is statistically significant [25,26]. In a recently published article by Glatter et al. [27], they report a case of Brugada syndrome that was successfully managed for over 13 years with sotalol. The authors speculate that the β-blocking and sodium channel pump-blocking properties of the medication somehow eliminated the trigger that initiates the lethal rhythm. More research needs to be done on this newly identified condition to determine if participating in athletics will put these patients at unnecessary risk. These patients will need to be thoroughly educated and counseled about their disease by an expert in order to allow them to make an informed decision.

Short QT syndrome

The QT interval represents ventricular depolarization and repolarization and, as previously discussed, there is a significant association between a prolonged QT interval and SCD. The short QT syndrome, is a recently identified autosomal dominant genetic disease, characterized by a QTc of less than 300 msec, symptomatic palpitations, and syncope. It is associated with atrial arrhythmias and SCD from ventricular fibrillation. The significance of the short QT interval, which represents a shortened time for ventricular repolarization, is believed to result in an easily induced ventricular fibrillation and sudden death in affected patients [28].

Gaita et al. [29] reported on two unrelated families with nine cases of SCD, two of the victims were known to have a short QT interval and five more members were found to have a shortened QT on ECG. Members of these families were evaluated because of syncope, palpitations, and at least one was successfully resuscitated from a cardiac arrest. The two sudden death victims and the five living members with short QT were found to have a QT interval of less than 280 msec and a QTc of less than 300 msec. The five living patients underwent EPS and were found to have short atrial and ventricular refractory periods, and all had an increased vulnerability to ventricular fibrillation. An ICD is the treatment of choice for patients identified as having short QT syndrome. Gaita et al. [28] demonstrated the effectiveness of quinidine on prolonging the QTc and decreasing the inducibility of the fatal arrhythmias.

This is obliviously an uncommon condition, but one that the sports medicine physician needs to know exists and rule out when the patient has symptoms or a family history that are consistent with the published reports.


Interpretation of the ECG of an athlete can be very challenging as the distinction between normal and potentially pathologic findings can be very subtle. A great majority of the abnormalities found in the ECG of an athlete will be normal variants. But, the combination of an ECG abnormality in association with red flags from the history and physical examination should lead to the athlete being withheld from competition until the physician can complete a more extensive evaluation.

The primary care sports medicine physician needs to be comfortable with the normal variants in the ECG of an athlete as well as the abnormalities indicative of relatively uncommon and potentially fatal conditions (Table 3). Consultation with an experienced cardiologist should always be sought in cases in which the ECG just does not look right and the sports medicine physician is uncomfortable with the athlete's story. The conditions presented in this article have ECG findings that the sports medicine physician just can not afford to miss. As long as all of these abnormal ECGs are referred for further evaluation no one will ever be able to criticize a practitioner for not practicing the standard of care.

Table 3
Table 3:
Summary of ECG abnormalities

The impact of a SCD on a community is impossible to estimate. Knowing that these conditions are uncommon and being diligent in the evaluation of athletes can allow both the athletes and the physician to feel that training and competition will be as safe as possible. Finally, the physician must remember that although a single normal ECG is not a guarantee of immortality, an abnormal ECG is not reason to disqualify an athlete without a thorough evaluation.

References and Recommended Reading

Papers of particular interest, published recently, have been highlighted as: • Of importance, •• Of major importance

1.•• Maron, BJ: Sudden death in young athletes.N Engl J Med 2003, 349:1064–1075.

Great review article from one of the experts in the field.

2. Maron BJ: Cardiovascular risks to young persons on the athletic field.Ann Intern Med 1998, 129:379–386.
3. O'Connor FG, Kugler JP, Oriscello RG: Sudden death in young athletes: screening for a needle in a haystack.Am Fam Physician 1998, 57:2763–2770.
4. Wen DY: Preparticipation cardiovascular screening of young athletes.Phys Sportsmed 2004, 32:23–30.
5. Corrado D, Basso C, Schiavon M, Thiene G: Screening for hypertrophic cardiomyopathy in young athletes.N Engl J Med 1998, 339:364–369.
6.•• Maron BJ, Thompson PD, Puffer JC, et al.: Cardiovascular preparticipation screening of competitive athletes.Circulation 1996, 94:850–856.

Consensus statement from the AHA on cardiovascular preparticipation screening.

7.•• Estes NAM, Link MS, Homoud M, Wang PJ: ECG findings in active patients differentiating the benign from the serious.Phys Sportsmed 2001, 29:67–74.

Excellent review article with great review of the parts of an ECG. Good resource for what are normal variants and what is concerning.

8.•• Basilico FC: Cardiovascular disease in athletes.Am J Sports Med 1999, 27:108–120.

Very detailed article describing the epidemiology of SCD. Thorough review of the ECG and echocardiogram findings of all the major potential cause of SCD. Great discussion on eligibility for participation based on diagnosis.

9.• Pelliccia A, Maron BJ, Culasso F, et al.: Clinical significance of abnormal electrocardiographic patterns in trained athletes.Circulation 2000, 102:278–284.

Good resource for the abnormalities that can be found on the ECG of an athlete. Classifies abnormalities on their potential significance.

10.•• Maron BJ, Thompson PD, Puffer JC, et al.: Cardiovascular preparticipation screening of competitive athletes. A statement for health professionals from the Sudden Death Committee (clinical cardiology) and Congenital Cardiac Defects Committee (cardiovascular disease in the young), American Heart Association.Circulation 1996, 94:850–856.

One of the mandatory references for the physician involved in screening and clearing athletes for athletic participation.

11.•• Estes NAM, Link MS, Cannom D, et al.: Report of the NAPSE policy conference on arrhythmias and the athlete.J Cardiovasc Electrophysiol 2001, 12:1208–1219.

One of the mandatory references for the physician involved in screening and clearing athletes for athletic participation.

12.•• Maron BJ, Isner JM, McKenna WJ: 26th Bethesda Conference; recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. Task Force 3; hypertrophic cardiomyopathy, myocarditis and myopericardial diseases and mitral valve prolapse.J Am Coll Cardiol 1994, 24:880–885.

One of the mandatory references for the physician involved in screening and clearing athletes for athletic participation.

13. Nishimura RA, Holmes DR: Hypertrophic obstructive cardiomyopathy.N Engl J Med 2004, 350:1320–1327.
14. Tabib A, Loire R, Chalabreysse L, et al.: Circumstances of death and gross and microscopic observations in a series of 200 cases of sudden death associated with arrhythmogenic right ventricular cardiomyopathy and/or dysplasia.Circulation 2003, 108:3000–3005.
15. Harrison TC, Kessler D: Arrhythmogenic right ventricular dysplasia/cardiomyopathy.Heart Lung 2003, 30:360–369.
16. DiMarco JP: Implantable cardioverter-defibrillators.N Engl J Med 2003, 349:1836–1847.
17. Lerman BB, Basson CT: High-risk patients with ventricular preexcitation - a pendulum in motion.N Engl J Med 2003, 349:1787–1789.
18. Pappone C, Santinelli V, Manguso F, et al.: A randomized study of prophylactic catheter ablation in asymptomatic patients with Wolff-Parkinson-White Syndrome.N Engl J Med 2003, 349:1803–1811.
19. Kass RS, Moss AJ: Long QT syndrome: novel insights into the mechanism of cardiac arrhythmias.J Clin Invest 2003, 112:810–815.
20. Moss AJ: Long QT syndrome.JAMA 2003, 289:2041–2044.
21.• Link MS, Wang PJ, Estes NAM: Ventricular arrhythmia in the athlete.Curr Opin Cardiol 2001, 16:30–39.

Excellent article with good explanations and examples of the significant ventricular arrhythmias. Useful tables and examples of abnormal ECGs.

22. Barkley KL: Arrhythmias.Medical Problems in Athletes. Edited by Fields KB, Fricker PA. Malden, MA: Blackwell Publishing; 1997:105–115.
23. Antzelevitch C, Brugada P, Brugada J, et al.: Brugada syndrome: a decade of progress.Circ Res 2002, 91:1114–1118.
24. Wilde AAM, Antzelevitch C, Borggrefe M, et al.: Proposed diagnostic criteria for the Brugada syndrome consensus report.Circulation 2002, 106:2514–2519.
25. Naccarelli GV, Antzelevitch C: The Brugada syndrome: clinical, genetic, cellular, and molecular abnormalities.Am J Med 2001, 110:573–581.
26. Huikuri HV, Castellanos A, Myerburg RJ: Medical progress: sudden death due to cardiac arrhythmias.N Engl J Med 2001, 345:1473–1482.
27. Glatter KA, Wang Q, Keating M, et al.: Effectiveness of sotalol treatment in symptomatic brugada syndrome.Am J Cardiol 2004, 93:1320–1322.
28. Gaita F, Giustetto C, Bianchi F, et al.: Short QT syndrome: pharmacologic treatment.J Am Coll Cardiol 2004, 43: 1494–1499.
29. Gaita F, Giustetto C, Bianchi F, et al.: Short QT syndrome a familial cause of sudden death.Circulation 2003, 108: 965–970.
© 2005 American College of Sports Medicine