Although the 36th Bethesda Guidelines for sports participation recommend that athletes with implanted cardioverter-defibrillators (ICDs) be disqualified from participating in sports (1), surveys of implanting physicians and sports medicine specialists indicate that the majority of athletes with ICDs are participating in some form of sports activity (2,3).
ICDs are implanted to treat episodes of sudden cardiac arrest (SCA) caused by ventricular fibrillation (VF) in high-risk individuals. Such individuals are identified either by having experienced a prior VF episode from which they were resuscitated (secondary prevention patient) or by having an underlying high-risk cardiac condition known to pre-dispose to VF (primary prevention patient). The epidemiology of SCA differs significantly in the athletic population compared with the general population, but the indications for ICD implant are the same in all patient groups (4). Significant outcome data demonstrating the value of the ICD in prolonging life in high-risk populations has been established (5-10). However, outcomes that have been obtained in the general population through studies and registry data may not necessarily apply to the athletic population because of the unknown reliability of the device under the conditions of sports participation. Further study is necessary to determine outcomes in the latter group. Here we discuss the issues surrounding ICDs in athletes: the definition of sudden death, SCA, and VF; the epidemiology of sudden death in the general population and in athletes; methods of defibrillation and how they differ from one another; the ICD system, implant technique, and indications for implantation; issues surrounding safety and efficacy of ICDs in athletes; return-to-play considerations; preliminary safety and efficacy data obtained from survey data of those who care for athletes with ICDs; and rationale for the recently launched ICD Sports Registry.
DEFINITION OF SUDDEN DEATH, SUDDEN CARDIAC ARREST, AND VENTRICULAR FIBRILLATION
Sudden death in both the general population and in athletes can occur because of a variety of conditions, including trauma, heat illness, asphyxiation, drowning, or SCA (11-18). The most frequent cause in atheletes is SCA caused by specific rhythm disturbances known as ventricular tachyarrhythmias, especially ventricular fibrillation (VP) caused by previously unsuspected underlying heart disease (11,12). The term "sudden death," when applied to an episode of SCA caused by VF, is probably somewhat of a misnomer in the modern era of automatic external defibrillators (AEDs) and ICDs. Instances of what used to be true "sudden death" caused by VF, with previously no hope of recovery, can now be treated successfully with prompt defibrillation applied either externally (AED) or internally (ICD). If such treatment is successful, it is possible to restore the victim to a stable rhythm and hemodynamics, but it is crucial to deliver the defibrillation shock as soon as possible. The earlier the rhythm can be treated with defibrillation, the higher the survival rate from such events (19-21).
EPIDEMIOLOGY OF SUDDEN DEATH AND SCA IN THE GENERAL POPULATION AND IN ATHLETES
In the general population of the United States, SCA occurs at a rate of 450,000 per year, far exceeding the incidence of stroke, lung cancer, breast cancer, or AIDS (13-18). In fact, SCA claims more than any of those other diseases combined. This figure amounts to 1,200 events per day, 50 per hour, or 1 every 80 seconds, with the majority of these episodes occurring in individuals with clinically recognized heart disease, particularly previous myocardial infarction or congestive heart failure (16,17). In the general population, 80% of the SCA events are caused by coronary artery disease, while another 15% are caused by primary cardiomyopathies. In the remaining 5%, SCAs are caused by various other conditions, channelopathies, valvular, and congenital heart disease (17).
The epidemiology of sudden death caused by SCA events in children, adolescents, and young athletes differs significantly from that of the general population. In the pediatric and adolescent population, SCA events occur at a rate of 7,000-15,000 per year (18), whereas in athletes, "sudden death" due to SCA occurs approximately 150-200 times per year, or 1 in 200,000 athletes (22). Athletes under the age of 35 yr are more prone to undetected myocardial disease, whereas athletes over age 35 are more prone to atherosclerotic coronary artery disease as the underlying cause of the sudden death or SCA episode. According to registry data of young athletes in the United States (11), of 387 athletes who suffered from sudden death, the most common cause is still hypertrophic cardiomyopathy, which accounts for 26% of the sudden deaths. However, commotio cordis (sudden death caused by VF due to a sudden blow delivered during the vulnerable period of the cardiac cycle), now accounts for 19% of the episodes, and anomalous coronary artery for 14% of the episodes. The remainder of cases in athletes are due to non-specific left ventricular hypertrophy, myocarditis, ruptured aortic aneurysms, right ventricular dysplasia, tunneled coronary arteries, aortic stenosis, coronary artery disease, myxomatous mitral valve disease, dilated cardiomyopathy, long QT syndrome, trauma, drug abuse, asthma, and heat illness.
It has been shown that athletes with underlying heart disease are 2.5 times more likely to have an episode of SCA during practice or competition compared with non-athletes with heart disease who are not actively engaging in vigorous sports (23). The preponderance of SCA events occurring during practice or competition has been attributed to enhanced cardiac irritability and exacerbation of ventricular arrhythmias under the conditions of catecholamine excess, or under the severe hemodynamic and/or metabolic stresses known to occur with intense athletics (1,22,23).
METHODS OF DEFIBRILLATION AND HOW THEY DIFFER FROM ONE ANOTHER
The most successful treatment for VF is prompt defibrillation, with rates of successful termination of the rhythm disturbance varying according to time between the onset of VF and application of the defibrillation shock (19). If the shock is applied within the first 30 sec, there is an approximate 90% chance of successful resuscitation from the VF event. However, success declines by 7%-10% each minute that time elapses, and there is a less than 10% chance of successful defibrillation after 10 min. The ability to deliver the shock quickly will vary according to the type of defibrillator applied. Results of external defibrillation are in the 5%-65% range for manual or automated external defibrillators (20,21). However, based upon their internal position, ICDs are able to interpret the cardiac rhythm and deliver the shock the quickest of all the devices, with success rates of defibrillation on the order of 95%-99% (24,25).
THE ICD SYSTEM, IMPLANT TECHNIQUE, AND INDICATIONS FOR IMPLANTATION
The ICD system has two components: the lead system and a mini-computer powered by a battery, all sealed in a titanium case (Fig. 1). ICD leads are flexible insulated wires with electrode tips. The electrode and conductive wire are typically manufactured of nickel or cadmium, and the insulation materials from silicone or polyurethane. Most contemporary ICDs use transvenous leads, but previously, ICDs most often used epicardial lead systems. Subcutaneous lead systems are currently under investigation. They are much easier to implant and avoid some of the complications associated with transvenous systems (26). Preliminary data indicate that these ICD systems are effective, but they appear to require twice as much energy to defibrillate, and efficacy has not yet been established (26).
To know if, when, and what type of therapy might be needed, the ICD constantly monitors or senses the cardiac rhythm, and logic circuitry determines whether defibrillation should be applied. The ability of the ICD to analyze rhythms and appropriately detect arrhythmias is called discrimination and is accomplished through the use of advanced software formulas called algorithms. The ICD case is made of titanium, a strong metal used to manufacture rockets and satellites, which is 10 times as strong as steel, but much lighter. The case is small (less than 35 cc in volume), lightweight (about 4-5 oz), and less than 2 inches wide and 0.5 inches thin.
During ICD implant, a small cutaneous incision is made in the upper chest, and the ICD leads are inserted into the subclavian vein and threaded into the heart. The ICD case is placed subcutaneously into the ICD "pocket" and connected to the leads. The defibrillation threshold (DFT), or the amount of energy necessary to successfully defibrillate the heart, is tested by inducing VF and waiting while the device detects, charges, and delivers the shock. The entire process of detection, charging, and delivery of the shock should require less than 20 sec. If the detection times and thresholds are acceptable, the incision is closed. As battery size has decreased over the years, newer models have allowed for small inconspicuous incisions and use in infants and children. Intracardiac electrograms are continually monitored via the lead system and can be stored in the mini-computer located in the ICD device for future downloading during a clinic visit. If VF is detected via the detection algorithm, a defibrillation shock can be applied within 8-15 sec in most cases. Internal shocks typically vary between 20-30 J.
Indications for ICD implantation can be classified according to whether the patient or athlete had a prior episode of VF from which he or she was successfully resuscitated (secondary prevention indication) or whether the patient or athlete is known to have an underlying cardiac condition known to be high risk for an episode of VF (primary prevention indication). Although there are no substantial data in athletic populations, research has shown that ICDs have improved survival in many of the conditions known to cause SCA in athletes. In hypertrophic cardiomyopathy (HCM), registry data in more than 500 patients with HCM has shown that the rate of ICD shocks for ventricular tachyarrhythmias (VF or ventricular tachycardia) was 10.6% per year for secondary prevention after SCA and 3.6% per year for primary prevention (9). Features of high risk in a primary prevention patient were defined as family history of sudden death, massive left ventricular hypertrophy, nonsustained ventricular tachycardia on Holter monitoring, and unexplained prior syncope (9). The likelihood of appropriate ICD discharge was similar whether patients had one, two, or three or more risk factors. The only death reported over the 3.7-yr follow-up period was arrhythmia in the setting of an ICD malfunction. Inappropriate ICD shocks occurred in 136 patients (27%). The authors concluded that in a high-risk HCM cohort, ICD interventions for life-threatening ventricular tachyarrhythmias were frequent but highly effective in restoring normal rhythm. Similar success with the ICD has been reported for other conditions that may cause sudden death in athletes, specifically long QT syndrome (10) and dilated cardiomyopathies (6,27). As athletes may have at least a 2.5 times higher risk of having an SCA event (23), the HCM registry data would suggest that the intervention rate for ventricular tachyarrhythmias might be as high as 25% for a secondary prevention patient and 10% for a primary prevention patient. Thus, one would expect a higher rate of ICD shocks in HCM athletes.
ISSUES SURROUNDING SAFETY AND EFFICACY OF ICDS IN ATHLETES AND RETURN-TO-PLAY CONSIDERATIONS
Because of the overwhelming success of the ICD in terminating VF quickly and successfully in high-risk populations, it is tempting to extrapolate such outcome data to the athletic population and allow sports participation in athletes who have undergone ICD implant for an underlying high-risk condition, such as HCM or long QT syndrome. However, the success of the ICD in the HCM registry data and in other conditions known to cause SCA in athletes cannot necessarily be assumed to be true for the athletic population. Thus, the 36th Bethesda Guidelines are very clear in that participation is not allowed in sports if one has had implantation of an ICD, regardless of the underlying condition (1). Several issues unique to athletes surround the safety and efficacy of ICDs in athletes, thereby impacting return-to-play considerations (Table 1).
Exercise exacerbates ventricular and supraventricular arrhythmias in multiple disorders (28,29), and in ICD patients (30,31), a phenomena most likely related to enhanced sympathetic tone, and elevated levels of circulating catecholamines. Detection algorithms are not perfect in their ability to discern ventricular rhythms from supraventricular rhythms. Thus, the exercising individual may experience a higher frequency of both appropriate and inappropriate ICD shocks. They can occur quite unexpectedly, causing a great degree of distress to the patient or athlete, with resultant decreased quality of life (32).
If appropriate ICD shocks do occur in the event of an appropriate VF or ventricular tachycardia episode while exercising, it is possible that the ICD shock may fail to convert a life-threatening arrhythmia. Shock failure may be due to any one of a number of reasons, including catecholamines, subendocardial ischemia, acute diffuse left ventricular dysfunction/dilation or stunning, markedly increased extracellular potassium, presence of toxins such as cocaine, ephedra, or alcohol, and upright posture while exercising. All of these have been shown to be either experimentally or clinically relevant (33-40).
The efficacy of the ICD during exercise is unknown, but these data suggest that arrhythmias during high catecholamine states may be harder to terminate, suggested by studies of epinephrine infusion during defibrillation testing (33), of circadian variation (34,35), and of laboratory-induced mental stress (36). For instance, in human subjects with implanted ICDs, intravenous infusion of epinephrine has been shown to significantly increase the amount of energy necessary to defibrillate. Baseline shocks of 25 J were successful 16 out of 16 times, but during epinephrine infusion this rate decreased by 25% (33).
Programmed energy levels, as determined by DFT testing at implant, may not be successful in terminating the rhythm disturbance, especially in the presence of confounding factors other than the catecholamines. Ischemia increases the DFT (37) and postshock re-initiation of VF (38). Prolonged endurance exercise has been associated with release of cardiac troponin and left ventricular dysfunction, suggestive of left ventricular stunning or ischemia (39,40). The chronic fibrosis that appears in hypertrophic cardiomyopathy is felt to be caused by repeated bouts of micro-ischemia (41). Because ischemia and left ventricular dysfunction are known to be associated with higher DFTs, this also may play a potential role in the failure of the ICD to defibrillate an athlete.
Intense exercise can markedly increase extracellular potassium, as high as twice the baseline level (42). Hyperkalemia not only enhances myocardial irritability, but it is known to diminish the ability of an ICD to terminate the rhythm (38,43). Some athletes may be taking toxins or supplements. Cocaine is known to be associated with higher DFTs (44), increasing the likelihood of failure to defibrillate in the clinical setting. The same is probably true for ephedra and other related compounds. Upright position has been reported to increase the DFT (45). As most sports are played in the upright position, this also may be a factor in failure of the shock to successfully terminate the rhythm disturbance.
The ICD leads are introduced in the narrow space between the clavicle and the first rib during the implant procedure. The lead is vulnerable to insulation and conductive element fractures, due to crushing of the lead by the bony structures. This vulnerability is likely to be more pronounced during sports or conditioning activities that require repetitive motion such as weightlifting. If such fractures occur in between clinic visits, the athlete may be at risk for failure of the ICD to successfully terminate the rhythm. The leads, device casing, battery, and logic circuitry were not designed to withstand the rigors of contact sports. Thus, failure of one of these components due to direct trauma also is a possibility. If an athlete sustains VF or receives a shock during practice or competition, there may be risk of harm due to momentary loss of consciousness or loss of body control. This would be of particular concern in the case of the athlete who is playing a contact sport. Finally, as the Bethesda Guidelines formed the basis of the 1996 decision of the court not to allow a basketball athlete to play with an ICD implanted, an important precedent was established regarding return to play for athletes with implanted ICDs (46,47). The guidelines are clear in stating "no play" with an ICD in place. Therefore, if an athlete does participate and the device fails for some reason, or if there is bodily injury sustained, there may be a liability issue. Until there are detailed outcome data on the safety and efficacy of ICD therapy in the athletic population, the true risk:benefit ratio is unknown.
PRELIMINARY SAFETY AND EFFICACY DATA OBTAINED FROM SURVEY DATA OF THOSE WHO CARE FOR ATHLETES WITH ICDs AND RATIONALE FOR THE RECENTLY LAUNCHED ICD SPORTS SAFETY REGISTRY
Several small series do report successful ICD conversions during exercise. Among a small group of patients with HCM, all appropriate shocks during competitive or vigorous activity were successful (48). In another study in a group of 23 actively exercising patients with ICDs who experienced 36 appropriate ICD shocks during vigorous activity, no shock failures or adverse events occurred (49). However, it is unlikely that the ICD patients reported in these series exercised or trained to the degree that an elite athlete would. Two recent surveys have attempted to gather information on those athletes who have been participating with ICDs (2,3).
In a 2006 survey of Heart Rhythm Society (HRS) members, recommendations by physicians to patients with ICDs regarding participation in sports varied widely, and most respondents individualized recommendations. Few respondents (10%) counseled patients with ICDs to avoid all activities more vigorous than golf or bowling, but most did, however, recommend against contact sports (76%). Some advised against competitive sports (45%) or sports with a particular risk of injury (35%), including those involving heights, such as rock climbing or bungee jumping. Many physicians individualized recommendations based on underlying cardiac disease (71%). While there was consensus among many physicians that hypertrophic cardiomyopathy, congestive heart failure, and ischemic disease should limit activity, opinions differed regarding how long QT syndrome and Brugada syndrome should affect sports participation. Some respondents lifted at least some restrictions after an arrhythmia-free period, most frequently 6 months or 1 yr.
Sports participation by patients with ICDs appears to be common. Overall, 70% of the HRS physicians report that patients in their practice engage in some form of sporting activity, with basketball, running, and skiing being the most commonly reported. Forty percent of the respondents report that patients had received ICD shocks during sports participation. Most commonly reported sports during which shocks occurred are running and basketball. While ICD shocks during sports were not uncommon, adverse outcomes of the arrhythmias and/or shocks received during sports were rare (Table 2). Overall, 1% of the physicians reported known injury to patient, 5% reported injury to the ICD system, and <1% reported failure of shocks to terminate the arrhythmia. The most common adverse events reported were lead fracture or lead dislodgement attributed to repetitive-motion activities, most commonly weightlifting and golf. Of nine specific patient injuries described, six were minor. Major injuries included two head injuries due to falls, one during running, and one on a treadmill. A neck injury occurred during hunting. Two deaths were reported. One occurred due to the head injury on a treadmill, and no details were given of the other. More than 70% of the HRS members felt that the guidelines should not be so restrictive.
A similar study was conducted among members of the American Medical Society for Sports Medicine (AMSSM). This society comprises specialists in sports medicine, who often serve as team physicians for sports teams at the high school, collegiate, Olympic, and professional level. This study differs from the one conducted in the HRS members in that numbers of athletes rather than numbers of physicians were used as the denominator in the statistical analysis. Despite this difference, the results were remarkably similar. Forty-three percent of the membership responded, and of the respondents, 17.1% had cared for 81 athletes with ICDs. Of the athletes with ICDs, 65.4% were allowed to participate in sports, and 30% had received a shock at some point during their athletic career (Fig. 2). These figures are very similar to what was observed among the HRS members. Overall adverse event rate was 13.2%, but of the shocked athletes, 43.8% experienced some type of adverse event due to the shock, such as failure of the shock to defibrillate (athlete survived), injury to the device, or injury to the athlete. Injury to the device included two lead fractures and one other nonspecified device injury, while injury to the athlete included abdominal laceration and two non-specified injuries. Although a lower figure than reported by the HRS respondents, 36% of the members of the AMSSM felt that the guidelines should be liberalized.
To further define the safety and efficacy of ICDs in the athletic population, the National ICD Sports Registry was launched. Any athlete or active individual with an ICD can be enrolled by contacting the coordinating center at Yale or any of the 30 participating centers (50). Data generated in this study will include appropriateness of ICD shocks, efficacy of such shocks, and any adverse events related to ICD shocks.
In summary, instances of SCA in athletes with known high risk underlying heart disease can be treated with implantation of an ICD. Although the Bethesda Guidelines state that the athletic population should not be participating in sports, because of concerns over safety and efficacy, preliminary survey data indicate that both the HRS membership (implanting electrophysiologists) and the team physicians (AMSSM membership) are recommending continuation in athletic activities in approximately 70% of athletes and patients with implanted ICDs. There appears to be a 30%-40% incidence of ICD shocks in the individual athlete who participates in sports, a figure somewhat higher than that seen in a non-athletic population. An ongoing national ICD Sports Registry will provide valuable information as to the safety and efficacy of ICDs in the athletic population.
1. Maron, B.J., and D.P. Zipes. 36th
Bethesda Conference: Eligibility Recommendations for Competitive Athletes with Cardiovascular Abnormalities. JACC
. 4:51-64, 2005.
2. Lampert, R., D. Cannom, and B. Olshansky. Safety of sports participation in patients with implantable cardioverter defibrillators: A survey of Heart Rhythm Society members. J. Cardiovasc.
3. Lawless, C.E., R. Lampert, B. Olshansky, and D. Cannom. Safety and efficacy of implantable defibrillators and automatic external defibrillators in athletes: Results of a nationwide survey among AMSSM members. Presented at the 2005 Annual Meeting of the American Medical Society for Sports Medicine. Austin TX.
4. Gregoratos, G., J. Abrams, A.E. Epstein, et al
. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: Summary article: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). Circulation
5. Ezekowitz, J.A., P.W. Armstrong, and F.A. McAlister. Implantable cardioverter defibrillators in primary and secondary prevention: A systematic review of randomized, controlled trials. Ann. Int. Med
. 138:445-452, 2003.
6. Bardy, G.H., K.L. Lee, D.B. Mark, et al
. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl. J. Med.
7. You, J.J., A. Woo, D.T. Ko, et al
. Life expectancy gains and cost-effectiveness of implantable cardioverter/defibrillators for the primary prevention of sudden cardiac death in patients with hypertrophic cardiomyopathy. Am. Heart J.
8. Maron, B.J., W.K. Shen, M.S. Link, et al
. Efficacy of implantable cardioverter-defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy. New Engl. J. Med.
9. Maron, B.J., P. Spirito, W.K. Shen, et al
. Implantable cardioverter-defibrillators and prevention of sudden cardiac death in hypertrophic cardiomyopathy. JAMA.
10. Wojciech, Z., A. Moss, J. Daubert, et al
. Implantable cardioverter defibrillator in high-risk long QT syndrome patients. J. Cardiovasc. Electrophysiol.
11. Maron, B.J., J. Shirani, and L.C. Poliac, et al.
Sudden death in young competitive athletes. Clinical, demographics, and pathological profiles. JAMA.
12. Maron, B.J. Medical progress: Sudden death in young athletes. New Engl. J. Med.
13. 2002 Heart and Stroke Statistical Update, American Heart Association.
14. U.S. Census Bureau, Statistical Abstract of the United States, 2001.
15. American Cancer Society. Surveillance Research, Cancer Facts and Figures 2001.
16. Zheng, Z., J.B. Croft, W. Giles, and G. Mensah. Sudden cardiac death in the United States, 1989 to 1998. Circulation.
17. Myerburg, R.J., and A. Castellanos. Cardiac arrest and sudden cardiac death. In: Heart Disease, A Textbook of Cardiovascular Medicine
, 6th ed. E. Braunwald, D.P. Zipes, and P. Libby (Eds.). W.B. Saunders, 2001.
18. Schindler, M.B., D. Bohn, P.N. Cox, et al
. Outcome of out-of-hospital cardiac or respiratory arrest in children. New Engl. J. Med.
19. Cummins, R.O. From concept to standard-of-care. Review of the clinical experience with automated external defibrillators. Ann. Emerg. Med.
20. Marenco, J.P., P.J. Wang, M.S. Link, et al
. Improving survival from sudden cardiac arrest: the role of the automated external defibrillator. JAMA.
21. Valenzuela, T.D., D.J. Roe, G. Nichol, et al
. Outcomes of rapid defibrillation by security officers after cardiac arrest in casinos. New Engl. J. Med.
22. Maron, B.J., and A. Pelliccia. The heart of trained athletes: Cardiac remodeling and the risks of sports, including sudden death. Circulation.
23. Corrado, D., C. Basso, M. Schiavon, et al
. Does sports activity enhance the risk of sudden cardiac death? J. Cardio. Med.
24. Goldberger, Z., and R. Lampert. Implantable cardioverter-defibrillators: Expanding indications and technologies. JAMA.
25. Anderson, K.P. Sudden cardiac death unresponsive to implantable defibrillator therapy: An urgent target for clinicians, industry and government. J. Interv. Card. Electrophysiol.
26. Parsonnet, V., A. Berstein, and D. Neglia. Nonthoracotomy ICD implantation: Lessons to be learned from permanent pacemaker implantation. Pacing Clin. Electrophysiol.
27. Bansch, D., M. Antz, S. Boczor, et al
. Primary prevention of sudden cardiac death in idiopathic dilated cardiomyopathy: The cardiomyopathy trial (CAT). Circulation.
28. Albert, C.M., M.A. Mittleman, C.U. Chae, et al
. Triggering of sudden death from cardiac causes by vigorous exertion. New Engl. J. Med.
29. Lampert, R., T. Joska, M.M. Burg, et al
. Emotional and physical precipitants of ventricular arrhythmia. Circulation.
30. Pires, L.A., M.H. Lehmann, R.T. Steinman, et al
. Sudden death in implantable cardioverter-defibrillator recipients: Clinical context, arrhythmic events and device responses. J. Am. Coll. Cardiol.
31. Papaioannou, G.I., and J. Klugar. Ineffective ICD therapy due to excessive alcohol and exercise. Pacing ClinElectrophysiol.
32. Schron, E.B., D.V. Exner, Q. Yao, et al
. Quality of life in the antiarrhythmics versus implantable defibrillators. Circulation.
33. Sousa, J., W. Kou, H. Calkins, et al
. Effect of epinephrine on the efficacy of the internal cardioverter-defibrillator. Am. J. Cardiol.
34. Kong, T.Q., J.J. Goldberger, M. Parker, et al
. Circadian variation in human ventricular refractoriness. Circulation.
35. Venditti, F.J., R.M. John, M.L. Hull, et al
. Circadian variation in defibrillation energy requirements. Circulation.
36. Lampert, R., D. Jain, M.M. Burg, et al
. Destabilizing effects of mental stress on ventricular arrhythmias in patients with implantable cardioverter-defibrillators. Circulation.
37. Qin, H., G.P. Walcott, C.R. Killingsworth, et al
. Impact of myocardial ischemia and reperfusion on ventricular defibrillation patterns, energy requirements, and detection of recovery. Circulation.
38. Swerdlow, C.D., A.M. Russo, and P.J. Degroot. The dilemma of ICD implant testing. Pacing Clin. Electrophysiol.
39. Middleton, N., R. Shave, K. George, et al
. Left ventricular function immediately following prolonged exercise: A meta-analysis. Med. Sci. Sport Exerc.
40. Shave, R.E., G.P. Whyte, K. George, et al
. Prolonged exercise should be considered alongside typical symptoms of acute myocardial infarction when evaluating increases in cardiac troponin T. Heart.
41. Maron, B.J. Hypertrophic cardiomyopathy: A systematic review. JAMA
42. Sejerstad, O.M., and G. Sjogaard. Dynamics and consequences of potassium shifts in skeletal muscle and heart during exercise. Physiol. Rev.
43. Sims, J.J., A.W. Miller, and M.R. Ujhelyi. Regional hyperkalemia increases ventricular defibrillation energy requirements: Role of electrical heterogeneity in defibrillation. J. Cardiovasc. Electrophysiol.
44. Chen, J., R. Haris Naseem, O. Obel, and J.A. Joglar. Habitual cocaine use is associated with high defibrillation threshold during ICD implantation. J. Cardiovasc. Electrophysiol.
45. Schauerte, P., D. Bjorn, K. Ziegert, et al
. Influence of body position on defibrillation thresholds of nonthoracotomy implantable defibrillators: A prospective randomized evaluation. J. Cardiovasc. Electrophysiol.
46. Maron, B.J., M.J. Mitten, E.F. Quandt, and D.P. Zipes. Competitive athletes with cardiovascular disease-The case of Nicholas Knapp. New Engl. J. Med.
47. Mitten, M.J., B.J. Maron, and D.P. Zipes. Task force 12: Legal aspects of the 36th Bethesda Conference recommendations. J. Am. Coll. Cardiol.
48. Begley, D.A., S.A. Mohiddin, D. Tripodi, et al
. Efficacy of implantable cardioverter-defibrillator therapy for primary and secondary prevention of sudden cardiac death in hypertrophic cardiomyopathy. Pacing Clin. Electrophysiol.
49. Davids, J.S., C.A. McPherson, C. Earley, et al
. Benefits of cardiac rehabilitation in patients with implantable cardioverter-defibrillators: A patient survey. Arch. Phys. Rehabil.