In the past 15 years there has been an increase in the options available for treating patients with malignant ventricular arrhythmias (MVA). While there are still nearly 300,000 episodes of sudden cardiac death secondary to MVA each year, 20%-30% of the patients now survive the acute event (21). In addition, there are about 100,000 patients with recurrent ventricular tachycardia or with syncope of unknown etiology (21). The technological, surgical, and pharmacologic advances of the past 15 yr have yielded a group of about a quarter of a million patients surviving with MVA. This improved treatment of malignant ventricular arrhythmias has also produced an increasing number of MVA patients who may require exercise testing or cardiac rehabilitation.
Patients who have survived an episode of sudden cardiac death, however, are a high risk group for two reasons. First, the annual recurrence rate is about 30%-40% (3,6,19). Second, a substantial number of these individuals have severely depressed ventricular function(10,15, Cardiac Pacemakers, Inc., (CPI) St. Paul, MN, unpublished statistics). Since their risk for cardiac arrest during exercise is substantial (27), exercise testing and training has been contraindicated in many centers. Recent experience(2,7,8,15,16,17,29,32,34), however, has indicated that exercise can be used safely and effectively in the evaluation and management of selected patients with MVA. This paper is a review of that experience and also presents some guidelines for exercise testing and training of this high risk population.
Exercise can produce a potentially arrhythmogenic condition and, therefore, may be useful in the evaluation and treatment of patients with cardiac arrhythmias. Candinas and Podrid (4) have suggested a number of mechanisms through which exercise creates an arrhythmogenic environment. These mechanisms are summarized in Figure 1. In addition to a decrease in vagal tone, the central features of these mechanisms are augmented sympathetic neural activity and an increase in circulating catecholamines during exercise. Such changes may contribute to arrhythmogenesis through one of three mechanisms.
First, stimulation of sympathetic neural activity and catecholamines increases the rate of spontaneous depolarization from ectopic foci. These responses to exercise enhance membrane automaticity and make arrhythmias more likely. A second mechanism for exercise-induced arrhythmogenesis is through triggered automaticity from delayed after-potentials. If a triggered after-potential can reach threshold, an action potential can occur. If this can become repetitive, it may set up an arrhythmia. Increases in catecholamines and sympathetic neural stimulation resulting from exercise enhances calcium influx into the cell and can thus increase after-potential amplitude. A final mechanism is via reentry. The differences of conduction and refractory properties of myocardial tissues that are adjacent to each other create an environment that is favorable to the development of arrhythmias. An appropriately timed stimulus can create a circuit and set up an arrhythmia. Through stimulation of the sympathetic nervous system and enhanced catecholamine drive from exercise, the electrophysiologic properties of the myocardium may be altered. Specifically, conduction velocity can be increased while refractory periods can be shortened in myocardial tissues.
In addition to neural/hormonal changes, exercise alters cardiac physiology through metabolic changes in the cell. Specifically, changes in blood electrolytes (hypokalemia) and decreases in cellular pH may contribute to exercise-induced ventricular tachycardia (VT). Figure 2 shows one of the metabolic changes that takes place in response to exercise. The graph depicts the blood lactate, as well as the heart rate, response to progressive exercise in a patient with a history of recurrent exercise-induced ventricular tachycardia. Figure 2 demonstrates that the onset of blood lactate accumulation (OBLA) occurred at a heart rate of 115 beats·min-1 in this patient. It is noteworthy that the patient had a brief self-terminating run of VT at peak exercise during this procedure. These data were collected after he had had an episode of ventricular tachycardia while warming up to exercise at a health club. The arrhythmia at the health club had required a defibrillatory shock from the patient's automatic implantable cardioverter-defibrillator.
When this patient's “warm-up” was reproduced in the laboratory(Table 1), his heart rate was 117 beats·min-1 during the first minute of activity and increased to a peak of 147 beats·min-1 by the end of warm-up. It is clear from Table 1 that virtually all of his activity at the health club was being performed during a period of lactate acidosis. While the exact mechanism for the arrhythmic event is unclear, it is possible that the accumulation of lactic acid may have contributed to a metabolic environment that was potentially arrhythmogenic (in this patient without overt cardiac abnormalities).
Additional mechanisms through which exercise may be arrhythmogenic are also included in Figure 1. Exercise can contribute to the development of cardiac arrhythmias through ischemic mechanisms secondary to the increase in myocardial oxygen demand required by exercise. Finally, myocardial stretch and contraction abnormalities might also play contributing roles (4).
Exercise testing produces a period of increased risk for the patient. It can play a key role in evaluating high risk cardiac patients. Information(such as the heart rate at the onset of a ventricular arrhythmia, peak heart rate response to exercise, the effectiveness of pharmacologic interventions, AICD function, evaluation of AICD discharges, exercise prescription, etc.) can be generated during an exercise test. The clinical usefulness of this information in the diagnosis and management of the patient, however, must be balanced against the risk of untoward cardiac events that may occur during the test. Several investigators have evaluated this risk. The results of six of these studies are summarized in Table 2. The risk of serious complications is no higher than 4%.
Two studies are particularly noteworthy. Young's group(34) evaluated 1377 exercise tests performed on 263 high risk ventricular arrhythmia patients. Only 2.3% of the tests yielded emergent complications, and 1.2% of the tests required electrical cardioversion. The most recent investigation, by Allen and coworkers (2) reports the experience of exercise testing 64 consecutive patients with a history of ventricular fibrillation or hemodynamically significant ventricular tachycardia. Eight percent of these tests produced sustained ventricular tachycardia. There were, however, no significant complications. The typical endpoints in the exercise tests were fatigue or dyspnea, with over 90% of the tests being terminated for one of these routine endpoints.
Exercise Testing Considerations
When exercise testing patients with MVA, significant attention should be paid to emergency procedures for the exercise laboratory. The procedures must be written, practiced regularly, reviewed, and modified as necessary. It is noteworthy that Young et al. (34) successfully resuscitated all 32 events in their 1377 tests. There were no deaths, myocardial infarctions, strokes, or any lasting morbid events. Unfortunately, neither the study by Young et al. (34) nor Allen et al.'s (2) investigation identified variables that were well correlated with and predictive of the occurrence of ventricular tachycardia during an exercise test. The only helpful association was a history of ventricular tachycardia during a previous exercise test. Twenty percent of Young et al.'s patients who developed an exercise-induced arrhythmia had had a prior arrhythmia during vigorous activity. Less predictive was the fact that Allen's group found that patients who did not have VT on ambulatory monitoring were unlikely to have it during a graded exercise test.
A useful approach to providing a safe test environment for MVA patients is anticipation of the test endpoint. This involves considering the questions that the test is intended to answer. It is then possible to identify what must occur during the test in order to answer these questions. When these points are considered before the test begins, the probable endpoint of the test can be predicted based on the underlying arrhythmia substrate and/or the therapy being used to treat the arrhythmia. This approach is applied to several patient subgroups below and summarized in Table 3.
Patients with cardiomyopathies and chronic heart failure typically have very limited exercise tolerance. Low level exercise protocols (e.g., modified Naughton or a slow speed modification of the Balke protocol) are recommended for this subgroup. The stages should be short (1-2 min in duration) and the increments between stages small (0.5-1 MET). The total exercise time will usually be short. These patients are often limited by peripheral muscle weakness as opposed to cardiorespiratory limitations. Consequently, the tests are often terminated by leg fatigue at low heart rates. Some patients with cardiomyopathies may even exhibit chronotropic incompetence. On the other hand, there are individuals in this category with high resting heart rates who become quite tachycardiac with even minimal exercise. In general, this group can be anticipated to have poor exercise tolerance and the test will be fairly brief in duration.
Some young patients with exercise-induced ventricular tachycardia have good exercise tolerance. This is a group that needs to be dealt with cautiously. They generally respond to exercise in ways that are analogous to those of the healthy normal population. The transition into ventricular tachycardia (VT), however, can be quite sudden. When exercise testing a patient with a history of VT related to exercise, caution should be used as the patient's heart rate increases. Since the onset of the arrhythmia is usually unpredictable, care must be taken when these patients approach or exceed 85% of their age-predicted maximum heart rate.
In some MVA patients ischemia may be the underlying substrate. Patients with a history of sudden cardiac death who show signs or symptoms of ischemia during exercise testing should not be pushed to 2-3 mm of ST segment depression. Also, exercise testing personnel should be made aware of the heart rate suppression properties of many antiarrhythmic medications. Very few of the patients on medications for malignant ventricular arrhythmias will achieve an age predicted maximum heart rate.
AUTOMATIC IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR (AICD)
A final area of consideration in exercise testing MVA patients involves those who have an AICD™. The device has proven to be extremely effective, nearly eliminating sudden cardiac death in the patients who receive it. A 5-yr follow-up of patients with malignant ventricular arrhythmias treated with the AICD indicated only about 4% had died suddenly(33). By comparison, Waller et al.(31) found only about 30% of patients who failed to respond to pharmacologic treatment of their MVA to be without sudden death during a 4-yr follow-up period.
The AICD has proven so effective in treating sudden death that its use has become widespread. Since 1985, when the device was approved by the FDA, the number of implants has increased in a virtually exponential fashion. In 1990 and 1991 more than 12,000 devices were implanted. By comparison, the first 10,000 implants were done during the 10-yr period between 1980 and 1990(Cardiac Pacemakers, Inc. (CPI), St. Paul, MN, unpublished statistics). With such rapid growth, most exercise laboratories can expect to perform an exercise test on a patient with one. It is essential that exercise laboratory staff have a strong background in the AICD's design and function. It is equally important that they understand the medical status of the patients who are treated with it and the special considerations required for testing them.
Exercise Testing Considerations
There are a number of considerations when exercise testing patients with implantable defibrillators (29). Of primary importance is protecting the patient from inappropriate shocks during exercise-induced sinus tachycardia. The staff must be aware of the device's heart rate cut-off point or points (i.e., the peak heart rate that the device will tolerate before it shocks the patient). They must also be aware of the sequence of therapies (anti-tachycardia pacing or shocks) that the device is programmed for. In addition to the regular exercise test staff, there must be one individual with specialized training in the care of patients with the AICD. This person is designated to divert clinically inappropriate shocks and deactivate the AICD when it begins to charge inappropriately (i.e., when the patient is not experiencing a ventricular tachyarrhythmia).
Several techniques can be utilized to protect the patient from inappropriate shocks. The choice is somewhat dependent upon the purpose of the test and the type of device that the patient has. Second generation AICD offer two choices. The device may be inactivated and external rescue (i.e., with a defibrillator) can be employed if the patient develops a malignant arrhythmia. Alternatively, the AICD may be left in its activated state and then monitored for inappropriate charging. This approach is useful when assessing the appropriateness of AICD discharges in patients who have recently been shocked by their defibrillator.
This approach uses a device called an AIDCHECK that monitors defibrillator charging activity. The AIDCHECK probe can be taped over the defibrillator on the surface of the patient's abdomen. If the AICD begins to charge, the display on the AIDCHECK will show the accumulation of time in the device's charge cycle. In addition to this advance of the charge time digits, the AIDCHECK will emit a constant tone. When the AICD begins to charge, the individual monitoring the device should then check the patient's rhythm. If the AICD is charging inappropriately (e.g., in response to sinus tachycardia), the shock can be diverted by using a donut magnet. This will deliver the AICD's energy pulse into its internal test load rather than through the leads to the patient. This is done by placing the magnet over the upper right hand corner of the AICD for 2-3 s. The magnet is then removed.
Most third-generation implantable cardiovertor-defibrillators offer another alternative since their activity can be inhibited by the magnet. The donut magnet is taped over the device during the exercise test. The patient's rhythm is monitored by the designated individual and if a malignant arrhythmia develops, the magnet can be rapidly removed. This allows the device to resume its normal monitoring and defibrillating functions. The patient is protected from inappropriate shocks while the magnet is in place over the device and also protected from a ventricular arrhythmia when the magnet is removed. It is possible to rapidly reprogram some third generation devices. This allows the test to be conducted with the device functioning according to its usual parameters. If it is necessary to increase the heart rate cut-off point during the test (in response to sinus tachycardia), this can be done quite quickly and easily.
Finally, the simplest alternative is to terminate the test as the patient approaches the device's heart rate cut-off point. This may be done with any implantable cardiovertor-defibrillator. The obvious limitation of this approach is that the information that the test was supposed to supply may be truncated by a premature endpoint.
It should be clear that exercise testing patients with the AICD requires appropriate equipment and personnel with the specialized training required to operate it.
INPATIENT EXERCISE TRAINING
The Medical College of Wisconsin participated in the clinical trials of a number of then-investigational antiarrhythmic agents and the original implantable defibrillator. A substantial amount of experience exercise training patients with malignant ventricular arrhythmias accrued as a result of these trials. The process was begun with inpatients in 1981. By 1988, 135 patients who had been hospitalized for evaluation and treatment of MVA had become involved in an inpatient exercise training program(15). During that time over 1200 patient-hours of experience exercising this population was gained.
These inpatients with malignant ventricular arrhythmias were referred to this exercise program for several reasons. The physical activity was useful in minimizing deconditioning secondary to the prolonged hospitalization. Owing to the rigid time schedules of clinical trials, several patients were hospitalized for 3-6 months. Such long hospitalizations not only held the potential for physical decompensation, but also were psychologically stressful. Exercise helped address both of these problems.
Additionally, survivors of sudden cardiac death developed self-efficacy through participation in an inpatient exercise program. The program helped them learn to live with a malignant ventricular arrhythmia. Finally, clinical information that was useful in the management of these patients was often derived from exercise training sessions. It provided the opportunity to monitor the patient's responses to a variety of activities at various intensities. In a number of cases patients failed pharmacologic interventions on the basis of arrhythmias noted during exercise in the Rehabilitation Laboratory.
While the indications for cardiac rehabilitation for patients with MVA were extremely broad, there were some exclusion criteria. Patients were not permitted to participate in the exercise program until they had undergone cardiac catheterization. It was necessary to define the substrate of the arrhythmia before initiating any exercise training. Patients whose heart failure was not adequately compensated or whose ischemia was not well controlled were excluded. Patients with hypotensive or symptomatic ventricular tachycardia were not included. During transitions in drug therapy some patients were not permitted to participate in the exercise training until they had been given adequate time for medication loading.
The intensity of the program was driven by the exercise tolerance of the patients. A significant portion of these patients had severely depressed left ventricular function. The addition of antiarrhythmic medications with negative inotropic effects produced a group of patients with very limited exercise tolerance. The average exercise heart rate of the patients participating in the inpatient training program was 107 beats·min-1 with a blood pressure of 143/74. Peak workload averaged 3.4 METs.
Arrhythmias during exercise were very common in this population. Nearly 80% of the patients had some type of ventricular arrhythmia. Thirty-one experienced ventricular tachycardia, four episodes of which were sustained. There were no episodes of ventricular fibrillation associated with the exercise program. Of the 31 patients who experienced ventricular tachycardia during exercise, over 80% of the episodes were asymptomatic. This was probably related to the rate of the ventricular tachycardia that occurred. In only 20% of the episodes did the rate of the arrhythmia exceed 175 beats·min-1. The antiarrhythmic medications that these patients were taking unquestionably contributed to the slower rate and therefore fewer symptomatic episodes of ventricular tachycardia occurred.
Twenty-three complications occurred during exercise training. Sixty-five percent of these were of a nature that is relatively routine for cardiac rehabilitation programs (e.g., mild chest discomfort). Of the other eight episodes, one was a life-threatening emergency. This emergent complication (1 per 1214 patients-hours of activity) was an episode of cardiac arrest(sustained VT with loss of consciousness) associated with exercise training. The patient was successfully resuscitated.
Complications were considered urgent if they required immediate medical intervention, led to termination of an exercise session, or necessitated transporting the patient back to the ward. There were seven such events (e.g., unrelenting chest pain or ventricular arrhythmias). There were three episodes of sustained, symptomatic ventricular tachycardia during exercise.
In response to each urgent complication the exercise session was stopped and the patient was seen by an electrophysiologist involved with their case. All patients remained stable throughout their episode and were transported back to the ward for reversal of their arrhythmia or for other treatment. The urgent complication rate was 1 per 173 patient-hours of exercise. The urgent complications associated with ventricular arrhythmias and the one episode of cardiac arrest may all have been proarrhythmic effects of the antiarrhythmic agents that the patients were taking at the time of the episodes. Virtually all commonly prescribed antiarrhythmic agents have the potential for serious proarrhythmic effects.
There were no differences in ejection fraction or presenting arrhythmia between the patients who experienced significant complications (urgent or emergent events) and those who did not. The group that experienced significant complications during exercise, however, were training at a significantly higher work load, heart rate, and systolic blood pressure than the patients who did not experience significant complications during exercise. The group with complications were working at nearly twice the MET level as those patients who did not have such complications.
OUTPATIENT EXERCISE TRAINING
A follow-up study (16) reviewed the training records of 42 patients who were seen in an outpatient cardiac rehabilitation program following hospitalization for the management of their malignant ventricular arrhythmias. The 9-yr experience with these patients included 1246 patient-exercise sessions. These patients also commonly experienced arrhythmias during exercise. Over 90% of the patients had ventricular arrhythmias during exercise. About 30% of the patients experienced ventricular tachycardia during the cardiac rehabilitation program.
There were no deaths and no emergent complications during exercise in this outpatient group. There were nine routine complications and nine complications that were urgent. These urgent complications included four episodes of increasing ventricular tachycardia and three episodes of symptomatic ventricular tachycardia. The rate of urgent complications (1 per 138 patient-hours of activity) was actually greater than when these patients were inpatients (1 per 173 patient-hours).
Ejection fraction, presenting arrhythmia, history of congestive failure, and age all failed to identify outpatients who were prone to complications. Exercise variables (i.e., workload, heart rate, blood pressure) were also noncontributory in predicting which patients would experience urgent complications during exercise. The patients who had any episode of ventricular tachycardia during an exercise session, however, were more than seven times more likely to experience an urgent complication during exercise than those who had no ventricular tachycardia during exercise. Consequently, even brief, relatively slow, asymptomatic episodes of ventricular tachycardia appeared to be a harbinger of urgent complications.
Exercise Risk Factors
Van Camp and Peterson's (27) evaluation of patients who experienced cardiac arrest during cardiac rehabilitation identified a number of risk factors for sudden death during exercise training. Included among these was a history of cardiac arrest. Previous work(24,25) indicated that this particular risk factor for sudden death during exercise needed further evaluation. We, therefore, identified 52 patients who participated in outpatient cardiac rehabilitation following an acute myocardial infarction that had been complicated by cardiac arrest (17). This group was matched (for demographic background, medical history, and exercise participation variables) with 51 cardiac rehabilitation patients who had had an acute myocardial infarction without cardiac arrest. There were no significant differences between the two groups in terms of age, sex, history of congestive failure, ejection fraction, or mode of therapy (medical management vs surgery vs PTCA). Nor were there differences in terms of hours of participation in cardiac rehabilitation, exercise training work loads, hemodynamic responses, or ratings of perceived exertion during exercise.
The results of this study indicated no differences between the two groups in the occurrence of arrhythmias during exercise. Virtually identical numbers of patients in each group experienced ventricular tachycardia and couplets during exercise. Simple ventricular arrhythmias were also extremely similar in terms of rate of occurrence. The number of complications during exercise were almost identical in the two groups. Although the trend was for the complications to be more urgent and less routine in the group with the myocardial infarction complicated by cardiac arrest, that trend did not reach statistical significance. The rate of urgent complications in that group was 1 per 218 patient-hours whereas in those patients with a myocardial infarction not complicated by cardiac arrest the occurrence of urgent complications was at a rate of 1 per 524 patient-hours. In this study the group with a history of cardiac arrest was not at increased risk during cardiac rehabilitation.
Relative Risk of Exercise
Before undertaking the exercise testing and/or training of a high risk cohort such as MVA patients, the risk-to-benefit relationship of exercise must be put into context. The question of inherent risk of sudden cardiac death during activity for the general population was addressed by Siscovick et al.(22) in their evaluation of people who died suddenly of cardiac disease in the Seattle area. They found that there was an increased risk of sudden cardiac death during vigorous activity when compared with periods of inactivity. Despite this relatively higher risk, exercise is a low risk activity for the general population(11,18,23,28,30). Even among cardiac patients the chances of sudden death during exercise are quite low. Haskell's (13) pioneer survey of cardiac rehabilitation programs reflected cardiac rehabilitation in its early stages. Even at that time the risk of fatal cardiac arrest associated with an exercise session was only about five per million patient-hours of participation. A more recent study indicates that current practices in cardiac rehabilitation have made the risk even lower. Van Camp and Peterson (26) found the risk to be about 1.3 fatalities per million patient-hours.
A comparison of the rate of emergency complications that have been reported in various populations (Table 4) indicates the high risk nature of the patients who have been hospitalized for evaluation and treatment of malignant ventricular arrhythmias. In Kelly et al.'s study(15), inpatients had a dramatically greater risk of cardiac arrest during exercise than that reported among outpatients in cardiac rehabilitation programs by other investigators(13,14,26). The relatively limited number of inpatient in Kelly's study (15) may overstate the one cardiac arrest that occurred. This subgroup of patients, nonetheless, must be considered very high risk and treated accordingly.
From the experience with both inpatients and outpatients who have experienced malignant ventricular arrhythmias, the following observations/recommendations about their participation in cardiac rehabilitation are made. First, there appears to be a cohort of particularly high risk patients who need to be treated with considerable caution. These are individuals with a history of MVA whose ventricular function is somewhat compromised yet they maintain very good exercise tolerance. An inpatient study(15) indicated that this group of patients (who did about twice the work and achieved considerably higher heart rates and blood pressures during exercise) were far more likely to experience urgent complications during exercise than those patients with very limited exercise capacity.
Second, the arrhythmogenic side effects of antiarrhythmic agents must be considered. The experience with flecainide and encainide has been well documented (5,20). In an inpatient study(15) it was felt that many of the arrhythmia-related urgent and emergent complications may well have been due to arrhythmogenic side effects. In addition, it is important to be cognizant of the long loading periods some antiarrhythmic agents have. Before allowing patients to participate in cardiac rehabilitation it should be established that their antiarrhythmic medications are at therapeutic levels. Amiodarone, for example, has a particularly long loading period. The effects of the major antiarrhythmic agents on the ECG, hemodynamics, and exercise capacity are summarized in ACSM's Guidelines (1).
Third, the staff must be well versed in the management of patients with an AICD. This means that they must clearly understand the operation of the device. Additionally, the staff must be apprised of the cut off rate and nuances of each patient's AICD. Patients must be able to monitor their pulse. Because of the rate-triggering nature of the AICD, a preexercise program exercise test is crucial in prescribing exercise for AICD patients. This is often done preoperatively.
In the rehabilitation management of these patients, it is clear that untoward events will occur. Our experience has been that these events are typically routine. Urgent events, however, do occur. They are usually not emergencies since the ventricular tachycardia tends to be relatively slow and not hemodynamically compromising. Our experience with the inpatient population(15) was that about 80% of the episodes of ventricular tachycardia occurred at a rate below 175 beats·min-1. The occurrence of any ventricular tachycardia in our outpatient group(16), however, indicated increased risk of a subsequent urgent event. Therefore, even brief asymptomatic episodes must be followed up immediately with referral back to the patient's physician. Also, the staff and the patients must clearly understand that the AICD functions as a safety net. This means that its role is not to prevent ventricular tachycardia, but rather to resuscitate patients who experience malignant ventricular arrhythmias. The program, therefore, must be well prepared with written and regularly practiced emergency procedures.
The programming of exercise for patients who are at high risk for sudden cardiac death is most prudently done when it is based upon the individual patient's exercise limiting factor. In patients who are limited by their heart(either by virtue of ischemia or cardiomyopathy) the prescription must be adjusted accordingly. This means a decrease in exercise intensity with an increase in exercise duration and frequency. Typically the best tolerated activities for these patients will be aerobic ones.
Some patients will be limited more by their body strength than by their heart. This may be the case even though many of these patients have very poor ventricular function and/or exercise-induced ischemia. This particular subgroup, despite having cardiac problems, are not truly limited by their myocardial function. They tend to be so weak and deconditioned (usually from prolonged periods of inactivity) that their body will not allow them to reach the limitation that their heart would impose. Exercise prescription for this group should rely heavily on ratings of perceived exertion. These patients should be encouraged to increase activity as tolerated. The emphasis should be placed on the development of muscular power particularly as it relates to body movement. Walking, cycling, and stair climbing are useful activities. The development of leg strength will improve these patients' ability to function on a day to day basis and, therefore, improve the quality of their lives.
Finally, there is a group of patients who are limited by the electrical instability of their heart. In many cases these patients can resume relatively normal exercise routines, although they may require some adjustment in the intensity of their activity. If intensity is reduced, it can be compensated for by increased duration and frequency of activity. Patients with exercise-induced ventricular tachycardia are often quite young and active. They often find it very difficult to accept the limitations of their disease. Given the coverage provided by the AICD, these patients may be able to participate in rather vigorous exercise training. This decision, of course, must be arrived at by the patient and his or her physician. Simply, some patients in this category are willing to accept the risk of being shocked by their AICD to allow them to participate in activities that they had engaged in prior to their initial episode of sudden cardiac death. If these patients make such a decision, the cardiac rehabilitation program should strongly encourage them to exercise in a safe setting. Ideally this would be a cardiac rehab program. If patients insist on exercise/activities outside the program setting, the importance of the availability of emergency support must be emphasized. Exercising alone should be adamantly discouraged. Finally, these patients should be counselled on the wisdom of reducing exercise intensity.
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CARDIAC REHABILITATION; EXERCISE; AUTOMATIC IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR; SUDDEN CARDIAC DEATH