We are all on a trajectory to heart disease. It’s called age.
(J.N. Cohn, University of Minneapolis, at the Annual Scientific Meeting of the Heart Failure Society of America, Toronto, Canada, 2004)
Heart Failure in an Aging Society
Two fundamental factors determine the growing prevalence of heart failure in the Western hemisphere: average life expectancy and age-adjusted incidence of chronic heart failure (CHF).
Since the 1840s the average maximum life expectancy has been increasing at a constant rate of 3 months per year with no change in sight.
1In most industrialized societies the age group over 65 years is the fastest growing proportion.
It is exactly in this age group that CHF is most prevalent: 6.6% of all women and 6.8%
of all men between 65 and 74 years are affected by CHF in the US. This number climbs to nearly 10% above 75 years of age (Figure 19-1).
2The combined impact of the aging population and the age distribution of CHF has caused an epi- demic growth in disease numbers. In the 22 years between 1979 and 2001 hospital discharges for CHF rose by 164% and today 79% of all hospital- ized patients are older than 65 years.
2Elderly patients with CHF pose a special task for cardiac rehabilitation because of the overlap of age- related and disease-associated impairment of exercise tolerance.
Training in Heart Failure – from Fear to Favor
Until the late 1980s chronic heart failure was widely regarded as a classical contraindication for exercise-based rehabilitation approaches in guidelines and clinical practice alike. Progressive immobilization was recommended for CHF patients with exercise intolerance as routine therapy to prevent any hemodynamic overload on the diseased left ventricle. It was assumed that patients with extensive myocardial damage and severely depressed left ventricular function had an excessive risk for exercise-related morbidity and mortality. However, this concept was shattered two decades ago by the lack of any clear relation between left ventricular ejection fraction and exercise capacity
3– a finding which led to the novel concept that peripheral factors might significantly contribute to the pathogenesis of exercise intolerance. This para- digm shift inspired a new generation of clinical researchers to objectively assess the clinical and hemodynamic effects of exercise in CHF patients.
The results of a whole series of prospective ran- domized training studies which unanimously confirmed an improvement in peak oxygen uptake by 12–21% ( +1.2 to +5.7L/min/m
2) with no exer- cise-associated additional morbidity or mortality being reported (Table 19-1). As a result exercise training is now recommended in national and international guidelines for the treatment of patients with chronic heart failure.
19
Exercise Training in Heart Failure
Stephen Gielen, Josef Niebauer, and Rainer Hambrecht
142
In this chapter both basic principles of exercise physiology in health and disease and the practical aspects of initiating a training program in CHF patients (including patient selection, training methods, and adaptation of individual training intensities) will be addressed.
Finally, clinical results and prognostic implica- tions of training interventions in CHF will be discussed.
20–24 25–34 35–44 45–54 55–64 65–74 75+
Ages 0
2 4 6 8 10
Percent of Population
Men Women
0.1 0.1 0.1 0.1 0.7 0.5 1.8 1.3
6.2
3.4 6.8 6.6
9.89.7
FIGURE 19-1. Prevalence of chronic heart failure by age and sex according to NHANES III (1988–1994) according to the American Heart Association.2Red bars represent men, white bars women. (Reproduced with permission, Heart Disease and Stroke Statistics-2005 Update, © 2004, American Heart Association.)
TABLE19-1. Effects of exercise training on peak oxygen consumption: results of random- ized trials
Author n Duration Etiology VO2max (L/min/m2) ∆VO2max (L/min/m2)
Coats 199042 11 8 weeks ICM 13.5 +3.2
Jette 199143 15 4 weeks post-MI 12.2 +3.6
Coats 199244 17 8 weeks ICM 13.2 +2.4
Belardinelli 199545 55 8 weeks DCM 15.0 +1.2
Kiilavuori 199546 20 12 weeks DCM/ICM 20.7 +2.2
Kiilavuori 199619 27 24 weeks DCM/ICM 19.3 +2.4
Keteyian 199647 40 24 weeks DCM/ICM 16.0 +2.5
Meyer 199748 18 3 weeks DCM/ICM 12.2 +2.4
Dubach 199749 25 8 weeks post-MI 19.4 +5.7
Belardinelli 199950 99 2 years DCM/ICM 15.7 +4.2
Hambrecht 200020 73 24 weeks DCM/ICM 18.2 +4.8
McKelvie 200251 181 12 weeks DCM/ICM 14.0 +1.4
Gianuzzi 20037 89 24 weeks DCM/ICM 13.8 +2.4
Niebauer 200552 30 8 weeks DCM/ICM 25.3 +2.7
DCM, dilative cardiomyopathy; ICM, ischemic cardiomyopathy; Post-MI, after myocardial infarction.
The Time Course of Training Adaptations
The physiological response to exercise follows a well-established pattern in both health and disease. The concept of the supercompensation cycle
4is based on the idea that a training stimulus disturbs the stability of the organism and induces physiological adaptations or training effects. This primary stimulus is called overload. An overload is characterized as physical exercise which demands more than the normal physical work capability of the organism and leads to a tem- porarily reduced muscular function resulting in fatigue.
The overload phase is followed by restoration, which implies that regenerative mechanisms restore the exercise capacity to pretraining levels.
The time course of the restoration is different for different organ functions: Typically, heart rate, ventilation, neurohormonal levels, and body tem- perature return to normal within minutes or hours, while it may take days to fill up carbohy- drate stores and to repair muscular damage.
The hallmark of the training cycle is the adap-
tation phase, in which the tissue and organ
damages are supercompensated. The physiological changes in this phase include increases in skeletal muscle mass, strength, mitochondrial density, key aerobic enzyme activity, and fuel storage capacity.
The cardiovascular system adapts to exercise by increasing capillary density in the exercised muscle, increased blood volume, increased left ventricular end-diastolic volume, and maximal stroke volume. Thereby each training cycle pro- duces a higher fitness level which allows for greater workload and training benefits in the sub- sequent training sessions. Once regular training is stopped, the adaptations are gradually lost as a result of disuse – a phase termed reversal (Figure 19-2).
Differences in Physical Responses to Exercise in Health and Disease
While the basic pattern of the supercompensation system is valid in both health and disease some important differences should be noted:
1. In the presence of cardiovascular disease exercise capacity is limited. As a result, lower than normal levels of physical exertion result in fatigue and in the temporary reduction of organ function during the overload phase.
2. A patient with cardiovascular disease will need more time to regenerate following an over- load, which implies that the supercompensation cycle is prolonged.
3. As a result of peripheral intrinsic alterations associated with certain forms of cardiovascular disease (i.e. chronic heart failure), the ability of the skeletal muscle to respond to an overload by muscle hypertrophy and improved oxidative energy metabolism may be impaired.
Why are these aspects important in cardiovas- cular rehabilitation? As indicated in Figure 19-3, training effectiveness critically depends on an optimal timing and dose of exercise. Ideally, a training session should be performed at the height of the adaptation phase. At this time the individual has the best physical preconditions to tolerate a second overload (Figure 19-3A). When training sessions are timed too late the training adaptations may already be lost (Figure 19-3B), when timed too early the individual may still be in the restoration phase so that a second overload could have detrimental effects and lead to further loss of function (Figure 19-3C).
The most important factors determining phys- iological adaptation and magnitude of improve- ments in exercise performance include age, intensity, duration and frequency of exercise, genetic background, and pretraining fitness levels.
It has to be kept in mind that the gains in physi- cal capacity achieved during prolonged training programs are greatest following initiation of the exercise program.
The molecular mechanisms involved in mediat- ing beneficial training effects are discussed in detail in Chapter 12. Suffice it to say that
24 48 72 96 72 96
Overload Restoration Adaptation Reversal
Hours
FatigueAdaptation
A B C D FIGURE19-2. The primary training stimulus is termed
“overload” (A) because it exceeds the organism’s current work capacity, resulting in temporary fatigue.
During restoration, organs return to pretraining levels (B). Training adaptation occurs as a supercompensa- tion due to structural changes and adaptations (C). A reversal of previously gained adaptations is possible once training is stopped (D). (Reprinted with permis- sion from Moyna.4)
endurance training partially reverses the intrinsic pathologic alterations in skeletal muscle metabo- lism and catabolism, improves ventilatory func- tion, reduces autonomic and neurohormonal activation, attenuates local and possibly systemic inflammatory activation, and improves endothe- lial dysfunction resulting in reduced afterload and higher stroke volume.
Patient Selection for Exercise Training in CHF
Patients with CHF have higher morbidity and mortality rates as compared to most other forms of heart disease (especially stable coronary artery disease). Therefore, current guidelines stratify CHF patients as a high-risk group for training interventions. As indicated above this implies a more detailed diagnostic evaluation before initia- tion of exercise training which includes echocar- diography and a 12-lead ergometry.
What are the potential risks of exercise training for CHF patients? The most widespread fear has long been the adverse effect of exercise training on
left ventricular remodeling after a myocardial infarction. In a single non-controlled clinical study, Jugdutt et al. reported a negative influence of training on left ventricular (LV) performance in post-infarct patients.
5However, several prospec- tive randomized clinical trials have since shown that training favorably affects LV geometry and function.
6,7The second major concern was a proarrhythmogenic adverse effect of training.
However, meta-analyses of controlled training trials did not substantiate this concern: There were 56 adverse events in the 622 CHF patients in training programs and 75 adverse events in the 575 subjects in the control group (P = 0.60).
8On a pathophysiological basis the reductions in neurohormonal activation and circulating cate- cholamines in training patients should beneficially affect the incidence of malignant arrhythmias. However, systematic studies in this area are still missing.
Indications for Exercise Training in CHF
Today, exercise-based cardiac rehabilitation is officially recommended by current ESC and
Fitness LevelFitness LevelFitness Level
+ – + –
+ –
Training session
A
B
C
FIGURE19-3. Fitness improvements are greatest when training sessions coincide with the peak of the adaptation phase (A). If timed later no significant gains in fitness are to be expected; if timed too early training sessions will result in worsening of function (C). (Reprinted with permission from Moyna.4)
AHA guidelines as an adjunctive therapy for patients with stable CHF, without any cardiac decompensation in the preceding 3 months, and with uptitrated guideline-oriented pharmacologi- cal therapy.
9,10While most training studies re- cruited primarily patients in NYHA class II, subgroup analysis shows that patients in more advanced CHF (NYHA class III) benefit equally from the training intervention.
11,12Contraindications for Exercise Training in CHF
Any patient who wants to start regular physical training in the presence of CHF has to pass two lists of contraindications, the first for exercise testing, the second for exercise training. Con- traindications for exercise testing apply because a maximal exercise test (ergometry, treadmill, or spiroergometry) is required to calculate the correct training heart rate (Table 19-2, A).
Contraindications for exercise training are less well defined. However, it is generally agreed that patients may not have any cardiac decompensa- tion in the preceding 3 months or any acute sys-
temic illness (Table 19-2, B). In addition to the list of clear contraindications, clinical situations in which there is an increased risk for training therapy are listed in Table 19-3. While the condi- tions described do not prohibit exercise they should be resolved whenever possible prior to the initiation of training interventions (e.g. by implantation of an internal cardioverter/defibril- lator in complex ventricular arrhythmias, espe- cially in ischemic cardiomyopathy).
In prospectively conducted exercise training studies in stable CHF patients, adverse events are surprisingly low, with post-exercise hypotension, atrial or ventricular arrhythmias, and worsening heart failure symptoms being the most common complications.
Although the risk to patients with ventricular arrhythmias during training interventions has never been prospectively evaluated, most studies have excluded patients with evidence of ventricular arrhythmias ( ≥Lown IV during Holter ECG).
Vigorous uncontrolled exercise may precipitate cardiac decompensation in CHF patients.
However, there are no reports of an increased rate of pulmonary edema in long-term submaximal training trials in stable CHF patients. In patients with stable compensated chronic heart failure (CHF) no additional risk of maximal exercise testing has been reported with no major compli- cations reported in one study of 1286 bicycle ergometer tests.
13Risk Stratification and Patient Screening
The American Heart Association (AHA) and the American College of Sports Medicine (ACSM) have published detailed guidelines on exercise
TABLE19-2. Contraindications to exercise testing (A) and exercisetraining (B)
A. Contraindications to exercise testing (according to AHA guidelines53) Acute myocardial infarction <2 days
Unstable angina with recent rest pain Untreated life-threatening cardiac arrhythmias Uncompensated congestive heart failure Uncontrolled hypertension
Advanced atrioventricular block Acute myocarditis and pericarditis Symptomatic aortic stenosis
Severe hypertrophic obstructive cardiomyopathy Acute systemic illness
B. Contraindications to exercise training
Cardiac decompensation in the previous 3 months
Progressive worsening of exercise tolerance or dyspnea at rest or on exertion over previous 3–5 days
Significant ischemia during low-intensity exercise (<2 METs, <50W) Uncontrolled diabetes
Acute systemic illness or fever Recent embolism
Thrombophlebitis
Active pericarditis or myocarditis
Myocardial infarction within the previous 3 weeks New onset atrial fibrillation
TABLE19-3. Increased risk for exercise training
<1.8kg increase in body mass over the previous 1–3 days Concurrent continuous or intermittent dobutamine therapy Decrease in systolic blood pressure with exercise NYHA functional class IV
Complex ventricular arrhythmia at rest or appearing with exertion Supine resting heart rate >100 beats/min
Preexisting co-morbidities limiting exercise tolerance
Patient with sign/symptoms of
heart failure
Initial evaluation and therapy
Unstable or NYHA IV Stabilized in NYHA
class II or III on appropriate treatment
Evaluate exercise tolerance
Optimize medical therapy. Consider for device support, transplant, or inotropes
Exercise-induced ventricular tachycardia,
ischemia or hypotension
Further diagnostic studies as indicated Impaired but no serious
exercise-induced sequelae of exercise
Cardiac rehabilitation at 50–70% of VO2max 3–5
times per week
FIGURE 19-4. Clinical evaluation of CHF patients prior to the enrolment into a training program according to current guidelines.
(Adapted from Braith.54) TABLE19-4. Risk stratification according to the recommendations of the AHA
AHA classification NYHA class Exercise capacity Clinical characteristic ECG monitoring
A. Apparantly healthy Men <45 years No supervision or monitoring
Women < 55years required
Without sympstoms, no major risk factors, normal exercise stress test
B. Stable cardiovascular I–II >6METs Free of ischemia or angina at rest or Monitored and supervised only during disease with low risk >1.4W/kg on the exercise stress test prescribed sessions (6–12 sessions).
for vigorous exercise body weight Stable CHF (EF ≥ 30%). Light resistance training may be
but unable to No ventricular arrhythmias included in comprehensive
self-regulate activity rehabilitation programs
C. Moderate-to-high risk III <6METs No ability to self-monitor exercise Continuous ECG monitoring during for cardiac <1.4W/kg Pathologic response to exercise rehabilitation until safety is complications during body weight test (drop in BP, signs of established. Medical supervision
exercise ischemia etc.), nsVT during exercise during all exercise sessions until safety
is established
D. Unstable patients. III–IV <6METs Unstable angina No physical activity recommended
Physical activity <1.4W/kg Uncompensated heart failure for conditioning purposes
for training body weight Uncontrollable arrythmias Attention should be directed to restoring
contraindicated patient to class C or higher
in clinical populations and encourage risk stratification of patients prior to initiating an exercise training program.
14A widely used risk assessment scheme was proposed by the AHA (Table 19-4).
15The majority of CHF patients will be classified as class B or C. Medical supervision including ECG monitoring is necessary until the clinical safety of the training program is established.
Before enrolment in a training program, a patient with CHF should be in a stable condition without clinical evidence of fluid overload. A typical patient evaluation should be performed by an experienced cardiologist and involves: medical history, clinical examination, a resting ECG, a symptom-limited ergometry, and echocardiogra- phy. Other supplementary options are: Holter ECG, 24-hour blood pressure measurements, stress echocardiography, chest x-ray, and, in a few cases, evaluation of left ventricular filling pres- sures with a Swan–Ganz catheter under stress conditions. If the clinical status of a patient is unclear and previous examinations/tests are lacking, invasive diagnostic measures should be undertaken in order to clarify the situation (Figure 19-4).
A thorough medical examination must also
be carried out in order to exclude patients
who have cardiovascular and/or orthopedic mus-
culoskeletal contraindications. Muscle atrophy – which may occur as a result of aging, long-term bed confinement, sedentary lifestyle or glu- cocorticoid therapy – must be evaluated and recorded.
It should be underlined that patients included in training studies have to be on optimized medical therapy and in stable clinical condition for at least 4 weeks before the initiation of the training program. It is recommended that patients should be uptitrated according to current guidelines on standard heart failure medication (especially ACE inhibitors and beta-blockers) prior to training. Training interventions in CHF are based on aerobic steady-state exercise sessions at 50–80% of the peak oxygen uptake for 15–30 min 3–5 times per week. In highly symptomatic patients with very low symptom- free exercise tolerance ( <75W) shorter training sessions at low intensity (50% of VO
2max) may be required. When patients tolerate this regimen well, first the session duration should be prolonged, then training intensity can be increased.
Selection of the Optimal Training Protocol
Training protocols vary in a number of variables:
– Exercise level: aerobic versus anaerobic.
– Exercise type: endurance versus resistance.
– Exercise application: systemic versus regional.
– Exercise method: continuous versus intermittent.
– Exercise control: supervised versus non- supervised.
Exercise Level: Aerobic Versus Anaerobic
Most of the training protocols to date are derived from classical protocols used in patients with coronary artery disease. Individual training intensities are fixed at 70–80% of peak oxygen consumption or chronotropic reserve. Exercise training at these conventional workloads, however, may be unsuitable for severely affected
CHF patients whose initial functional exercise capacity is very low. Moreover, intermittent exercise at workloads >70% of peak VO
2exposes the heart to periodically elevated LV filling pressures. Based on small exercise trials, some authors hypothesized that the elevated LV filling pressures induce further LV dilation.
5However, large trials in ischemic patients with LV dys- function did not reveal any deleterious effect of exercise on LV volume, function, or wall thickness.
6,7,16Nevertheless, aerobic exercise training at low workloads ( ≤50% of peak aerobic capacity) appears to be a promising approach to physical training in patients with severely compromised LV function because exercising at low workloads does increase peak aerobic capacity and vascular flow capacity of the lower limb while exposing the left ventricle to lower wall stress than that associated with conventional workloads.
17–19Exercise Type: Endurance Versus Resistance
Endurance training leads to a reduction in after- load with a decrease in systemic resistance at rest and at maximal exertion as well as to a small improvement in LV ejection fraction.
20Similar data for resistance training in CHF patients do not exist. Aerobic endurance training thus still forms the basis of training therapies for CHF patients.
Critical appraisal of (predominantly) isometric
resistance training (hand-grip training, stress
time >3min) is based on older studies that found
a drastic rise in afterload along with an acute
reduction in cardiac output
21and an increase
in the severity of mitral regurgitation.
22In
contrast to these findings, 2 × 10 repetition
leg-press exercises at 70% of maximal capacity
or interval training do not cause a clinically
relevant decrease in ejection fraction/increase
in systolic blood pressure.
23,24By shortening
the isometric and lengthening the isotonic
exercise phase, it is possible to avoid hemody-
namic strain. Pure resistance training in CHF
patients leads to an increase in muscular
strength. There is, however, no accompanying
increase in maximal O
2uptake.
25It is only by
combining resistance and endurance training that
the important prognostic marker VO
2max can be improved.
26Experimental studies with animals have shown that resistance training leads to enhanced local expression of insulin-like growth factor I (IGF-I).
It may therefore be possible that supplemen- tary, individually adapted resistance training of specific extremities positively influences the cata- bolic breakdown of muscle tissue which is often associated with congestive heart failure. Specific data relating to this area still lacking.
To summarize, patients in risk groups B and C (compare Table 19-4) may benefit from a resis- tance training program with short stress phases (maximal capacity 10 repetitions) at <60% MVC, interrupted by phases of muscle relaxation, without causing hemodynamic deterioration. As a supplementary training modality, resistance training can complement, but not replace, the well-established aerobic endurance training.
Exercise Application:
Systemic Versus Regional
Segmental training has been proved to be effective in CHF patients in improving muscle force and functional status.
27,28The low hemodynamic burden on the myocardium makes segmental exercise suitable in particular for selected patients in NYHA class IV, who are often unable to engage in sufficient whole body exercise.
Nevertheless, no study to date has specifically compared the long-term effects of different modes and levels of exercise training in CHF with regard to functional work capacity and LV function.
Exercise Method: Continuous Versus Intermittent
Limited information is available for isometric training or interval training with short bouts of stimuli on peripheral muscles. First results from Meyer et al.
29demonstrated that interval training permits more intense exercise stimuli on peri- pheral muscles with minimal cardiac strain as compared with hemodynamic response during ergometry.
Derived from controlled training studies, exercise is usually recommended for 20 to 60 minutes on 3 to 5 days per week. The lower and upper cut-off level regarding frequency and duration of exercise sessions, however, is not known.
Exercise Control: Supervised Versus Non-supervised
There are no convincing data that home-based exercise training is less safe than strictly super- vised exercise training. Experience from con- trolled trials of physical training in Europe demonstrated higher symptomatic benefit after combined home- and hospital-based train- ing programs than in the hospital-based only programs, which may reflect improved patient compliance with the former protocol.
30However, it is currently recommended to initiate a training program in heart failure patients only under supervised conditions. Home-based training can be started as soon as the safety of the training protocol has been established and the patient is acquainted with the safety precautions associated with exercise (i.e. control of training pulse).
Initiation of Training Therapy and Progression of Training Intensity
In most training intervention trials, a minimal symptom-free exercise tolerance of 25 W is required for the initiation of the training program. In patients with very low exercise toler- ance ( <50W),training is started with several short training sessions of 5 ( −10) minutes per day at 50% of peak oxygen uptake. At higher baseline exercise capacities the initial training session duration can be 10–15 minutes. An adequate warm-up and cool-down period consisting of stretching or aerobic exercise at a very low inten- sity is also recommended.
As the training adaptations progress, first train- ing duration, then training intensity are gradually increased aiming at 20 min of exercise at 60–70%
of VO
2max for 5 days per week (Figure 19-5).
Clinical Effects of Exercise in Chronic Heart Failure
Prognostic and Symptomatic Effects
The results of the ExTraMATCH meta-analysis of the ESC with a total of 801 CHF patients documented a significant reduction of total mortality by 35% (odds ratio 0.65; CI 0.46–
0.92, P = 0.015), and of hospitalization by 28% (odds ratio 0.72; CI 0.56–0.93, P = 0.018).
11With regard to symptomatic benefit a recent meta-analysis of randomized controlled trials by the European Heart Failure Training Group revealed an improvement of peak VO
2by up to 2 mL/kg/min with a range of +14 to +31% increase versus control patients. Although modest in absolute terms, this increase of about 20% trans- lates into a considerably better quality of life for most patients.
Cardiac function is not worsened by exercise training; indeed, a small but significant improve- ment of ejection fraction and reduction in car- diomegaly was observed in one prospective randomized trial.
20Based on this trial, improved endothelium-dependent vasodilation
31with reduced total peripheral resistance – both at rest and at peak exercise – is a major contributing factor to the increase in ejection fraction (Figure
19-6). The improvement of endothelium- dependent vasodilation is not limited to the trained limb but is a systemic training effect if the muscle mass involved is large enough to elicit increases in cardiac output during exercise ses- sions.
32However, beneficial adaptations of the respiratory, neurohormonal, and autonomic system are also involved.
Interactions with Medication
Current guidelines require patients to be upti- trated on a combination therapy of ACE inhibitors, beta-blockers, diuretics, spironolac- tone, and digitalis according to clinical status. The question naturally arises how these medications might affect training response in CHF patients.
This concern is especially related to beta-blocker therapy as it affects the heart rate response to exercise.
According to a small, non-randomized French study in patients with stable CHF, the effect of exer- cise training as measured by ergospirometry was not influenced by the presence or absence of beta- blocker treatment.
33This holds true despite lower training heart rates among patients under beta- blockade. However, patients should be uptitrated to their optimal individual beta-blocker dose prior to the initiation of the training program.
50% VO
2max; 5-10 min./unit Training Duration
Training Frequency
Intensity
Initial Phase Phase of Workload Increase
50%→ 60% → 70% VO2max
FIGURE19-5. The training pyramid illustrates the gradual increase in training duration, frequency, and intensity which occurs at the beginning of a training program in CHF patients.
Special Patient Subgroups
Patients with ICDs
The evidence that cardiac mortality is reduced in CHF by implantation of internal cardio- verters/defibrillators (ICDs) is mounting, fuelled by prospective randomized trials such as the MADIT-II and the COMPANION study. While biventricular pacing was associated with sympto- matic improvement, the biventricular ICD group benefited from a reduced rate of sudden cardiac deaths resulting in lower cardiac mortality.
Rehabilitation institutions have long been reluctant to offer training programs to CHF patients with ICDs. The major concerns were based on the notion that ICD patients represent a high-risk subgroup for ventricular arrhythmias, and that most rehabilitation facilities lack the equipment, personnel, and expertise to treat patients effectively after a shock delivery.As a con- sequence, only specialized institutions have eval-
uated training post ICD implantation. In these small studies, however, training appears to be both safe and feasable.
34,35Certain safety concerns remain and should be addressed.
Risk of Training-Related Shock Delivery and Device Failure
In a single-center non-randomized follow-up study, the rate of ICD malfunction was reported to be 10.2% (n = 12 patients), requiring reopera- tion in 3 and reprogramming in 9 patients.
36While no exercise-related shocks were observed in this study, Vanhees reported that 3 out of 95 patients experienced adequate shocks for ventric- ular tachycardia (VT) during exercise. These patients terminated the training program. In addi- tion, one patient had several shocks the day after training. Two additional patients had asympto- matic VTs terminated with overdrive pacing – one during exercise testing, one during a training session.
35FIGURE19-6. Effects of exercise training on cardiac dimensions and ejection fraction. Note that ejection fraction is improved as a con- sequence of reduced afterload and improved preload rather than by intrinsic myocardial effects.
Risk of Inadequate Shocks During Exercise- Induced Supraventricular Tachycardias
Inadequate ICD discharges triggered by supraven- tricular tachyarrhythmias are well recognized in ICD patients
37and may induce life-threatening ventricular arrhythmias in individual patients.
38,39In the recent Vanhees study
35inadequate defibril- lator discharge during an exercise session occurred in one patient but did not result in any proarrhythmic complications. Other studies did not observe any training session-related inade- quate ICD discharges.
Special Recommendations for Training Interventions in ICD Patients
• While no excess mortality was observed in the non-randomized observational ICD training studies, close cooperation is needed between rehabilitation centers and electrophysiologists to determine the optimal training heart rate for the patient, so that he remains below the thresh- old for VT detection. In patients with atrial fibrillation optimal pharmacological rate control should be established prior to initiating a training program.
• Maximal exercise testing in an institution with ICD support should be performed prior to the training intervention to rule out exercise- induced ventricular arrhythmias.
• Given the relatively high ICD malfunction rate of 10.2% in one study, it seems prudent to check the ICD function after the first 2–4 weeks of training therapy.
Elderly Patients
In addition to having heart failure, elderly people often suffer from disability caused by mental depression, low aerobic fitness levels, low skeletal muscle mass, and presence of orthopedic co- morbidities. Despite these factors, the elderly benefit equally from cardiac rehabilitation, but from a lower baseline.
Evidence Base for Beneficial Training Effects in the Elderly
Despite the demographic changes and the high proportion of elderly people among patients hos-
pitalized for CHF, systematic studies comparing training effectiveness between younger and older CHF patients are still scarce. In a meta-analysis of 14 training studies, Piepoli identified only 14 out of 134 patients (10%) >70 years of age.
40In this minor subgroup, clinical symptoms were significantly improved after training; however, peak oxygen uptake was unchanged. A recent observational study in 17 CHF patients between 61 and 91 years, on the other hand, 6 months of exercise training resulted in a 23% increase in VO
2max.
41While clearly more studies are needed to compare the symptomatic effectiveness of train- ing between younger and older CHF patients, Piepoli recently presented a large mortality meta- analysis of CHF training studies. A total of 117 patients ≥60 years were included,of whom 52 were randomized to exercise training.
11No difference in mortality reduction by training was found between younger and older CHF patients (hazard ratio 0.64 ≥60 years and 0.65 <60 years, P = 0.74).
This is remarkable since age itself is the best pre- dictor of death.
Recommendations for Exercise Training in Elderly CHF Patients
• When initiating aerobic exercise the exercise intensity should be carefully weighted against a higher risk of injuries with higher workloads.
Even workloads as low as 60–65% of the maximal heart rate have documented effects on exercise capacity. To avoid orthopedic injuries ergometer training is preferably to walking or jogging.
• To antagonize the loss of muscle mass endurance exercises are often supplemented with moderate-intensity resistance training (e.g. elastic bands) with 8–10 set repetitions at 40–60% of the 1-repetition maximum.
• The aim of exercise-based rehabilitation in the
elderly is the improvement of locomotor coor-
dination, endurance, and muscle force so that
patients are able to perform the physical duties
of their daily life. Therefore, the primary goal is
prevention of disease-associated disability and
hospitalization, and maintenance of indepen-
dent living.
Future Perspectives of Training Interventions in Heart Failure
The reliability of practical recommendations is always related to the soundness of the study data- base. Three areas can be identified where there is clearly a need for further trials:
1. While meta-analyses indicate a prognostic benefit of training in CHF patients the final ran- domized mortality study is still pending. It has recently been started in the US (HF-ACTION study: Heart Failure – A Controlled Trial Investi- gating Outcomes of exercise traiNing) and will finally settle the debate about the training-related mortality reduction in patients with CHF.
2. There is still uncertainty on the issue whether exercise training can safely be initiated on an outpatient basis. The vast majority of training studies in CHF started the training program in hospital with close monitoring of training sessions by experienced staff. While this is clearly optimal therapy it would exclude thou- sands of patients from the benefits of training interventions if in-hospital training was required for all patients. Future studies need to identify subgroups in whom it is safe to offer monitored training sessions without concomitant hospital- ization.
3. Resistance training is being increasingly employed in CHF patients in clinical practice.
However, the database for such modifications of established aerobic training programs is not sound. While meta-analysis clearly indicates a prognostic benefit of endurance training for CHF, similar data are lacking for resistance exercise.
Large-scale randomized studies comparing aerobic, resistance, and combined training pro- grams in CHF are still pending.
The majority of people involved in cardiac rehabilitation share a practical, “hands-on”
approach to training interventions and may tend to modify training programs based on personal experience rather than clinical studies. Without doubting the value of experience, we have to remember that training interventions in CHF must be regarded in the same way as powerful medications with a need for optimal dosing, con- sideration of side-effects, and close clinical follow-
up by an experienced cardiologist. We are there- fore well advised to demand the same level of evi- dence for training interventions as for pharmaceuticals. Such a way of proceeding will not only assure the optimal benefit and safety for the patient but provide the best chances to receive adequate funding in times of shrinking healthcare resources.
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