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Heart failure
Exercise training in heart failure: practical guidance
  1. Viviane M Conraads,
  2. Paul J Beckers
  1. Department of Cardiology, Antwerp University Hospital, Edegem, Belgium
  1. Correspondence to Professor Viviane Conraads, Department of Cardiology, Antwerp University Hospital, Wilrijkstraat 10, 2650 Edegem, Belgium; viviane.conraads{at}uza.be

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Regular physical exercise modulates cardiovascular (CV) risk and improves endothelial function. As such, exercise training (ET) prevents the development and progression of atherosclerotic lesions. In patients with established coronary artery disease, ET has consistently shown a 15–31% reduction in all cause and cardiac mortality.1

Prevention is not a chief therapeutic target in the management of chronic diseases. In the case of chronic heart failure (CHF), treatment mainly concentrates on reducing hard end points. It should be stressed, however, that maximal aerobic capacity is a powerful, yet underestimated, predictor of outcome.2

Exercise intolerance, with pronounced fatigue and dyspnoea even at low exercise load, impairs autonomy and quality of life in CHF patients. Exercise training is by far the most efficacious way to improve physical performance. A 15–30% increase in aerobic capacity in stable CHF patients has been repeatedly demonstrated following endurance training.

Controversy remains as to whether ET favourably affects outcome and which training modality suits these patients best. A critical issue, which is also applicable to the community at large, is the problem of non-adherence to prescribed exercise regimens.

This article provides general information on the clinical application of ET and includes practical guidance on how to prescribe exercise for CHF patients.

Multifactorial origin of exercise intolerance defines targets of exercise training

To understand the relation between cardiac performance and exercise capacity in healthy subjects, it is useful to recall the Fick equation:

VO2=Q (CaO2 − CvO2) where VO2 is oxygen consumption, Q is the cardiac output, CaO2 is the arterial oxygen content, and CvO2 is the venous oxygen content

Intuitively, disturbed cardiac function and haemodynamics are often considered the sole determinants of exercise intolerance in CHF patients. The demonstration of a poor relationship between peak oxygen consumption (Vo2peak) and resting left ventricular ejection fraction, however, underscores the fact that this view is too simplistic. As heart failure progresses, the second factor in this equation (reflecting the ability to transport oxygen through vasodilated arteries and to use it by working muscles) gains importance. Peripheral changes, which significantly impact exercise capacity in CHF patients, include skeletal muscle abnormalities, ventilatory inefficiency, increased ergoreceptor activity, and endothelial dysfunction.3 Exercise training in CHF patients modifies these peripheral factors, rather than exclusively improve cardiac performance. By increasing nitric oxide (NO) bioavailability, counteraction of activated neurohormonal and inflammatory pathways, as well as anti-oxidative effects, ET reduces peripheral vasoconstriction, corrects endothelial dysfunction and enhances endothelial repair.4 These changes parallel observed ET induced increases in Vo2peak.

Objective assessment of maximal aerobic capacity in CHF is mandatory

Exercise prescription needs to match individual requirements and patients' characteristics, such as the degree of physical and cardiac impairment and the presence of muscle wasting. Intensity should be high enough to be effective, but safe margins need to be respected. It is therefore mandatory to first exactly measure exercise capacity.

Why perform maximal cardiopulmonary exercise testing?

Maximal exercise testing, with ventilatory expired gas analysis (cardiopulmonary exercise testing, CPET), is the most precise and therefore preferred method. Estimations based on tests without gas analysis are popular in healthy subjects (ie, fitness facilities), but issues such as chronotropic incompetence and the use of cardiovascular drugs prohibit accurate extrapolations in CHF patients.5 Objective measurement of Vo2peak, in addition to other prognostic parameters derived from CPET, is considered the gold standard to predict outcome and to direct advanced treatment options in CHF. With regard to ET, integration of CPET derivatives, allows: (1) calculation of effective and safe training intensity; (2) functional and risk classification; and (3) assessment of benefit following a training programme.

An important and useful submaximal index is the ventilatory anaerobic threshold (VAT). This point is defined as the exercise level at which ventilation (VE) starts to increase exponentially, relative to the increase in Vo2. Relative hyperventilation occurs to eliminate excess carbon dioxide (CO2) production, which compensates for increased lactate formation. Exercise training delays the occurrence of anaerobic metabolism (VAT) and this phenomenon is clinically relevant (figure 1). Indeed, daily life tasks rarely demand peak performance, but are conducted at a submaximal workload. As such, augmenting the workload that can be achieved and sustained without limiting complaints of dyspnoea and fatigue (ie, before reaching VAT) is a major target of ET, especially in CHF patients.

Figure 1

Schematic presentation of the relation between exercise intensity and lactate concentrations. During incremental exercise, lactate is maintained at a steady state value (±1 mmol/dl), until contribution of anaerobic metabolism to energy generation increases. This occurs as the capacity of the cardiovascular system to transport oxygen reaches its maximum. Whereas the initial transition occurs gradually and starts at the ventilatory anaerobic threshold (VAT; start of increase of lactate level from 1 to 4 mmol/dl), the respiratory compensation point (RCP; above 4 mmol/dl lactate) marks the point of rapid lactate accumulation and ensuing exercise cessation. The blue line illustrates the evolution after exercise training (ET). The red arrow shows how ET will lead to higher Vo2 at the time VAT occurs.

Cardiopulmonary exercise testing in practice

Patients should be submitted to CPET in a non-fasting state and without interruption of medical treatment on the day of testing. Most centres use ramp protocols, with small increments, aiming at a total duration of 8–12 min. Based on physical activity, New York Heart Association (NYHA) classification, medical information, and prior exercise testing, physicians ought to carefully determine starting workload and the magnitude of each step. Overestimation of a patient's capacity will lead to rapid lactate accumulation and premature cessation of effort. Workloads that are too small will unnecessarily prolong the test and cause fatigue, without reaching the actual maximal aerobic capacity. Most physiology laboratories in Europe prefer bicycle ergometry to treadmill testing. While the former is probably safer in patients who are severely debilitated and not stable on their feet, Vo2peak during treadmill exercise is systematically 10–15% higher because of larger muscle Vo2peak involved. Care should be taken to avoid rail handling during treadmill exercise. Interpretation of CPET requires insights into exercise physiology. Description into depth, however, is beyond the scope of this paper and the reader is referred to recently published guidelines on this issue.6 Figure 2 shows the basic and essential parameters that can be derived from CPET. This information is required to determine Vo2peak and to calculate ET intensity, relative to Vo2peak. Vo2peak and Vo2max are not interchangeable terms. In fact, true Vo2max is attained when the rise in Vo2 ceases, despite further increase in workload. Flattening of the Vo2 curve, however, is not often demonstrated. Instead, Vo2peak is reported as the highest Vo2 averaged over a 20–30 s period, achieved at presumed maximal effort. For the sake of simplicity, the term Vo2peak is used throughout this article.

Figure 2

Schematic presentation of the relation between exercise intensity and ventilatory gas analysis, as measured during cardiopulmonary exercise testing. Lactate measurement is often replaced by expiratory gas analysis during cardiopulmonary exercise testing. Start of the exponential rise of ventilation (to eliminate the excess carbon dioxide (CO2) that is produced because of lactate accumulation), compared to oxygen consumption (Vo2), also identifies the ventilatory anaerobic threshold (VAT). An even more pronounced rise in ventilation, compared to CO2 production, marks the respiratory compensation point (RCP). This is the point beyond which buffering mechanisms have reached their maximum and acidosis occurs. This evolution explains why, beyond past the RCP, further continuation of exercise is limited and is accompanied by excessive hyperventilation. Markers of ‘true’ maximal effort, necessary in order to determine Vo2peak: failure of Vo2 to further increase, despite increasing work rate (so-called ‘Vo2 plateau’); attainment of RCP; increase of respiratory exchange ratio (CO2 production/Vo2) above 1.1–1.15.

Electrical devices are increasingly implanted in CHF patients. Exercise testing is useful to determine the workload threshold, above which heart rate might inappropriately trigger implantable cardioverter defibrillator (ICD) shocks. Moreover, CPET is the optimal exercise testing modality to guide fine-tuning of biventricular pacemakers during exercise.

The disadvantages of CPET, such as the need for expertise, dedicated equipment and associated costs, have led to a search for alternatives. Submaximal exercise evaluation using the 6 min walk test is increasingly implemented to assess the effects of drug treatment and other interventions. Although reproducibility seems acceptable, improvement as a mere result of repetitive testing may be problematic. In order to prescribe exercise intensity or to accurately determine prognosis in CHF patients, CPET cannot be substituted by the 6 min walk test.

Practical implementation of exercise training in CHF patients

Patient evaluation before exercise training

Box 1 summarises the history and clinical evaluation of CHF patients, who are potential candidates for ET. Comorbidities that may prevent adequate training or impose additional risk need to be identified and addressed properly. It is strongly recommended to fully optimise evidence based pharmacological treatment and electrical devices before starting the ET program. Since many centres will use target heart rate to define exercise training intensity, changing β-blocker dose, for example, during the actual training programme will interfere with prescribed exercise intensity. High resting heart rate will identify patients who might benefit from up-titration of β-blockade. It also identifies patients with a small heart rate reserve (difference between maximal and resting heart rate), and, as a consequence, limited capacity to increase aerobic performance. On the other hand, combining different treatment modalities, such as cardiac resynchronisation therapy (CRT) and ET, will yield superior results, and ET should be started after implantation.

Box 1 Patient assessment before exercise training (ET)

  1. History and clinical examination:

    • Symptoms, NYHA classification, signs of congestion

    • Exercise induced angina or arrhythmia

    • Compliance with diet and pharmacological treatment

    • Comorbidities, some of which may complicate ET (eg, locomotor problems and frailty, obstructive lung disease, diabetes mellitus causing glucose fluctuations during exercise)

  2. Treatment assessment: optimal pharmacological treatment and implantation of electrical devices based on current guidelines

  3. Resting ECG: sinus rhythm or atrial fibrillation, resting heart rate

  4. Laboratory testing: blood urea nitrogen (BUN), creatinine, electrolytes, haemoglobin, cardiovascular risk factors, biomarkers

  5. Echocardiography: degree of systolic dysfunction, dimensions, left ventricular filling pressures, pulmonary arterial pressure, valve dysfunction

  6. Anthropometric measurements: weight, length, body mass index, body composition (% lean and fat mass), muscle strength

  7. Cardiopulmonary exercise testing

Electrolyte abnormalities and impaired renal function are common findings in patients on diuretics and should be corrected first. In addition, cardio-renal anaemia has been demonstrated in up to 30% of large CHF populations. Anaemia as such will impair aerobic capacity and may elicit exercise induced myocardial ischaemia. Echocardiography is the preferred tool to obtain additional imaging. It supplements clinical assessment by providing measurements of filling pressures and the degree of compensation, and identifies underlying valve disease. Box 2 provides information on contraindications for ET in CHF patients. It is important to assess carefully current symptoms and signs of congestion, since safety and efficacy of ET have not been sufficiently studied in unstable and NYHA functional class IV patients.

Box 2 Contraindications for exercise training

Cardiac

  1. Symptoms and signs of congestion, unstable or NYHA functional class IV

  2. Exercise training induced:

    • Myocardial ischaemia

    • Hypotension

    • Non-sustained or sustained ventricular tachycardia

    • Atrial fibrillation (until resolved)

  3. Valve dysfunction that is amenable to surgery

Extracardiac

  1. Active inflammatory disease, fever, including peri-myocarditis

  2. Cerebrovascular or musculoskeletal disease preventing exercise testing or training

  3. Severe obstructive lung disease, leading to arterial oxygen desaturation

  4. Uncontrolled diabetes, thyroid dysfunction, hypo- or hyperkalaemia, hypovolaemia

Intuitive concerns about training patients with severely impaired left ventricular dysfunction or remodelling are not supported by objective demonstration of harmful effects. Many CHF patients that are considered too old, or have developed severe muscle wasting, improve their physical performance with the help of an adapted training programme. Whereas the implementation of electrical devices may caution both physicians and patients to avoid exercise, ICD and CRT patients can safely participate in an exercise training programme with favourable results. Although reports are limited to small series, the spectrum of underlying disease severity is progressively broadened. Patients with primary pulmonary hypertension, patients activated on a transplant list, and even those supported with assist devices seem to derive benefit from tailored ET.

Exercise training: modality, intensity, duration, frequency

There is a considerable gap between the firm recommendations to implement ET in CHF patients and the lack of clearly delineated practical guidelines. Each training facility seems to use its own recipe, which varies in setting (home based versus supervised), duration, frequency, exercise modality and intensity, fitness equipment, exercise testing, etc. Because of the differences in training facilities, and even more relevant, the diversity of patients in terms of exercise capacity and specific physical limitations, centres usually apply ‘tailored’ instead of a universal exercise prescription.

Typically, rehabilitation services start mobilisation and education early on, during hospital admission, and set the stage to discuss and to motivate CHF patients to engage in formal ambulatory ET. For patients residing in remote areas, initial in-hospital training might be an option, followed by home based training after a couple of weeks. In most European countries, however, training programmes consist of ambulatory supervised sessions, usually three (to five) times weekly, during a period of 12–16 weeks. Duration of training is variable, depends on initial physical capacity, and will evolve as patients get fitter and stronger. For severely debilitated patients, exercise times as short as 10–15 min, at low intensity (40–50% of Vo2peak), sometimes repeated several times a day, are the only means of progressively increasing aerobic capacity. For those who are extremely deconditioned and struggle with severe muscle wasting, the initial focus should be on strength training in order to increase muscle force and mass, before endurance training can even be considered. CHF patients are not different from healthy subjects with regard to detraining; as soon as 2–3 weeks after exercise cessation, training effect wanes. Hence, ET is deemed to be a life long ‘treatment’.

Endurance or aerobic training

Walking, cycling, rowing, and calisthenics are the most common applied training modalities for cardiovascular patients in general, and for CHF patients in particular. Cycling is usually preferred; low workloads are possible, power output is reproducible, and the weight of the patient is supported, which reduces the risk of injuries. In addition, infrastructure requirements are manageable. Workloads that are prescribed for indoor activities cannot reliably be extrapolated to outdoor exercise, since environmental conditions may differ significantly. Beneficial effects on maximal aerobic capacity have been shown with steady state aerobic exercise at intensities that vary between 50–80% of Vo2peak, although usually intensity between 70–80% is prescribed. Because of the strong relation between heart rate and oxygen uptake, similar percentages of heart rate peak or heart rate reserve are also used for guidance. The rate of perceived exertion (RPE; Borg scale that ranges from 6–20) should be considered as an adjunctive measure of exercise intensity, but by no means replaces objective measures. From a practical standpoint, heart rate monitors are used during actual ET and patients are instructed to aim for the heart rate achieved at the predefined percentage of Vo2peak during CPET. In case of irregular rhythm, such as atrial fibrillation, aiming at a certain workload, again at the chosen percentage of Vo2peak, is an alternative. Depending on initial exercise tolerance, exercise duration and frequency should be adapted.

The scheme in figure 3 provides a traditional flow chart for prescribing endurance ET for CHF patients. Each training session will start and end with a (5 min) warming-up and cooling-down period, involving stretching and flexibility exercises. As patients improve, duration first and then intensity can be gradually increased. Most rehabilitation centres will re-evaluate patients after 4–6 weeks, with formal CPET, in order to adjust exercise intensity and assess progression. Although used in some centres, when available, there is no formal need for remote rhythm monitoring in most patients.

Figure 3

Endurance training prescription. Each training session should start and end with stretching and flexibility exercises. Depending on the degree of physical intolerance, as assessed by objective evaluation of Vo2peak, patients are classified and exercise intensity, as well as duration of training sessions, is defined. With time, duration first, followed by intensity, are increased. It is advisable to reassess physical performance during the actual training period and to adjust training intensity accordingly.

Dynamic resistive or strength training

Classical weight lifting is a popular way of ‘body shaping’, usually practised by healthy subjects in fitness centres, but does not have a place in the rehabilitation of cardiovascular patients. Dynamic resistive exercises, on the contrary, have become an integral part of contemporary exercise programmes for low risk cardiovascular patients.7 Although much less information is available on effect and safety in CHF patients, experience is growing and initial results are encouraging. Sustained maximal isometric exercise (weight lifting) causes an excessive rise in blood pressure and lowers stroke volume. This is very different from dynamic resistive exercises. CHF patients are advised to train smaller muscle groups, which are solicited in a dynamic way, and at low to moderate intensity. Patients should be instructed in the correct lifting techniques to avoid the Valsalva manoeuvre. Most commonly, dynamic resistive exercise is integrated in so-called circuit weight training, which involves both endurance and resistive exercise training, on an alternate base. Although elastic rubber bands are useful, exact exercise intensity is difficult to assess and dedicated fitness machines are preferable.

Figure 4 illustrates how a typical resistive exercise scheme may be deployed. In order to prescribe exercise intensity, objective measurement of muscle strength and adequate reporting is mandatory. Usually, exercise is implemented at 50–70% of the one repeated maximum (1RM, the highest weight that can be lifted once with correct form throughout a complete range of motion). With multifunctional fitness machines, several muscle groups can be trained in a sequential manner, starting with small volume sets and progressively increasing. Figure 5 provides a schematic example of how endurance and resistance exercise can be combined in circuit weight training.

Figure 4

Dynamic resistive exercise training prescription. After objective assessment of the 1RM (one repeated maximum) of different muscle groups, a small set of dynamic resistance exercises, at low intensity, is started. Care is taken to avoid Valsalva manoeuvres. Again, training volume, and at a later stage, training intensity is increased. At least 1 min of recovery should be allowed in between different exercise sets. The pictures illustrate the different patterns of muscle groups, exercised by a heart failure patient.

Figure 5

Example of circuit weight training. This is a typical example of a circuit weight training programme, useful to train patients who suffer from severe muscle weakness. The initial focus clearly is on muscle strengthening, with progressive introduction of longer endurance training periods, as patients become stronger. Orange boxes = muscle strengthening; blue boxes = endurance training periods.

The added value of strength training for disabled CHF patients is that it also incorporates upper body exercises. To complete daily life tasks, CHF patients are often hindered by skeletal muscle weakness of upper limbs. Secondly, these physical tasks are usually not conducted at maximal effort. Combined endurance–resistance ET has been shown to be particularly effective in improving submaximal exercise tolerance—that is, the ability for sustained exercise, at a level before overt dyspnoea and fatigue develop.8 Lastly, haemodynamic load during exercise is determined by the percentage of muscle mass used. By increasing strength of a certain muscle group, the percentage of muscle mass solicited, in order to lift a certain weight, will be lower and hence cardiovascular load will be reduced.

Beneficial effects of exercise training

Quality of life and exercise capacity

A systematic review of randomised controlled trials on ET in CHF patients demonstrated improvement in terms of health related quality of life in seven out of nine studies.9 From the data of 848 randomised patients, a mean increase of 2.16 ml/kg/min in Vo2peak was calculated.

Peripheral changes

ET has been demonstrated to decrease circulating catecholamine concentrations, it has anti-inflammatory and anti-oxidative effects, it reduces natriuretic peptide concentrations, and increases shear stress and NO bioavailability in CHF patients.10 The latter is extremely relevant, since aerobic capacity in CHF patients strongly relates to endothelium dependent vasodilation. Regular physical training also tackles muscle wasting and restores the anabolic–catabolic dysbalance, as well as hyperactive muscle ergoreflexes.

Cardiac and haemodynamic changes

In a randomised controlled trial of moderate endurance ET in mainly ischaemic CHF patients, Belardinelli et al11 demonstrated increased myocardial thallium uptake as soon as 2 months after. In addition, diastolic function seems to ameliorate with ET, as suggested by a higher peak left ventricular filling rate.12 Although peak cardiac output increases, through higher stroke volume, Hambrecht and colleagues13 provided data to support lower peripheral vascular afterload, rather that intrinsically better myocardial performance, as an explanation.

From a recent meta-analysis, it was concluded that endurance ET reverses left ventricular remodelling.14 Significant reductions in both end-systolic and end-diastolic volumes are accompanied by enhanced left ventricular ejection fraction. The results for combined endurance–resistance training were not convincing, although these studies are fewer in number, and were conducted more recently, on top of optimised modern anti-remodelling medical treatment.

Hard end points: morbidity, mortality, and safety

Larger single centre studies conducted in this field, as well as a recently published meta-analysis,15 have suggested significant benefit in terms of hard end points. Because of the lack of adequate power of these trials, the multicentre randomised controlled HF-ACTION (Heart Failure: A Controlled Trial Investigation Outcomes of Exercise Training) trial was highly welcomed.16 A total of 2331 patients, with left ventricular ejection fraction ≤35% and NYHA functional class II–IV, were randomised 1:1 to either the training group or the usual care group. Following 36 supervised sessions, patients in the training arm were asked to train at home and received specific instructions. After a median follow-up time of 30.1 months, it was concluded that ET for this cohort of relatively young (59 years), mainly male (72%) and moderately impaired (NYHA II–III) CHF patients was safe. There was a non-significant reduction in the risk for the primary end point (all cause mortality or all cause hospitalisation), which after adjustment for pre-defined prognostic predictors, gained significance (−11%, p=0.03). The fact that, after 3 months, the median increase in Vo2peak was only 0.6 ml/kg/min (∼4%) suggests that the training stimulus might have been insufficient. This sobering result points at the Achilles' heel of the intervention; long term adherence to ET is extremely challenging, even more so in patients with comorbidities. After 10–12 months, the median exercise time was only 74 min per week, which is considerably less than the 120 min goal. These limitations notwithstanding, there was a modest, but significant, improvement in quality of life as measured by the Kansas City Cardiomyopathy Questionnaire.

Future directions

Guidelines for the treatment of CHF, issued by the European Society of Cardiology in 2008, propose ET as a class IA indication.17 Investigations that assessed the effect of ET, however, are strongly biased against women and the elderly. As a consequence, it remains unclear whether current results can be extrapolated to the typical CHF patient, who is very likely to be over 65 years of age and female in 40–50% of cases. Because of lack of data, physical training for heart failure patients with preserved ejection fraction, who suffer equally from impaired exercise tolerance, was not discussed in this paper.

The major obstacle to benefiting fully from structured ET programmes is related to poor long term compliance. A dose–response analysis of the HF-ACTION trial strongly suggests that with increasing exercise volume, maximal exercise capacity, quality of life, hospital admission, and mortality significantly improve.18 Clinical (eg, comorbidity) as well as psychological (eg, depression) and socioeconomic factors may influence compliance with ET, but adequate strategies to enhance adherence remain to be further developed and tested. A successful way to increase long term benefit of ET should include patients' personal input. In a randomised pilot trial, we recently demonstrated that activities that match individual preferences, including group activities, involving family or friends, help patients to continue their effort.19 Other training modalities, such as aerobic interval training,20 as well as the identification of possible responders, a priori, are necessary to develop more efficacious exercise programmes and optimise the use of limited resources.

Exercise training in patients with heart failure: key points

  • Exercise training (ET) is an evidence based adjunct treatment modality with a strong impact on physical performance and quality of life.

  • Tailored ET is advised instead of a ‘one size fits all’ approach.

  • Cardiopulmonary exercise testing is the method of choice to evaluate exercise capacity objectively and define training intensity.

  • Thorough assessment of patients before training is necessary, but restrictions to ET have been progressively abandoned.

  • The benefits of ET entail both central and peripheral adaptations and are clinically translated into anti-remodelling effects, reduced morbidity and mortality.

  • Poor long term adherence to exercise prescription is the main obstacle to durable effects.

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References

  1. Data from a cohort of 2105 heart failure patients confirm that, even in the β-blocker era, Vo2peak is a strong and independent predictor of mortality.

  2. Comprehensive overview that provides insight into how exercise training in CHF patients affects peripheral determinants of exercise intolerance.

  3. Important and general information on how functional capacity in cardiovascular patients should be assessed.

  4. Up-to-date review on the indications for CPET, providing thorough insights into both exercise physiology and the multitude of parameters that can be derived from exercise testing, supplemented with ventilatory expired gas analysis.

  5. Scientific statement on the current applications of resistance training in cardiovascular patients.

  6. Thorough meta-analysis on the impact of ET in CHF patients, including quality of life and exercise capacity.

  7. Review on current knowledge of mechanisms by which ET has beneficial effects in patients with CHF.

  8. First large randomised study showing the significant benefit of endurance ET in CHF patients on endothelial dependent vasodilation.

  9. Meta-analysis on the effect of ET in terms of reversed left ventricular remodelling and systolic function in patients with CHF.

  10. Important information in this meta-analysis consists of the demonstration of a significant reduction in both hospitalisation rate and mortality for patients allocated to ET.

  11. Largest randomised controlled trial conducted to date, in which more than 2000 CHF patients were allocated to ET or usual care. After predefined adjustment for prognostic determinants, the combined end point of all cause mortality or all cause hospitalisation was reduced by 11%.

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Footnotes

  • Competing interests In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. The authors have no competing interests.

  • Patient consent Obtained.

  • Provenance and peer review Commissioned; not externally peer reviewed.

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