Fatigue in patients with cardiovascular disease

Annales de réadaptation et de médecine physique 49 (2006) 392–402 http://france.elsevier.com/direct/ANNRMP/

Literature review

Fatigue in patients with cardiovascular disease J.M. Casillas a,*, S. Damak a, J.C. Chauvet-Gelinier b, G. Deley a, P. Ornetti a a

Inserm ERITm 0207, pôle rééducation–réadaptation, CHU de Dijon, 23, rue Gaffarel, 21079 Dijon cedex, France Service de psychiatrie et d’addictologie, CHU de Dijon, 3, rue du Faubourg-Raines, 21079 Dijon cedex, France

b

Received and accepted 3 April 2006

Abstract Fatigue is a frequent complaint during cardiovascular disease and can sometimes constitute the first clinical manifestation of this disease. It is responsible for deterioration of the quality of life and prognosis. Although physical and mental fatigue are often intimately interrelated, these two aspects of fatigue correspond to different pathophysiological mechanisms and different clinical features and the neurobiological links between the two are only just beginning to be studied. Physical fatigue is related to loss of efficacy of the effector muscle, due to multiple causes: mismatch of cardiac output during exercise, muscle and microcirculatory deconditioning, neuroendocrine dysfunction, associated metabolic disorders. Mental fatigue corresponds to predominantly depressive mood disorders with a particular entity, vital exhaustion. The diagnostic approach is designed to eliminate other organic causes of fatigue. Functional tests investigating physical (exercise capacity) and mental dimensions (mood disorders) can be used to analyse their respective roles and to propose personalized management, in which rehabilitation has an essential place due to its global approach. The objective of this reduction of fatigue is threefold: to improve independence, to improve quality of life and to limit morbidity and mortality. © 2006 Elsevier SAS. All rights reserved. Keywords: Cardiovascular diseases; Depression; Fatigue; Heart failure; Rehabilitation

1. Introduction Fatigue can be defined as an unpleasant feeling of inability to perform physical or intellectual efforts (physical fatigue, mental fatigue), occurring prematurely during activity and resulting in an alteration of the subject’s usual performances and quality of life. It is a key symptom in the course of cardiovascular disease [163], as it constitutes a common presenting complaint, although its real prevalence has not been clearly established, essentially due to the difficulty of quantifying fatigue [92]. It is particularly frequent in heart failure and is often associated with a 50% reduction of physical capacities [93,163], but it is also observed during coronary artery disease without ventricular dysfunction. The intermittent claudication of peripheral artery disease is a localized form of muscle fatigue.

* Corresponding

author. E-mail address: [email protected] (J.M. Casillas).

0168-6054/$ - see front matter © 2006 Elsevier SAS. All rights reserved. doi:10.1016/j.annrmp.2006.04.003

This review will successively discuss the pathogenesis and assessment of fatigue in atheromatous disease, before considering the management of fatigue. 2. Pathogenesis of fatigue in cardiovascular disease The distinction between physical fatigue and mental fatigue appears to be more appropriate than the classification between peripheral fatigue (process intervening distal to the neuromuscular junction) and central fatigue (process intervening proximal to the neuromuscular junction) [21]. This approach, based on physical and mental dimensions, facilitates correlations with the clinical reality of cardiovascular disease. The common step is the final phase of integration of sensations in the brain (interoceptive sensitivity). We will not discuss this step in detail, as it is poorly elucidated, but probably has a similar organization to that of pain, pleasure and arousal, involving, in particular, dopaminergic and serotoninergic mediators. Analysis of this process is complicated by its subjective components [44]. The proposal of complex models integrating the various aspects of

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fatigue therefore appears to be a promising approach for the future [1]. 2.1. Physical fatigue Physical fatigue corresponds to loss of efficiency of the effector muscle, which can be due to very diverse causes in the context of cardiovascular disease, as several steps of energy production can be altered, resulting in real exercise intolerance: ● this is primarily due to mismatch of cardiac output to the body’s needs. It may be due to heart failure related to disorders of contractility (systolic heart failure) or left ventricular filling (diastolic heart failure) [135], diagnosed in routine clinical practice on the basis of clinical, echocardiographic, metabolic (VO2) and laboratory (Brain Natriuretic Peptide) criteria. However, these situations are complex and intricate, involving, in particular, preload and afterload as well as abnormalities other than ischaemic heart disease (valvular heart disease, arrhythmias, ventricular desynchronization, etc.). Consequently, determination of ventricular ejection fraction at rest, which is widely used in the diagnosis of heart failure, is not correlated with exercise intolerance [36,165]. Measurement of gas exchanges during exercise is a more valid marker and a reliable prognostic factor [98]. Although it is used in Weber’s classification to diagnose the severity of heart failure [160], it cannot distinguish the central component (cardiac output) from the peripheral component (arteriovenous oxygen difference) of the oxygen transport and utilization chain. Certain noninvasive measures, currently under development, provide additional information on the haemodynamic abnormalities responsible for exercise intolerance: systolic and diastolic echocardiographic parameters at rest and at the end of exercise linked to tissue Doppler [44], measure of cardiac output on exercise by thoracic impedancemetry [31] and by inert gas rebreathing [52]; ● muscle fatigue is also related to the peripheral muscle deconditioning inducing poor adaptation to exercise. This form of exercise intolerance is dominated by alteration of muscle oxidative metabolism. Phosphorus 31 nuclear magnetic resonance spectroscopy has demonstrated the consequences of muscle deconditioning with premature acidosis associated with creatine phosphate depletion during exercise and an abnormally long creatine phosphate resynthesis time during the recovery phase [37]. These abnormalities are particularly marked in patients with heart failure [42], also associated with impaired muscle aerobic metabolism leading to premature lactic acidosis during exercise [97]. This deconditioning is often worsened by a sedentary lifestyle, a major risk factor for cardiovascular disease [89], but also by decreased physical activity reduction as a result of exercise-induced symptoms (angina, intermittent claudication, palpitations, malaise, etc.): the patient limits his or her activity to avoid inducing anxiogenic painful symptoms;

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● an alteration of endothelial function is also responsible for disorders of microcirculatory adaptation in cardiovascular disease. Exercise capacity is limited according to the degree of alteration of NO-dependent vasodilatation [125,170]. The combination of muscle metabolic disorders and perfusion disorders during chronic heart failure plays a predominant role compared to insufficient cardiac output in the pathogenesis of exercise intolerance [164]; ● Neuroendocrine disorders, especially stimulation of the sympathetic nervous, renin-angiotensin-aldosterone and arginine-vasopressin systems, are increasingly incriminated in the pathogenesis of cardiovascular disease, particularly heart failure. These disorders are responsible for numerous harmful effects that impair exercise capacity: vasoconstriction, increased peripheral resistances, increased blood volume, ventricular remodelling [32,123]; ● respiratory impairment is frequent in severe heart failure, related to abnormalities of the ventilation/perfusion ratio [159] and responsible for harmful reflex hyperventilation probably due to excessive activation of muscle chemoreceptors and ergoreceptors [132]. Fatigue is then aggravated by dyspnoea, which is usually correlated with increased pulmonary artery pressure [98]. Respiratory failure can be related to chronic obstructive pulmonary disease associated with cardiovascular disease, as both diseases share a major risk factor, smoking; ● metabolic diseases associated with cardiovascular diseases (dyslipidaemia, diabetes, obesity) can worsen exercise intolerance [153], and insulin resistance is particularly involved in muscle deconditioning associated with heart failure [34]. 2.2. Mental fatigue Mental fatigue usually corresponds to a feeling of loss of vitality, lassitude, and the term “asthenia” is often used. A depressive tendency is predominant. In cardiovascular disease, this mental fatigue is more frequent in women [148]. These mood disorders can constitute all of the patient’s symptoms and must not be neglected, as they determine the prognosis. Advanced forms of mental fatigue essentially present in two ways: 2.2.1. Vital exhaustion Vital exhaustion is an entity associating unusual and persistent fatigue, loss of energy, a feeling of dejection and irritability [11]. It represents a risk factor for cardiovascular morbidity and mortality comparable to dyslipidaemia [12,121,129], and can be at least partially explained by an abnormal lipid profile [83] or decreased fibrinolytic capacity [86]. Various neurobiological hypotheses have been proposed, based on dysfunction of the hippocampus [45]. The type of personality plays an important role in development of this syndrome. Patients presenting anxiety and social inhibition (type D of 16-item Personality type-D Scale) [39] are the most frequently affected [116]. Similarly, pattern A (combining impatience, competition and compulsive workers),

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essentially considered in its “hostility” dimension, would act synergistically with vital exhaustion to generate coronary events [85]. Moreover, vital exhaustion resembles depression and is often associated with depression in cardiovascular disease [168], as the sadness, apathy and psychomotor retardation characteristic of depression are often associated with fatigue and irritability [102]. 2.2.2. Depression Depression is frequent in the course of cardiovascular disease [75,109]. It affects about 50% of post-infarction patients [50,141] and during chronic heart failure [60]. Also it represents an independent risk factor that significantly increases the morbidity and mortality [15,51,118]. The reduction of heart rate variability, reflecting a hyperadrenergic state, predisposing to arrhythmias [96], and correlated with depression in coronary patients, partly explains this impact [156]. Depletion in cerebral neurotransmitters, essentially serotonin, is involved in this autonomic dysregulation [8]. These findings open the way to new treatment options [101], as the links between mood disorders and the development of cardiovascular disease are beginning to be clarified by progress in neurobiology, involving neuronal circuits, neurotransmitters (serotonin, dopamine, etc.) and gene transcription of protein synthesis in the pathogenesis of depression [82]. The neurobiological approach to behaviours leading to the development of cardiovascular disease, especially addiction to smoking, is a very likely approach of the future [81] in order to explain, in particular, the link between depression and addiction [87]. 3. Diagnostic approach 3.1. Distinguish between fatigue and dyspnoea Fatigue is a subjective, polymorphic symptom that is difficult to analyse. However, it must be evaluated in routine clinical practice because one of the major objectives of treatment in cardiovascular disease is to reduce this unpleasant feeling. The clinician must start by distinguishing fatigue from dyspnoea which may be associated: difficulty breathing, accompanied by feeling of discomfort or oppression. The presence of dyspnoea associated with fatigue in a patient with cardiovascular disease is an argument in favour of an organic cause for these symptoms.

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This evaluation can be limited to a simple walk test or may require more sophisticated investigations; the second step consists of eliminating an aetiology other than cardiovascular disease (infection, cancer, inflammatory syndrome, neuromuscular disease, etc.) by complementary investigated guided by clinical findings; it is then essential to ensure that one of the problems frequently associated with cardiovascular disease is not responsible for fatigue or does not exacerbate fatigue. Multiple and interrelated causes are frequently observed. The list is long: hypertension or hypotension, drug treatments (betablockers, cardiac glycoside overdose, diuretics, etc.), fluid and electrolyte disorders (potassium, sodium), uncontrolled diabetes mellitus, anaemia, combination of sleep apnoea, chronic respiratory failure, renal failure, liver disease, endocrine causes (hypothyroidism or hyperthyroidism), etc. At least a laboratory work-up must be performed (complete blood count, liver function tests, serum electrolytes, serum creatinine, uraemia, thyroid function tests, blood glucose, proteinuria, etc.). Sleep apnoea syndrome raises a particular problem, as this is now a frequently identified cardiovascular risk factor, which, due to the associated asthenia and daytime sleepiness, raises problems of differential diagnosis with common fatigue [29]. The indications for nocturnal measurement of oxygen saturation and polysomnography must therefore be very large, as the prevalence of this syndrome is more than 50% in patients with heart failure [137] and real treatment options are available [134]; an associated disability (neurological, orthopaedic, etc.) able to explain or at least worsen exercise intolerance by the excess energy expenditure that it induces, must be excluded; early cognitive disorders may present in the form of mental fatigue and are frequent in chronic heart failure. Impaired intellectual performance can be secondary to cerebrovascular disease or decreased cerebral blood flow, which can be induced by exercise [73]. Impaired cognitive performance can be detected by psychometric tests.

3.3. Evaluate fatigue related to cardiovascular disease When a cardiovascular origin is considered to be probable, fatigue must be quantified and its physical and/or mental dimension must be specified, as physical and mental factors are usually interrelated.

3.2. Eliminate another cause for fatigue

3.3.1. Circumstances of onset The circumstances of onset can help to guide the diagnosis:

● The first step consists of distinguishing physiological physical fatigue occurring after intense or even unusual exercise. This is not always easy in practice, as fatigue is such a common symptom, frequently described in vague terms, often by elderly patients with reduced functional capacities. In these circumstances, evaluation of exercise capacity is particularly useful to eliminate real exercise intolerance.

● in favour of an organic cause: fatigue increasing during the day, stable, without major mood disorders, related to exercise and improved by rest; ● in favour of a psychological origin: starts in the morning, associated with apathy, sleep disorders and sexual disorders, loss of appetite, variable over time, not improved by rest and sometimes paradoxical positive effect of activity. It is

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particularly important to detect depression, as it can determine both the functional and the vital prognosis. Finally, the search for stressful of life events (bereavement, work stress, retirement, etc.) also appears to be necessary, due to the intricate relations between these events, depression and cardiovascular disease [122]. However, these circumstances of onset are not sufficient and objective assessment of fatigue is essential. It is based on a battery of tests designed to quantify the various physical and mental dimensions of fatigue. 3.3.2. Generic scores The use of a fatigue score would appear to be the simplest and least expensive methodology. However, it is insufficient as it is unable to discriminate between the mental and physical components, and it is not correlated with objective physical parameters such as the exercise test in patients with coronary artery disease [38] or peak VO2 in chronic heart failure [166]. Most generic scores validated in French are designed to evaluate fatigue correlated with cancer [46,57]. They investigate the behavioural, physical, cognitive and affective dimensions. Rhoten’s score [127] is one of the simplest to use, as it is composed of a visual analogue scale from 0 (no fatigue) to 10 (total exhaustion) and is correlated with the Multidimensional Fatigue Inventory comprising 20 items evaluating physical and mental aspects [46,136]. It is similar to the visual analogue scale developed by Krupp for multiple sclerosis [88]. Piper’s score comprises 22 items each scored from 0 to 10 [57]. Pichot’s scale comprises three themes, including one for fatigue composed of eight questions with four levels of response that is easy to complete, and a score greater than 20 is considered to be pathological [119]. There is also a large number of generic scores not validated in French that will not be discussed here [20,71,72,103,105,131,139,151,155,161]. Note that the Dutch Fatigue Scale [164] has been validated in patients with heart failure [146]. By definition, these generic scores are unable to distinguish the respective roles of physical and mental components of fatigue in cardiovascular disease. A more specific approach is therefore necessary. 3.3.3. Assessment of physical fatigue In practice, this assessment is based on clinical interview and demonstration of objective signs of fatigue. 3.3.3.1. Specific questionnaires. As the patient’s description of his or her feelings of fatigue is insufficient and as generic scores are inappropriate, two reproducible methods adapted to large numbers of patients are proposed: ● Borg’s score: this score is used to measure the perception of the level of activity during exercise and therefore the physiological intensity of this exercise [24,25]. It comprises 15 levels on a scale ranging from 6 (very mild activity) to 20

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(very strenuous activity), and the extreme physical fatigue preceding discontinuation of the exercise corresponds to the highest levels. Borg’s score is validated to define the intensity of work during retraining, especially when heart rate cannot be used (arrhythmia, drug-induced chronotropic effect) [7], as the desired level of exercise is usually situated between 12 and 16. Borg’s score is also useful to guide physical activity in patients with stabilized heart disease [77]. However, this score presents a marked interindividual variability for equivalent levels of exercise [171]. It also appears difficult for patients to distinguish between feelings of fatigue and dyspnoea [164]; ● the New York Heart Association (NYHA) classification represents the international reference for functional evaluation of chronic heart failure based on the circumstances of onset of dyspnoea [48]: ○ I: symptoms with strenuous activity; ○ II: symptoms with moderate activity (rapid walking, flights of stairs, etc.); ○ III: symptoms with mild activity (dressing, personal hygiene, etc.); ○ IV: symptoms with the slightest activity or at rest. 3.3.3.2. Functional quantification. Observation of the usual symptoms of physical fatigue (muscle weakness, tremors, cramps, disorders of the coordination, etc.) is not sufficient to assess the severity of fatigue and to guide treatment decisions. Other objective parameters of exercise capacity must be used: ● measurement of muscle strength and endurance; Maximum muscle strength is reduced during cardiovascular disease, especially in the presence of left ventricular dysfunction. For example, maximum strength of the quadriceps is reduced by about 30% in patients with heart failure, both for isometric [28] and isokinetic [107] contractions. This deficiency affects quadriceps endurance in the same proportions and is not modified by electrostimulation [106]; This muscle fatigue can be more accurately quantified by spectral analysis applied to surface electromyography. In patients with coronary artery disease, this abnormal muscle fatigue is reflected by a premature increase of motoneuron recruitment (increased Root Mean Square with early recruitment of low frequencies evaluated by Median Frequency) [54]. Correlations between electromyographic parameters and decreased endurance and muscle strength are also observed in patients with heart failure [130]. Similar alterations demonstrated in peripheral artery disease have been shown to be reversible in response to physical reconditioning [117]; ● an exercise test represents the most conventional method to assess decreased physical performance in the context of cardiovascular disease, as fatigue constitutes the usual limiting factor during this test [166]. Data obtained from the patient’s clinical history and fatigue scores also frequently underestimate the data provided by exercise tests for the evaluation of fatigue symptoms [167];

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Measurement of gas exchanges during the exercise test allows investigation of the entire chain of oxygen binding, transport and utilization, essential for oxidative phosphorylation. It is a validated criterion of cardiopulmonary and metabolic performance [158]. When a plateau is reached during a progressive exercise test, it usually means that the patient’s maximum capacities have been reached [144]. In subjects with cardiovascular disease, this plateau is generally not reached and, in these subjects, the peak VO2 is determined, as it reflects maximum oxidative capacities and therefore the highest degree of physical fatigue. Weber’s classification distinguishes 4 levels of severity of heart failure as a function of peak VO2 values [160]: ○ > 20 ml/kg/min Class A: no repercussions or very mild heart failure; ○ 16 to 20 ml/kg/min Class B: moderate repercussions; ○ 10 to 15 ml/kg/min Class C: marked repercussions; ○ < 9 ml/kg/min Class D: severe repercussions. The ventilatory threshold corresponds to a hyperventilation phenomenon during the progressive exercise test. It provides complementary information to peak VO2. It can be defined as the point beyond which there is a non-linear increase of the ventilatory equivalent for oxygen (VE/VO2), with no concomitant elevation of the ventilatory equivalent for carbon dioxide (VE/VCO2) [157]. In contrast with peak VO2, it is a submaximal parameter independent of patient motivation [111]. It corresponds to a well tolerated level of exercise (preceding onset of physical fatigue) and effective in terms of physical reconditioning especially in the case of heart failure [104]. The slope of the VE/VCO2 relation has been more recently demonstrated to be an objective parameter of exercise capacity, as it reflects oxygen extraction in the lungs and oxygen utilization in the muscles. An increase of this slope indicates decreased exercise capacity [150]. The slope of the relation between VO2 and the power developed during an exercise test also represents a marker of energy efficiency, as reduction of this slope is correlated with the severity of heart disease [78]. The essential limitation of this metabolic analysis remains the difficulty of distinguishing between the peripheral component (muscle) and the central component (cardiac) of exercise intolerance. The use of noninvasive methods to determine cardiac output during exercise, such as thoracic impedancemetry [31] and inert gas rebreathing [52], and evaluation of the oxygen extraction capacity in muscles by the infrared spectroscopy technique [61], should allow more reliable quantification of these components in the future. Furthermore, in patients with severe ventricular dysfunction, infrared spectroscopy can demonstrate cerebral hypoperfusion during exercise and recovery [84] and could constitute a method of detecting the harmful effects of exercise; ● Walk tests; A walk test is a complement or even an alternative to the exercise test for the analysis of exercise capacity. A standardized walk test can therefore be proposed in order to confirm the reality of physical fatigue. The 6-minute walk test is the most

extensively validated test and the most widely used in the context of cardiovascular disease, especially in patients with heart failure [63]. It constitutes a prognostic factor for morbidity and mortality [23] and is correlated with aerobic capacities and NYHA classification [85]. It is reproducible and particularly adapted to elderly patients who are unable to perform a maximum exercise test [113]. It represents a simple method of evaluation of the efficacy of a treatment for exercise intolerance [115,138]; ● physical activity is reduced in the case of chronic fatigue and quantification of physical activity is part of the evaluation of the global functional repercussions. Usual methods are based on the use of specific scores or accelerometric methods [30]. 3.3.4. Evaluation of mental fatigue 3.3.4.1. Generic measuring instruments. To our knowledge, no score validated in French has been developed to specifically measure mental fatigue in the course of cardiovascular disease. The Maastricht questionnaire, comprising 21 items each classified according to 3 levels, has been used to define vital exhaustion and relate this syndrome to the development of coronary events [9,10]. The Global Mood Scale comprises 20 items investigating negative aspects (malaise, fatigue) and positive aspects (energy, sociability) of the mental state of patients with coronary artery disease [38]. It has demonstrated the positive impact of retraining and the absence of a predictable correlation between this score and exercise capacity data. 3.3.4.2. Clinical approach to fatigue in depression: data derived from the clinical interview. Several clinical features can sometimes be helpful to identify mental fatigue in major depression, starting with the typical chronology with very severe symptoms at the beginning of the day (where even the slightest activity becomes an effort), classically followed by improvement in the evening [55]. A particular form of mental fatigue corresponds to the concept of psychomotor retardation in depression, ranging from moderate loss of vitality (minimal lethargy) to major asthenia, when the patient is constantly bedridden. Various degrees of loss of mental energy can therefore be detected according to the impact of depression. The depressed subject may complain of a simple lack of energy, then suffer from a massive loss of motivation (abulia), and finally present major psychomotor inhibition constituting an extreme catatonic form of melancholia. The mental component of fatigue in the course of major depression therefore takes on very specific clinical forms that should be recognized and quantified by means of validated measuring instruments. 3.3.4.3. Major depression measuring instruments. The depression scores used during cardiovascular disease are: the Beck Depression Inventory [18,141], the Hamilton Depression Scale [17,70,140,142,156], the Hospital Anxiety and Depression

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Scale [74], the Structured Clinical Interview for DSM-IV [47, 150], and the 90-item Symptom Checklist [41]. 3.4. Assess the repercussions on the patient’s independence and quality of life This is the most global dimension of the evaluation, designed to assess the efficacy of therapeutic intervention on fatigue related to cardiovascular disease. Generic disability scales can be used to assess independence when the functional repercussions of this fatigue are severe, essentially advanced heart failure in the elderly, who frequently present multiple disabilities. The Functional Independence Measurement (FIM), the AGGIR scale, or Barthel’s index [94] can be used. The most widely used quality of life scales are generic scales allowing comparison with other types of diseases [80]. They are essentially the MOS SF-36 (Medical Outcome Study 36-item Short Form), the NHP (Nottingham Health Profile), the SIP (Sickness Impact Profile) or even the Euro-QoL [6]. The SF-36 is the scale most frequently used. Specific quality of life scales are available, essentially designed for chronic heart failure: the MLwHF (Minnesota living with Heart Failure) [90], validated in French [27], is the scale most frequently applied. The combination of a generic score and a specific scale is recommended [64]. 4. Management of fatigue in the course of cardiovascular disease 4.1. Physical fatigue 4.1.1. Some pharmaceutical treatments Some pharmaceutical treatments can act on the clinical features of fatigue. A reduction of neuroendocrine abnormalities by angiotensin-converting enzyme inhibitors and beta-blockers is one of the leading objectives of treatment in cardiovascular disease, resulting in a reduction of morbidity and mortality. Angiotensin-converting enzyme inhibitors are part of the firstline treatment of heart failure, as, in the same way as diuretics, they reduce symptoms by improving exercise tolerance [162]. There is an growing body of evidence in favour of the prescription of angiotensin-converting enzyme inhibitors to all patients with cardiovascular disease, even without ventricular dysfunction [133], and angiotensin receptor antagonists can be used in the case of intolerance [56]. Note that concomitant treatment with a beta-blocker (or an alpha blocker) does not reduce this impact on exercise capacity in patients with moderate heart failure [49]. Aldosterone antagonists have also been shown to have a complementary impact during heart failure [35]. Insulin resistance, which is a major cardiovascular risk factor, especially for the development of heart failure, is involved in exercise intolerance, particularly due to the alterations of muscle metabolism [34]. Glitazones, a new class of oral antidiabetic drugs acting on insulin resistance, improve physical capacities in type 2 diabetes [124].

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4.1.2. Non-pharmaceutical treatments Non-pharmaceutical treatments are also designed to improve symptoms by acting on haemodynamic conditions. The list of such treatments is long, reflecting technological progress: coronary revascularization, ventricular resynchronization (multisite stimulation), heart transplantation, ventricular assistance, artificial heart, cell therapy (stem cells), gene therapy, etc. 4.1.3. Physical reconditioning Physical reconditioning occupies a special place, as it acts on various alterations responsible for physical fatigue: ● on cardiac function: increased myocardial perfusion [33] due to improvement of coronary endothelial function [67]. This allows an improvement of cardiac output during exercise in patients with stable coronary artery disease [59,108] and an increased ejection fraction in patients with heart failure [68], although this does not appear to be constant [99]; ● a mean increase of 20% of maximum aerobic capacities due to a predominant impact on muscle oxidative metabolism: increase of oxidative enzyme performances and capillary density in striated muscle fibres in patients with coronary artery disease [4,147], with a similar impact, demonstrated for a long time, on occlusive peripheral artery disease [76]. The improvement of muscle oxidative capacities in patients with heart failure can be demonstrated by phosphorus 31 nuclear magnetic resonance spectroscopy with reduction of the depletion of creatine phosphate and ADP synthesis during exercise and acceleration of creatine phosphate resynthesis during the recovery phase [2]; ● reduction of peripheral resistance by improvement of endothelial dysfunction resulting in more effective muscle perfusion [58]. Reduction of peripheral resistance, together with reactivation of NO-dependent vasodilatation [26], participates in improvement of aerobic performances in patients with coronary artery disease or heart failure [66]; ● reduction of the hyperadrenergic state with restoration of autonomic regulation [95] associated with increased heart rate variability [169] and an antiarrhythmic effect [22] in patients with coronary artery disease without ventricular dysfunction and in patients with heart failure [3]; ● metabolic impact: improvement of dyslipidaemia [43,152], control of obesity [126], reduction of insulin resistance [172]; ● improvement of ventilatory capacities in patients with heart failure [99] with improvement of alveolocapillary diffusion [62], contributing to resolution of dyspnoea. These effects of physical reconditioning result in lowering of the fatigue threshold with improvement of exercise capacity in patients with heart failure [19] or stable coronary artery disease [59]. The effects of physical reconditioning in patients with stable coronary artery disease are superior to those observed after angioplasty [69]. In patients with intermittent clau-

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dication, the claudication distance is improved by an average of 150% after physical reconditioning [91].

after rehabilitation for peripheral artery disease with [53] or without intermittent claudication [100].

4.1.4. Ergonomic measures Activity management education (distribution of tasks and rest periods to avoid reaching an excessive level of fatigue), domotic devices, technical aids, and domestic help will be necessary when the severity of the fatigue affects the patient’s independence. These compensatory measures are essentially used in severe heart failure, and are primarily designed to maintain the patient at home.

5. Conclusion

4.2. Mental fatigue

● eliminate other organic causes of fatigue as well as cognitive disorders; ● determine the physical and mental dimension of fatigue, must be based on the use of tests assessing the various aspects of the functional consequences of this fatigue, essentially depression scores and evaluation of exercise capacity. In routine clinical practice, appropriate management acting on the various factors of fatigue can be proposed on the basis of this assessment. Due to its global approach, rehabilitation occupies an important place in this management.

Various modalities of management of mental fatigue have been proposed: psychotherapy, behavioural stress management techniques, relaxation, pharmacological treatments. Psychological management can improve vital exhaustion and reduce the associated cardiovascular morbidity [14]. Coronary angioplasty does not appear to have the same impact [13]. Note that patients with a type D personality tend to be refractory to treatment, especially retraining [40]. In the context of depression, serotonin reuptake inhibitors can improve heart rate variability after acute coronary syndrome, reflecting correction of the autonomic equilibrium in favour of the parasympathetic system [101]. They are also present a better cardiovascular safety than tricyclic antidepressants [79]. However, there is no experimental evidence of the efficacy of treatment on cardiovascular morbidity and mortality at the present time. Multifactorial treatment of depression is now an integral part of the global management of patients during retraining [16]. Achievement of the defined objectives of physical reconditioning appears to be a decisive factor for improvement [128]. Relaxation techniques are effective, particularly on mood disorders and somatic symptoms of cardiovascular disease [149].

Fatigue is a frequent complaint among patients with cardiovascular disease. It directly determines their daily activities, their independence and quality of life. The mental component of fatigue is now considered to be a risk factor for cardiovascular morbidity and mortality. However, fatigue is difficult to analyse in view of its subjective nature. A diagnostic approach designed to:

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4.3. Global management Global management corresponds to optimal control of risk factors and is designed to slow the progression of atherosclerosis while limiting the symptoms of cardiovascular disease. Cardiac rehabilitation, due to its multidisciplinary intervention, integrates both personalized secondary prevention measures and physical reconditioning [5]. It helps to limit progression of coronary artery disease [65,110]. The clinical efficacy of physical reconditioning has been confirmed by several meta-analyses demonstrating a 20% to 25% reduction of cardiovascular mortality after retraining in patients with coronary artery disease [112,114,145] or heart failure [120]. The probable impact of this control of progression of atherosclerosis on fatigue has not been evaluated. In contrast, the improvement of quality of life in response to cardiac rehabilitation has been demonstrated in these patients [143,154], and

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