Beneficial effects of exercise

There are multiple benefits of exercise for patients with VHD. A 12-week aerobic exercise programme for symptomatic women with MVP revealed that compared with control subjects, the exercise group showed an improvement in functional capacity and well-being, with an associated reduction in anxiety scores and the frequency of symptoms.8 Exercise-based rehabilitation prior to cardiac surgery is associated with a lower risk of post-surgical complications and reduction in the length of hospital stay.9 Similarly, aerobic exercise, when initiated early after cardiac surgery, has demonstrated improved functional capacity and quality of life.10 In an animal model, regular exercise at an early age prevented the development of aortic valve sclerosis by preservation of endothelial integrity, reduction in inflammation and oxidative stress and inhibition of the osteogenic pathway.11

Potential harms of exercise

The potential adverse effects of exercise on VHD are summarised in figure 1.12–17 Consequently, patients with VHD may be predisposed to arrhythmias and adverse outcomes when participating in exercise due to the additional adrenergic surges and increased haemodynamic load on an already dilated, hypertrophied ventricle (figure 1). Endurance training causes volume loading on the ventricles, resulting in chamber enlargement, whereas isometric training increases peripheral vascular resistance, causing transient hypertension and pressure loading which may result in left ventricular (LV) hypertrophy, with most sports reflecting a mixed picture.18–20 An overlap exists between the cardiovascular adaptations to exercise and the pathophysiological effects of VHD (figure 2).17–19 21

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Figure 2

Venn diagram demonstrating the potential overlap between cardiac adaptations to exercise and valvular heart disease (VHD).17–19 21 Such adaptations are relevant to individuals who participate in high-volume (>4 hours per week), high-intensity endurance sport. LGE, late gadolinium enhancement; LV, left ventricle; LVEF, left ventricular ejection fraction; LVH, left ventricular hypertrophy; PA, pulmonary artery; RV, right ventricle; sPAP, systolic pulmonary artery pressure.

General principles

All patients with VHD should receive an exercise prescription, and should be encouraged to fulfil the minimal recommendations, unless there are specific concerns. These comprise of at least 150 min of moderate intensity aerobic exercise per week, supplemented by strength training and exercises that improve balance.22 Exercise prescription should be based on the principles of shared decision-making, particularly in the context of limited evidence to support exercise recommendations in patients with VHD. The physician should balance objective clinical parameters and existing exercise recommendations with the individual patients’ wishes and aspirations.

Assessment

A flow chart for the assessment of individuals with VHD with key considerations is shown in figure 3.

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Figure 3

Flow chart for the assessment of individuals with valvular heart disease. BP, blood pressure; CPET, cardiopulmonary exercise testing.

Step 1—history: a comprehensive medical history is necessary with particular emphasis on the underlying primary VHD diagnosis and previous interventions. Following a detailed account of cardiac symptoms, the physician should ascertain the patient’s functional status, the current type, volume and intensity of exercise and the patient’s exercise-related aspirations.

Step 2—physical examination: a thorough physical examination should be performed, including observing for any signs of connective tissue disorders.

Step 3—baseline imaging: echocardiography remains the cornerstone of assessment of VHD and should adhere to published guidelines.13 In the majority of patients, echocardiography suffices to assess the severity of the valve lesion, its impact on ventricular size and function and assessment for signs of pulmonary hypertension. Aortic diameters should be measured using standard methodology. If dilated, serial measurements are paramount as the rate of increase in aortic diameter is important for risk stratification. Cardiac MRI has an increasing role, particularly in cases where quantification of the valvular lesion is challenging with echocardiography or more detailed assessment of the ventricular size/function, aorta or myocardial tissue is necessary.

Step 4—exercise testing: the focus of exercise testing is to assess the patient’s functional capacity, exertional symptoms, the haemodynamic (blood pressure (BP)) response to exercise, and identify exercise-induced arrhythmias or myocardial ischaemia. The test should reflect the intensity of the exercise prescribed. Any abnormalities detected during exercise testing should prompt further evaluation and, if required, appropriate treatment or intervention before the patient can re-enter the assessment algorithm. Cardiopulmonary exercise testing (CPET) is the investigation of choice as it enables a more comprehensive assessment of haemodynamic parameters, as well as more accurate classification of exercise intensity by identifying ventilatory thresholds, particularly in patients with impaired cardiac function or those on beta-blocker therapy (figure 4).7 23 The use of CPET is dictated by local expertise and resources and in most centres is likely to be reserved for individuals with moderate-to-severe valvular disease who engage in high volume and intensity exercise. Some individuals may require exercise echocardiography, particularly when discordance exists between symptoms and severity of valve disease. Exercise echocardiography may inform the severity of the valve lesion, long-term outcome and monitoring frequency.6 24

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Figure 4

Examples of exercise prescription based on the ‘FITT’ (Frequency, Intensity, Timing, Type) principle. The examples of exercise/sports provided across different intensities are only indicative as many can be adapted to different intensities. The haemodynamic and ventilatory threshold parameters are based on recent classification.31 ᵃRevised Borg Category-Ratio scale—scale of rating of perceived exertion ranging from 0 (no exertion) to 10 (maximal exertion). bpm, beats per minute; HR max, maximum heart rate; mph, miles per hour; RM, repetition maximum; RPE, rate of perceived exertion; VO₂ max, maximum oxygen consumption.

Step 5—exercise prescription: the physician should provide specific prescription that addresses frequency, intensity, time and type of exercise/sport as per the ‘FITT’ (Frequency, Intensity, Timing, Type) principle. The prescription should offer an outline of both aerobic and strength training, similar to what is depicted in figure 4.7 There is limited evidence to support detailed advice on strength training. High-intensity/low-repetition numbers (≥70% of 1 repetition maximum (RM)) is more effective in increasing muscle strength and evidence suggests that it may have lower acute cardiovascular demands compared with low-intensity/high-repetition numbers strength training.25 However, heavy weights and Valsalva manoeuvre exercises may induce symptoms in patients with severely stenotic lesions and one should consider increasing the number of repetitions and sets prior to increasing weights. Most cardiologists have limited knowledge of exercise prescription to offer sufficient granularity as suggested by the 2020 European Society of Cardiology Sports Cardiology guidelines. As such, they may outline the basic principles of exercise prescription and then consider referral to a health and fitness professional for further advice.

Step 6—follow-up evaluation: the specific interval of re-evaluation will be dictated by the severity of the valve lesion, the volume and intensity of exercise and whether the patient participates in recreational or competitive sport. Individuals with moderate-to-severe valvular disease who engage in high-intensity exercise are likely to require more frequent follow-up (6–12 months). New symptoms should prompt discontinuation of the patient’s exercise regime and re-evaluation.

Aortic valve regurgitation

Aortic regurgitation (AR) causes volume and pressure loading of the LV with progressive dilatation and hypertrophy. The haemodynamic impact of AR may overlap with the sequelae of high-volume, high-intensity endurance exercise and occasionally it may be challenging to distinguish physiology from pathology, particularly with eccentric jets where the severity of AR may be underestimated (figure 2). In athletic individuals, the regurgitant volume may be increased due to the lengthening of diastole as a result of increased vagal tone and subsequent bradycardia.6 Moreover, isometric exercise is associated with increased aortic wall tension and may worsen AR. In contrast, static exercise provokes a reduction in preload resulting in reduced LV stroke volume and regurgitant volume.26

Asymptomatic individuals with mild or moderate AR may participate in all levels of exercise and sports if the parameters shown in figure 5 are fulfilled. An exercise test is useful to confirm asymptomatic status and functional capacity in those with moderate or severe AR. Exercise stress echocardiography may have a role as the absence of contractile reserve is associated with deterioration of symptoms and LV function during the medium-term follow-up of initially asymptomatic patients with severe AR.24 Individuals with severe AR may participate in low and moderate-intensity exercise, if the LV is not dilated, the left ventricular ejection fraction (LVEF) remains >50%, the aortic root is within normal dimensions or mildly dilated, and exercise stress testing is normal. Low-intensity exercise should be recommended for individuals with a dilated LV, LVEF ≤50%, significant aortic root dilatation or exercise-induced arrhythmias.

Aortic stenosis

Aortic stenosis (AS) increases LV afterload, resulting in LV hypertrophy, increased myocardial oxygen demand and myocardial fibrosis. LVEF and cardiac output are usually preserved but there is a risk of sudden cardiac death due to outflow obstruction, coronary hypoperfusion and ventricular arrhythmias.7 27 In asymptomatic individuals with moderate and severe AS, exercise testing can provide information relating to haemodynamic response to exercise, inducible myocardial ischaemia and arrhythmias. A progressive drop in systolic BP (SBP) with exercise, or failure to increase SBP by at least 20 mm Hg, identifies individuals at higher risk.28 Even in the context of an asymptomatic individual with a normal exercise test, current recommendations are conservative and advise low or moderate-intensity exercise and sports in those with moderate AS and low-intensity exercise in those with severe AS (figure 5).

Bicuspid aortic valve

BAV may be complicated by AS, AR or aortopathy. The impact of exercise on patients with BAV and its natural history is not fully understood. Aortic root dimensions in patients with BAV have been shown to progressively enlarge over a 5-year follow-up period but with no significant difference between athletes and non-athletes.29 Another study of athletes with BAV, matched with sedentary individuals with BAV and athletes with a tricuspid aortic valve, did not demonstrate progression of valve disease over 3 years.30 In longer-term follow-up studies, the majority of athletes with BAV had a benign clinical course and progression of root dilatation, valve stenosis or regurgitation likely occurred independently of athletic activity.31 A cautious approach to sports activities is advisable when the ascending aorta is above normal limits. In the absence of aortopathy, exercise recommendations for individuals with BAV are identical to individuals with tricuspid aortic valve dysfunction.7 32

Mitral regurgitation

Mitral regurgitation (MR) causes volume loading on the LV and associated LV enlargement and eccentric hypertrophy in the early stages when many individuals remain asymptomatic, before decompensating causing progressive and irreversible structural and functional changes.33 Occasionally, it may be challenging to distinguish the effects of regular, high-volume, high-intensity endurance exercise from those of MR, particularly with eccentric jets where the severity of MR may be underestimated (figure 2). It is thought that repeated bouts of augmented stroke volume associated with intense exercise may exacerbate the progression of LV dilatation and secondary MR. Imaging studies have shown that secondary MR often becomes more severe during exercise or with other changes in loading conditions.34 35 The majority of these studies focus on MR in relation to ischaemic heart disease or heart failure, both of which are associated with exercise restrictions.7 Novel indices may also help to further risk-stratify individuals with MR. Studies in patients with primary and secondary MR suggest that the presence of exercise-induced pulmonary hypertension, even in asymptomatic individuals, defined as systolic pulmonary artery pressure (sPAP) ≥60 mm Hg on echocardiography, predicts development of symptoms and cardiac morbidity and mortality.36

Asymptomatic individuals with mild or moderate MR may participate in all exercise and sports if they have a good functional capacity, left ventricular end-diastolic dimension <35 mm/m² in men and <40 mm/m² in women, EF ≥60%, sPAP <50 mm Hg and absence of complex arrhythmias during exercise. Individuals with severe MR may participate in low and moderate-intensity exercise, if the above conditions are met. All other individuals should be encouraged to participate in low-intensity exercise or regular physical activity. Individuals on long-term anticoagulation therapy for atrial fibrillation should avoid contact/collision sport.

Mitral valve prolapse

MVP is the most common cause of primary MR.37 The mechanical strain of MVP on papillary muscles and the adjacent myocardium is thought to be responsible for myocardial scarring, which may predispose to potentially life-threatening arrhythmias.38 Aside from the severity of MR, current exercise guidance takes into account specific markers of increased risk of sudden cardiac death in MVP (box 1). If any of these features are present, the individual is advised to refrain from high-intensity exercise and sports.7 38–41 As arrhythmia is a key factor in MVP, investigations should include an exercise test and ECG monitor, irrespective of valve severity, particularly for those who wish to engage in high-intensity exercise. Individuals with inferior T-wave inversion or evidence of ‘uncommon’, complex or exercise-induced ventricular arrhythmia should be considered for cardiac MRI to assess for myocardial fibrosis affecting the basal inferior/inferolateral wall.39 42

Mitral stenosis

Mitral stenosis (MS) is most commonly caused by rheumatic heart disease. More recently, mitral annular calcification (MAC) has been identified as a cause of the increasing prevalence of MS in the elderly. MS obstructs ventricular filling, resulting in left atrial dilatation and hypertension, thus predisposing to atrial arrhythmias. Remodelling of the pulmonary vasculature over time results in pulmonary hypertension, so a minority of individuals with severe MS remain truly asymptomatic on exercise.43 One of the most important parameters to guide exercise is sPAP. Those with an sPAP >40 mm Hg should refrain from participating in moderate or high-intensity exercise (figure 5).6 7 Exercise testing is useful in providing additional information on an individual’s haemodynamic response to exercise and exercise-induced arrhythmias. A recent study compared exercise echocardiographic parameters in subjects with MAC who underwent symptom-limited supine bicycle exercise with a propensity-matched control group of individuals without MAC. In patients with severe MAC, the mean mitral valve gradient was greater at rest and rose more during exercise than control subjects. The same differences were seen with sPAP, derived from tricuspid regurgitation velocities. As a result, individuals with MAC had a reduced exercise time and were more likely to stop due to dyspnoea.44

Tricuspid valve disease

Tricuspid regurgitation (TR) is most commonly secondary to left heart disease or pulmonary hypertension and exercise guidance is mainly based on the underlying aetiology. The prevalence of moderate-to-severe TR increases with age, estimated to affect >5% of women aged ≥70 years.45 A study assessing invasive CPET parameters in individuals with moderate and severe TR in the absence of significant left heart disease found that these individuals had a reduced stroke volume and heart rate response and thus impaired cardiac output reserve, compared with controls. Consequently, those with TR had an impaired exercise capacity.46 According to current guidance, asymptomatic patients with TR of all severities may participate in all exercise and sports providing the sPAP is <40 mm Hg, the right ventricle is not significantly dilated with preserved systolic function and have a good functional capacity and absence of arrhythmias on exercise testing.47

Pulmonary valve disease

Pulmonary valve stenosis is usually seen in the context of congenital heart disease, while pulmonary regurgitation (PR) is commonly acquired secondary to left-sided pathology or lung disease that results in pulmonary hypertension and dilated pulmonary arteries. Individuals with mild stenosis (<40 mm Hg) may participate in all exercise and sports, while those with moderate-to-severe stenosis should refrain from participating in high-intensity exercise. Asymptomatic patients with PR of all severities may participate in all exercise and sports providing the sPAP is <40 mm Hg, the right ventricle is not significantly dilated with preserved systolic function and have a good functional capacity and absence of arrhythmias on exercise testing.48 49

Valve replacements or repairs

Cardiac rehabilitation programmes after valve intervention should be considered in all patients to facilitate graduated return to physical activity and exercise.10 The rate of progression will be dictated by the individual patient characteristics, complexity of procedure and haemodynamic and rhythm sequelae. In patients who are anticoagulated or patients who have undergone valve repair, the risks of physical trauma during athletic competition must also be considered. These individuals should be advised to refrain from high-impact, contact sports.

There are limited data on the natural history of valve replacements or repair in patients who exercise intensively. Exercise testing in these individuals, up to an intensity consistent with the sport they wish to engage in, is recommended, noting that exercise tolerance after mitral valve replacement is often much lower than after aortic valve replacement, particularly if there is residual pulmonary hypertension.50 Current guidance recommends that those who are asymptomatic with valve replacements receive the same exercise advice as those with moderate native valve disease provided the ventricular function is preserved and sPAP is within normal limits.

Conclusion

All individuals with VHD should be encouraged to reduce sedentary behaviour and engage in at least 150 min of physical activity every week, including strength training. The great majority of individuals encountered in everyday clinical practice, with mild and moderate VHD, will be able to participate in the exercise and sports they wish, including high-intensity exercise and even competitive sports. Individuals with severe VHD, particularly when associated with symptoms or adverse haemodynamic or arrhythmic sequelae, require more meticulous evaluation and are likely to be subjected to some exercise limitations.