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Lifestyle advice for patients with ICDs: physical activity – what is healthy and what is contraindicated

Implantable cardioverter-defibrillators (ICDs) have proven their effectiveness in the primary and secondary prevention of sudden cardiac death (SCD) and their indications are now well defined and outlined by international recommendations. These recommendations encompass a vast range of diseases, ranging from purely electrical abnormalities (channelopathies) in morphologically healthy hearts to extremely advanced cardiac disease with severe left ventricular function impairment. Approximately 40% of the observed reduction in SCDs is a direct consequence of a reduction in coronary heart disease and other cardiac conditions. Lifestyle modifications are thus one of the most effective approaches in preventing SCDs in the general population.

Arrhythmias, General

Keywords: implantable cardioverter-defibrillator, lifestyle, physical activity, sudden cardiac death, ventricular arrhythmias



Approximately 50% of cardiac arrests occur in individuals without known heart disease; most suffer from undiagnosed ischaemic heart disease [1]. As a consequence, the most effective approach to prevent sudden cardiac death (SCD) in the general population begins with the quantification of the individual risk of developing ischaemic heart disease based on risk score charts, followed by the control of risk factors such as serum cholesterol levels, serum glucose levels, blood pressure, smoking and body mass index [2]. Approximately 40% of the observed reduction in SCDs is a direct consequence of a reduction in coronary heart disease (CHD) and improvement in other cardiac conditions [3].

Role of physical activity

Implantable cardioverter-defibrillators (ICDs) have proven their effectiveness in primary prevention mainly in cardiac ischaemic disease and other secondary causes of SCD, with their indications now well categorised and outlined by international recommendations. These recommendations cover a vast range of diseases, ranging from exclusively electrical abnormalities (channelopathies) in morphologically healthy hearts to extremely advanced cardiac disease with a severe left ventricular (LV) function impairment. Therefore, amongst patients with ICDs, sporting activities may cause problems, especially for those with preserved heart function.

Recent US recommendations suggest waiting at least six weeks after implantation prior to engaging in recreational sport following a satisfactory stress test. During patient follow-up, the presence of ventricular arrhythmias (VA) treated by the implanted defibrillator will result in the recommendation to reach at least three months without a new ventricular event prior to the resumption of physical activity [4].

Moderate leisure-time physical exercise is safe and clinically recommended for most individuals with ICDs [5]. The benefits of physical activity for secondary prevention are also well known [6], and, for ICD patients in particular, participation in exercise training programmes may reduce their risk of ICD shocks [7]. In Europe, the 2005 recommendations advise sports activity in ICD patients [5]. These recommendations permit low to moderately dynamic sports and static sports, according to Mitchell's classification, and not sports with a risk of collision, leaving few sporting options (billiards, bowling, cricket, golf, shooting, curling, yoga, table tennis, volleyball) [8]. These recommendations are based on expert consensus given the potential harm, but without large-scale studies to justify them. Until 2015, consensus statements [5,9] advised against participation in sports more vigorous than golf for patients with ICDs. The potential dangers of sports for the defibrillator wearer, hypothetical or real, are many, including appropriate shocks (severe VAs), inappropriate shocks (incorrect analysis of patient cardiac rhythm as VAs), physical injuries related to physical activity, and worsening of the underlying cardiac condition.

Often the VA occurrence may be associated with a transient loss of consciousness that can be potentially dangerous for the athlete or spectator, even if the ICD reduces VA episodes that are severe [10]. Intense exercise doubles the rate of SCD in patients with potentially arrhythmogenic cardiac disease [11], due to increased catecholaminergic secretion (e.g., adrenaline and noradrenaline), potential acidosis, dehydration and electrolyte disturbances. Environmental factors (e.g., extreme weather conditions, altitude and heat), can be potentially  deleterious to the patient and, along with exercise-induced ischaemic conditions, lead to the onset of VA events, reducing the effectiveness of defibrillations [12]. Moreover, physical activity can lead to misinterpretation of VA by ICDs due to acceleration of the heart rate (sinus tachycardia), or through triggering by misdiagnosed supraventricular arrhythmias (atrial fibrillation [AF] flutter, junctional tachycardia). Similarly, additional T waves related to effort may be misinterpreted by ICDs as a second QRS (double counting of the T wave) which may appear as doubling of the actual heart rate, leading to the ICD interpreting it as a VA. Intense physical activity is also a factor associated with premature detrition of defibrillation leads, resulting in complications such as inappropriate shocks and the need for reintervention to readjust the leads and the device.

Some cardiac diseases may be intensified by physical activity. This is demonstrated in right ventricle (RV) arrhythmogenic dysplasia, which is known to increase the pressure load on the RV induced by physical effort, including endurance training, promoting ventricular fibro-adipose remodelling between disjoint cardiomyocytes [13]. Patients with extremely advanced cardiopathies, especially those patients with dilated cardiomyopathies, or patients with residual coronary ischaemia, may also experience worsening of the cardiac disease through intense and repeated exercise [14]. Given these risks, sports in ICD patients could clearly be dangerous. However, we should keep in mind that some of these theoretical risks are not necessarily proven and that physical activity has a significant role in reducing cardiovascular morbidity and mortality. The psychological impact of the cessation of physical activity is significant, with depression even occurring in some ICD patients when sports are excluded.

In 2015, the North American recommendations paved the way for participation in highly competitive sports subject to the absence of VA over a three-month period and appropriate patient counselling with the guideline information: "the decision to participate in the sporting activity must be taken into account and inform the athlete that it could increase the risk of appropriate and inappropriate shocks and the risk of injury to the device in sports where the physical impact is important/intense" [4]. It is critical to know the type of sport and to evaluate the traumatic risk on ICD pockets and how to avoid them (sports with intense physical contact such as rugby, American football and combat sports, lower-risk sports, e.g., soccer and basketball, or those which can provoke friction on the ipsilateral costoclavicular lead, for example volleyball, swimming and racket sports) [15]. Finally, ICDs do not prevent loss of consciousness, and therefore its occurrence during the practice of some sports (motorsports, mountaineering, and skiing) may endanger the safety of patients and spectators.

In 2017, the multinational, prospective, observational ICD Sports Safety Registry demonstrated that, in 440 participants for a median follow-up of 44 months, athletes with ICDs engaged in vigorous competitive sports did not sustain physical injury or failure to terminate arrhythmia, despite the occasional events of inappropriate and appropriate shocks [16]. The two deaths reported were unrelated to competitive activity and dysfunction rates were stable at 5% at 5 years and 11% at 10 years, similar to an age-matched population. The appropriate shocks were common, around 10% during the follow-up period and mainly affected patients with RV arrhythmogenic dysplasia. Shocks were not more frequent when participating in competitive sports was compared to standard physical activity. Similar trends were also observed in the subgroup of top athletes practising sport intensively which reinforces the change in recommendations made two years earlier [16].

The underlying cardiac disease should be considered prior to making a recommendation (in particular, RV arrhythmogenic cardiomyopathy), as exercise increases disease progression [13] and arrhythmias. Athletes with this condition who often train and compete at high intensities should discuss their specific situation with their cardiologists and electrophysiologists. The ICD settings can be adjusted to identify the difference between a healthy rise in heart rate from exercise and that related to an abnormal heart rate or rhythm. ICDs are not the most convenient devices for sports practice. However, they substantially minimise the risk of SCD. These data can guide a more informed and tailored physician and patient decision, allowing sports participation for athletes with ICDs whilst remaining supportive of the eligibility recommendations [4]. In daily practice, patients with ICDs should take some precautions when performing physical activities. Prior to starting or returning to physical exercise, these patients should be clinically stable, with their ICD settings customised and adequately programmed. They need to be properly instructed about their cardiac condition and to comprehend their ICD’s limits. Ideally, ICD patients should always carry their device identification card and, if possible, they should exercise accompanied by someone who knows about their condition and is able to manage an emergency related to their cardiac status. Individuals with ICDs must bear in mind that these devices may suffer configuration changes due to magnetic or electrical fields.

We have seen that a difference between recreational and competitive sport was not found in the US registers but remains valid for medico-legal reasons in Europe since the practice of recreational sport is not covered legally, unlike competitive sport. It is also necessary to take into account the intensity of the sport and its duration as this can condition the appearance of metabolic disorders or lead to cardiopathy progression. Exercise prescription for individuals with ICDs varies. However, the four fundamental pillars of physical activity prescription (frequency, intensity, time/duration, and type of exercise) are simple and can be remembered using the acronym FITT.

Healthy weight and diet

One way to help reduce the cardiac risk of patients with ICDs is to maintain a healthy weight, which should be calculated by their body mass index (BMI) (a person’s weight in kg divided by the square of height in metres) to find out whether they are at a healthy weight or not. Another usual measure is waist circumference which is used for the same purpose. Women whose waistline is more than 35 inches or men whose waistline is more than 40 inches are considered overweight. While BMI and waist circumference can be helpful tools to determine whether ICD patients are obese, only a trained healthcare professional can assess their health status and risks. Obesity is an increasing concern worldwide, with a global prevalence of 13% [17]. A high BMI is associated with hypertension, arrhythmias, dyslipidaemia, and diabetes, and it increases the risk of cardiovascular morbidity and mortality caused by end-stage renal disease, coronary heart disease (CHD), provoking myocardial infarction and advanced heart failure (HF) leading to VA and SCD [18]. Even small changes to diet can impact substantially on cardiac health. Simple steps can keep these patients fit. For instance, ingesting foods containing whole grains, including a diversity of fruit and vegetables, reducing salt (sodium) and sugar, restricting consumption of high-fat foods (red meat, cheese, and baked goods), decreasing the intake of bad fats (saturated and trans fats, such as butter and solid shortening), which can raise the harmful LDL cholesterol levels in the bloodstream and reduce the beneficial HDL cholesterol levels, and replacing bad fats with good ones (monounsaturated and polyunsaturated fats, such as sunflower, soybean, corn and olive oils) which do not raise LDL cholesterol levels may have health benefits when eaten in moderation. However, patients with ICDs should be encouraged to have a conversation with their cardiologists before making changes to their diet.

Tobacco smoking

Recently, a meta-analysis summarised data on smoking status and the risk of SCD [19]. There was a threefold increase in the risk of SCD amongst current smokers, a 38% increase in the relative risk among former smokers and a twofold increase in the risk among ever-smokers compared to never-smokers. In a separate analysis of studies that compared current smokers with non-current (never + former) smokers, there was a twofold increase in the risk. This is consistent with the primary analysis, as the inclusion of former smokers together with never-smokers would have contaminated the reference group and led to an underestimation of the true association between smoking and SCD. There was a 58% increase in the relative risk per 10 cigarettes per day. However, only two studies were included in the dose-response analysis. The positive associations were observed across geographic location and sex, although the number of studies in some subgroups was modest [19]. The current findings strongly support interventions and policies to control tobacco use.

Alcohol consumption

No long-term randomised trials on alcohol consumption have been conducted. The available evidence is from observational studies (including meta-analyses of numerous studies) in which confounders affect the effect of alcohol. These studies usually compare alcohol users with non-users; the baseline features of non-users are different from those of users. Studies on the dose dependency of the cardiovascular effects of alcohol show a decrease at low doses for HF and SCD and an increase at higher alcohol levels of more than 80 g/day (J or U curve shaped). Alcohol has both direct pro-arrhythmic effects and consequences for metabolic, nervous and endocrine parameters, which secondarily affect arrhythmia incidence. AF is the most common arrhythmia after alcohol intake and its complications (especially stroke) increase with alcohol dose [20].

Low, medium and high dosages of alcohol sometimes have conflicting results. Single alcohol doses in non-drinkers are to be distinguished from low, medium (moderate) and high (excessive) alcohol doses in chronic drinkers. Ingested amounts of alcohol are given as a drink or in grams (g) of ethanol. Acute alcohol doses have consequences other than chronic intoxication. An alcohol dose in chronic alcoholics has different effects from the same dose in abstainers. Alcohol is often a starting or companion substance of other pro-arrhythmically active substances. Therefore, their impact on individual cases is difficult to separate. However, the protective effects of alcohol on pre-existing cardiovascular diseases, in particular atherosclerotic heart disease, are known.

Conversely, chronic alcohol abuse can lead to alcoholic cardiomyopathy. Interactions between cardiovascular drugs and alcohol have been described. Experimental and clinical findings diverge in different studies. Thus, alcoholic beverages containing impurities can modify the effect of alcohol, meaning that equal doses of pure alcohol in different preparations can have different effects. These factors make it difficult to assess the alcohol effect on a case-by-case basis. Information on alcohol consumption is not always reliable.

Not infrequently, however, identical and significantly higher alcohol doses do not lead to the same picture of alcoholic cardiomyopathy, thus a variation in genetic susceptibility is present. Finally, we can consider that an identical pathophysiological process may also occur in patients with coronary, valvular, inflammatory or myocardial heart disease of an entirely different cause. In these patients, especially those with HF, pre-existing arrhythmias from other causes can be increased by triggering mechanisms (especially extrasystoles, critical frequencies, electrolyte shifts, adrenergic imbalance, acidosis), but also by perpetuating the culprit stimuli. Therefore, HF patients, even those with ICDs, can be at an increased risk of SCD.

Relationships between excessive alcohol consumption and arterial hypertension have long been known. The incidence of arterial hypertension, however, doubles as a result of excessive consumption of alcohol, which potentially leads to LV hypertrophy, increasing the risk of both atrial arrhythmias and VA.

The precondition for any treatment of alcohol-related cardiac arrhythmias is the avoidance of harmful agents and medical treatment of HF, in the case of alcoholic cardiomyopathy. Alcohol-related arrhythmias do not have special treatments. Therapeutic trials with magnesium, carnitine, thiamine or other vitamins have not demonstrated efficacy. Hence, treatment follows the known rules of antiarrhythmic medication and includes anticoagulation for thromboembolic prevention in the setting of AF. Further therapeutic strategies, such as pulmonary vein isolation in AF or the implantation of ICDs as primary or secondary prevention of VA, should be avoided as long as there is a prospect of alcohol abstinence. If successful, previously severe arrhythmias will often disappear altogether. If the lifestyle change is not successful, the exhaustion of all therapeutic options will only improve the arrhythmia slightly.

We advise ICD patients who do not consume alcohol to continue abstinence and not consume alcohol solely for the potential cardiovascular disease risk reduction. The same advice applies to individuals who have underlying medical diseases that prohibit alcohol use. However, patients who choose to drink low amounts of alcohol, i.e., less than one unit per day (or less than 15 g/day) or less than 100 g/week, may experience benefits for their health and are not prohibited from drinking.



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Notes to editor


Márcio Galindo Kiuchi1, MD, MSc, PhD, FESC, FEHRA, FHFA; Markus P. Schlaich1,2,3, MD, FESC, FAHA; Jan K. Ho1, MBBS; Revathy Carnagarin1, MD, MSc, PhD; Humberto Villacorta4, MD, PhD, FESC

  1. Dobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit/Medical Research Foundation, University of Western Australia, Royal Perth Hospital, Perth, Australia;
  2. Departments of Cardiology and Nephrology, Royal Perth Hospital, Perth, Australia;
  3. Neurovascular Hypertension & Kidney Disease Laboratory, Baker Heart and Diabetes Institute, Melbourne, Australia;
  4. Cardiology Division, Department of Medicine, Universidade Federal Fluminense, Niterói, Rio de Janeiro, Brazil


Address for correspondence:

Dr Márcio Galindo Kiuchi, School of Medicine, Royal Perth Hospital Unit, The University of Western Australia, Level 3, MRF Building, Rear 50 Murray St, Perth, WA 6000, Australia.

Tel:  +61 8 9224 0382; Fax: +61 8 9224 0374



Author disclosures:

The authors have no conflicts of interest to declare.



The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.