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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Dr. Hein Heidbuchel,
For physicians evaluating athletes (or other individuals who want to engage in leisure time sports activities) a major focus is to prevent the development of arrhythmias that can have potentially life-threatening consequences. Preparticipation evaluation aims to detect underlying disease that may predispose to arrhythmias, both structural (like cardiomyopathies) and electrical. Moreover, an increasing number of athletes present with atrial fibrillation (AF), with exercise as a likely contributing causative factor. AF by itself is not a life-threatening disease but it may be associated with difficult management decisions. Prof. M. Borggrefe (Mannheim, Germany) recapitulated that cardiovascular causes are responsible for 56% of athletes dying suddenly on the field. Moreover, 90% of those occur during exertion. Due to better detection, primary electrical disorders (“channelopathies”) like Brugada syndrome, long and short QT syndrome, and catecholaminergic polymorphic VT (CPVT) form an increasing proportion of these cases, maybe even up to one quarter. Nevertheless, good data about the risk during exertion of patients with a known channelopathy are scarce, making founded recommendations concerning sports participation difficult. In general, European recommendations not only exclude symptomatic and phenotypically overt patients from competitive sports participation, but also recommend the same attitude for asymptomatic gene carriers with the same mutations. In Brugada syndrome, for instance, although cardiac arrest usually develops at rest and not during exercise, there is concern that the vagally-dominant remodelling that occurs in athletes may contribute to an increased risk at rest. Moreover, there is data that increasing central body temperature during sports may lead to increasing repolarisation abnormalities and hence risk. It needs to be stressed, however, that strong data are lacking. Also given the low event rate in BS patients in general (like demonstrated in the FINGER registry with over 1000 BS patients), one could argue that a more liberal eligibility could be defended. Further research is definitely needed. For long and short QT syndromes, an additional problem is the overlap in QTc intervals between a normal population and affected individuals, which is especially true for specific genotypes (like SQTS 4 and 5). On the other hand, for the rare condition of CPVT, which is the result of a mutation in the ryanodine receptor or calsequestrin, it is clear that exercise will aggravate the calcium-handling problems and propensity for arrhythmias. More than mild to moderate exercise therefore cannot be recommended to such patients. Prof. G. Thiene (Padova, Italy) focused his presentation on arrhythmogenic right ventricular cardiomyopathy (ARVC). Since the first description of the syndrome in 1988, when some were still doubting the abnormality of a phenotype with negative T-waves in the right precordial leads and ventricular premature beats (VPB) with a left bundle branch morphology, it has evolved into an accepted leading cause of sudden death in athletes. The pathologic hallmark is fibrofatty replacement of the ventricular wall, which can also be demonstrated via cardiac MR imaging. In recent years, it has become clear that the phenotype is not only restricted to the right ventricle, but can also involve (and sometimes even predominantly so) the left ventricle. ARVC contributes a relative risk of 5.4 for sudden death during exertion. Preparticipation screening including an ECG is often able to detect the cardiomyopathy at an early stage and has contributed to the reduction of sudden death in athletes as observed in Italy between 1988 and 2010. Indeed, right precordial negative T-waves are very uncommon after puberty and therefore should alert to ARVC. Suspicion for the condition can trigger more sophisticated evaluation with late potentials (present in about 1 out of 3 cases), echocardiography (relatively insensitive), cardiac MRI (although sometimes false negative too), and even voltage mapping in the RV outflow tract. The latter approach may also help differentiate from idiopathic RVOT ectopy, especially in ARVC forms that are localised to the RVOT. Although animal models have shown a training-dependent development of a functional ARVC phenotype in plakoglobin-deficient mice, and although there are data that endurance sports may result in an ARVC phenotype in man, there still is no consensus as to how far exercise can induce or facilitate the phenotype. Indeed, some investigators have raised the possibility of exercise-induced ARVC as a continuum from inherited ARVC (which is usually caused by mutations in the desmosomes). Prof. F. Carré (Rennes, France) highlighted the fact that the most common proarrhythmic inherited condition is hypertrophic cardiomyopathy (HCM), with a mutation prevalence of 1/500 in the general population. The hallmark histologic features are myofibrillar disarray, myocyte hypertrophy, insterstitial fibrosis, and abnormalities of the small coronary arteries. Again, the ECG has a high sensitivity to raise suspicion about the presence of HCM (mainly due to deep negative T-waves in the left precordial leads that are present in 80-85% of cases). Echocardiography is the first line investigation to confirm the diagnosis, with LV wall thickness of the septum or posterior wall ≥14 mm, or a septal/posterior wall ratio of >1.3, being diagnostic. The diagnosis in athletes however can be difficult, since there is overlap with the hypertrophic adaptations of the athlete’s heart. Other elements may be of help in the differential diagnosis, like small LV cavity <45 mm, increased left atrial size, or diastolic dysfunction. On the other hand, CMR is evolving into a more powerful evaluation tool, able to detect hypertrophy at sites that are difficult to image echocardiographically (like the apex, anterolateral or posterior wall). Moreover, CMR has the added benefit to being able to reveal areas of fibrosis, which have been shown to be related to the propensity for arrhythmias and hence constitute an important prognostic finding. If there is still uncertainty, also evaluation of family members can be of help. Although detraining may reveal absence of regression of hypertrophy in HCM, it is used less often nowadays in the diagnostic work-up, also because some animal data indicate that a paradoxical response can be observed. It is also important to stress that negative genetic testing cannot give a definitive exclusion. It is still unclear what constitutes the most important mechanism for arrhythmogenesis in HCM athletes. Different mechanisms have been proposed like changes in calcium handling, ischemia, increased catecholamines, acidosis, or ion disturbances. Indeed, some have shown important K+ changes during (increased) and immediately after exercise (with a rapid decrease to lower values than pre-exercise values) which certainly can contribute. Therefore, the official recommendations disqualify any symptomatic HCM patients from more than mild competitive sports. How far such restrictions also apply to asymptomatic and phenotypically negative gene carriers (i.e. without manifest hypertrophy) is still a matter of debate, with European recommendations so far being more restrictive than American ones. Prof. Lluis Mont (Barcelona, Spain) discussed a less lethal but much more prevalent form of arrhythmia in athletes, namely atrial fibrillation (AF). There is more and more epidemiological data that point to regular and intense physical activity as an independent risk factor for the development of this arrhythmia. Often, AF only develops in the forties or later, explaining why studies evaluating younger athletes could not find a relationship with AF. Nevertheless, AF prevalence in ex-athletes in their sixties may go up to more than 15%. The Physicians Health Study has shown an almost linear relationship between the frequency of vigourous sports and the relative risk of developving AF. Some have argued that a genetic predisposition may explain the association, but in contrast to familial forms of AF that have a high penetrance and become evident at young age, the reverse is true for sports-related AF. Moreover, familial AF is very rare. Also, the observed dose-response relation argues against genes as the sole explanation for sports-related AF. The pathophysiology of sports as risk factor for AF is most likely due to an interaction between atrial dilatation, increased vagal tone, increased atrial ectopy, and maybe even interstitial fibrosis. Indeed, a rat model of endurance training, developed in Dr. Mont’s lab, showed a progressive increase of fibrogenetic markers in parallel with the development of AF inducibility. In any case, the fact that sports may be a risk factor for a related ‘cardiac injury’ under the form of AF does not negate its beneficial effects on cardiovascular health in general!
Arrhythmic events during sport
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