Cardiovascular remodelling in the conditioned athlete is frequently associated with physiological ECG changes. Abnormalities, however, may be detected which represent expression of an underlying heart disease that puts the athlete at risk of arrhythmic cardiac arrest during sports. It is mandatory that ECG changes resulting from intensive physical training are distinguished from abnormalities which reflect a potential cardiac pathology. The present article represents the consensus statement of an international panel of cardiologists and sports medical physicians with expertise in the fields of electrocardiography, imaging, inherited cardiovascular disease, cardiovascular pathology, and management of young competitive athletes. The document provides cardiologists and sports medical physicians with a modern approach to correct interpretation of 12-lead ECG in the athlete and emerging understanding of incomplete penetrance of inherited cardiovascular disease. When the ECG of an athlete is examined, the main objective is to distinguish between physiological patterns that should cause no alarm and those that require action and/or additional testing to exclude (or confirm) the suspicion of an underlying cardiovascular condition carrying the risk of sudden death during sports. The aim of the present position paper is to provide a framework for this distinction. For every ECG abnormality, the document focuses on the ensuing clinical work-up required for differential diagnosis and clinical assessment. When appropriate the referral options for risk stratification and cardiovascular management of the athlete are briefly addressed.
Complex ventricular arrhythmias do not necessarily represent a benign finding in endurance athletes. An electrophysiological study is indicated for risk evaluation, both by defining inducibility and identifying the arrhythmogenic mechanism. Endurance athletes with arrhythmias have a high prevalence of right ventricular structural and/or arrhythmic involvement. Endurance sports seems to be related to the development and/or progression of the underlying arrhythmogenic substrate.
This consensus paper on behalf of the Study Group on Sports Cardiology of the European Society of Cardiology follows a previous one on guidelines for sports participation in competitive and recreational athletes with supraventricular arrhythmias and pacemakers. The question of imminent life-threatening arrhythmias is especially relevant when some form of ventricular rhythm disorder is documented, or when the patient is diagnosed to have inherited a pro-arrhythmogenic disorder. Frequent ventricular premature beats or nonsustained ventricular tachycardia may be a hallmark of underlying pathology and increased risk. Their finding should prompt a thorough cardiac evaluation, including both imaging modalities and electrophysiological techniques. This should allow distinguishing idiopathic rhythm disorders from underlying disease that carries a more ominous prognosis. Recommendations on sports participation in inherited arrhythmogenic conditions and asymptomatic gene carriers are also discussed: congenital and acquired long QT syndrome, short QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, arrhythmogenic right ventricular cardiomyopathy and other familial electrical disease of unknown origin. If an implantable cardioverter defibrillator is indicated, it is no substitute for the guidelines relating to the underlying pathology. Moreover, some particular recommendations for patients/athletes with an implantable cardioverter defibrillator are to be observed.
A small proportion of the athletes (26%) was asymptomatic. Paroxysmal atrial fibrillation remained stable in half of the athletes whereas the arrhythmia changed into permanent atrial fibrillation in a minority of this population.
There is a sport-specific left ventricular adaptation in endurance athletes. The triathlon heart and the heart of a cyclist differ significantly from a marathon heart.
One of the hallmark symptoms of patients with chronic heart failure (CHF) is exercise intolerance. Therefore, exercise testing has become an important tool for the evaluation and monitoring of heart failure. Whereas the maximal aerobic capacity (peak VO(2)) is a reliable indicator of the severity and prognosis of heart failure, submaximal exercise parameters may be more closely related to the ability to perform daily activities. As such, oxygen (O(2)) uptake kinetics, describing the rate change of O(2) uptake during onset or recovery of submaximal constant-load exercise (O(2) onset and recovery kinetics, respectively), have been shown to be useful parameters for objectively evaluating the functional capacity of CHF patients. However, their evaluation in this population is not a routine part of daily clinical practice. Possible reasons for this include a lack of standardisation of the assessment methodology and a limited number of studies evaluating the clinical use of O(2) uptake kinetics in CHF patients. In addition, the pathophysiological mechanisms underlying the delay in O(2) uptake kinetics in these patients are not completely understood. This review discusses the current literature on the clinical potency and physiological determinants of O(2) uptake kinetics in CHF patients and provides directions for future research. (Neth Heart J 2009;17:238-44.Neth Heart J 2009;17:238-44.).
The upper limit of blood lactate resulting in a lactate steady state during prolonged exercise is called the maximal lactate steady state (MLSS). The purpose of this study was to investigate the lactate response to steady-state exercise during a field test in elite endurance athletes. Plasma lactate levels were assessed in 13 elite triathletes and 13 elite cyclists (mean +/- SD; age 23.7 +/- 5.1 yr; HT 180.2 +/- 6.3 cm; WT 70.3 +/- 5.9 kg; VO2 max 68 +/- 3.7 ml/min/kg) during a 40 km-long time trial on a bicycle (4 km course x 10 laps). The steady state was demonstrated by monitoring the heart rate and timing every course run. The lactate levels were expected to correspond to MLSS. The mean level of lactate during the time trial was 7.4 +/- 2.5 mmol/l. Five athletes maintained plasma lactate levels which exceeded 10 mmol/l or more for almost 1 h. The large value of individual variability was conspicuous (range 3.2-12.2 mmol/l). These values exceeded all previous reported levels for MLSS from other investigators. Our observations are important in sport medical practice since the different lactate responses to exercise are used as parameters in training management.
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