Physical Exercise and the Athlete’s Heart
Regular physical exercise reduces cardiac morbility and mortality, preventing atherosclerosis. In contrast, sudden death may occur in competition athletes, as a consequence of ventricular tachy-dysrhythmias in association with different cardiovascular situations, whether congenital or acquired. Particularly over the last decade, research has systematically dealt with the identification of the limits of the criteria of the athlete’s heart in order to allow the systematic outlining of the risk cardiovascular illnesses underlying sudden death (MS).
The cardiocirculatory modifications associated to the practice of exercise in aerobiosis are secondary to the increase of the consumption of oxygen by the muscular tissue, and are generally expressed by an increase in cardiac debit arising from the raising of the heart rate and of the systolic volume. In a more specific manner, among other factors, the type of sport is of crucial influence. Dynamic or isotonic exercise is associated to the reduction of peripheral resistances, to the increase in arterial pressure and to a circulatory pattern of volume overload. Yet static or isometric exercise accompanies an increase of peripheral resistance and of systodiastolic arterial pressure, setting up a pattern of pressure overload. Although the long distance race is close to the dynamic model and weight-lifting is paradigmatic of static exercise, most sports have mixed components, of differing importance.
The activity of regular exercise or sport is accompanied by electrophysiological alterations and modifications in ventricular remodelling which contribute towards maintaining the cardiac debit high and the parietal stress low. Thus, as a response to overload, one observes the increase in parietal thickness and of the left ventricular mass, which is most remarkable and has no ventricular dilation in isometric sports (concentric hypertrophy), while there is an increase in the dimensions of the cardiac chambers in the activities of the dynamic kind (eccentric hypertrophy) . (Studies with magnetic resonance have made it possible to state that physiological dilation is balanced out for both left and right ventricles . It should be stressed that in the process of conditioning the ventricular systolic function remains normal while the pattern of diastolic function, assessed by transmitral Doppler tissue flow, is normal or “supra-normal”. Recent studies have shown alterations in the myocardic deformation associated to sports of the static type, but their meaning has not been made clear. Adaptation by the autonomous nervous system to athletic conditioning is also a part of the physiological response to regular exercise, with a raising of the vagal tonus vagal and sympathetic inhibition, expressed as sinusal bradycardia and alterations in the auricular-ventricular conduction on the nodal level . The degree and nature of the response also depend on the sex, nature and degree of training and on genetic and ethnic factors .
The modifications described form the pattern of athlete’s heart, as a physiological response to continued physical training. In extreme situations the cardiac modifications may be close to those described for some myocardiopathies that are associated to risk of sudden death and are a counter-indication to competitive sport, with the differential diagnosis often being complex.
Sudden Death in the Athlete
Sudden death in an athlete is a rare but terrifying event, with values that vary according to the series, higher with age and in the male sex. A very well characterised series from the region of Veneto, in Italy, indicates an incidence of 2.1/100,000 athletes per year . Death appears in 80% of the cases during sports and in 20% after exercise, suggesting that this is the precipitating factor . In the older age group sudden death is more frequently associated to coronary atherosclerotic disease, through intense exercise and due to myocardial stroke or ischemic ventricular arrhythmia. In fact, if exercise has a preventive role for atherosclerosis in the incipient phase, it may have a deleterial effect if it is not efficiently controlled in the pre-clinical established disease. In the young athlete (=35 years old) an important number of cardiovascular studies is the substratum for cardiac sudden death by ventricular tachycardia/fibrillation.
Hypertrophic myocardiopathy, with a genetic base and which is characterised by hypertrophy, fibrosis and structural disarrangement of the ventricular myofibrillas forms over one third of the sudden death situations in the United States (Fig. 1). This situation may be confused with athlete’s heart, particularly when the thickness of the ventricular wall reaches 15-16 mm, a criterion that forms a grey zone . Arrhythmogenic myocardiopathy of the right ventricle, also a genetic disease that is expressed as dilation, dysfunction and fibrolipidic infiltration of the right ventricle (Fig. 2), was indicated as the substratum for sudden death in one quarter of the cases in the region of Veneto. Its diagnosis uses clinical criteria, ECG, genetics, imagiology (ecocardiography/magnetic resonance) . Other situations underlying sudden death include congenital coronary diseases, premature coronary disease, myocarditis, dilated myocardiopathy, conduction disturbances, Wolff-Parkinson-White or the canalopathies, of difficult diagnosis (congenital Short QT and Long QT syndromes, Brugada and catecolaminergical ventricular polymorphic tachycardia). The dissection of the aorta or non-cardiac etiologies may rarely form an etiological situation.
Prevention of Sudden Death by Pre-Participation Screening
Medical evaluation of the athletes allows identification of asymptomatic individuals with a risk of sudden death. The protocol is not universally established. In the United States only the clinical history is assessed, with a special emphasis on family history. Analysis of the efficiency of this screening shows it is not very sensitive and specific . In Italy the screening process is obligatory for all those who practice competitive sport. Besides a full clinical history, taken by sports doctors, it includes ECG as the single examination. In the cases of suspicion of cardiopathy other diagnostic methods are carried out ranging from ecocardiography to Holter monitoring, to ergometry or to magnetic resonance, to electrophysiological study and others, following a diagnostic algorhythm . This strategy has been efficient in reducing the incidence of sudden deaths from 3.6/100,000 in 1980 to 0.4/100,000 patients/year in 2004. Despite the economic impact of the screening strategies, their benefit is widely demonstrated in the results in Italy, the only country where preventive attitudes are legislated and are compulsory. However, the guidelines of the European Society of cardiology now recommend this strategy of assessing athletes.
.jpg)
Fig. 1. Hypertrophic myocardiopathy. Picture of the left ventricle obtained by magnetic showing septal hypertrophy with fibrosis
(in white, arrow).seta).
Fig. 2. Arrhythmogenic myocardiopathy of the left ventricle. Picture of dilation and aneurism (arrow) of the left ventricle, obtained by magnetic resonance.seta).
Ana G. Almeida
Associate Professor of Cardiology
University Clinic of Cardiology
Faculty of Medicine of the University of Lisbon
anagalmeida@gmail.com
REFERENCES
Fagard RH. Impact of different sports and training on cardiac structure and function. Cardiology Clinics 1997;15:397–412
Pelliccia A, Maron BJ, Culasso F, et al. Clinical significance of abnormal electrocardiographic patterns in trained athletes. Circulation 2000;102:278–84
Karjalainen J, Kujala HM, Stolt A, et al. Angiotensinogen gene M235T polymorphism predicts left ventricular hypertrophy in endurance athletes. J Am Coll Cardiol 1999;34:494: 9
Corrado D, Basso C, Rizzoli G, et al. Does sports activity enhance the risk of sudden death in adolescents and young adults? J Am Coll Cardiol 2003;42:1959–63
Corrado D, Maron BJ, Basso C, Pelliccia A, et al. Sudden cardiac death in athletes. In Gussac I, Antzelevitch C (eds.) Electrical diseases of the heart, 2008. London: Springer-Verlag, pp.911–23
Maron BJ. Distinguishing hypertrophic cardiomyopathy from athlete's heart: a clinical problem of increasing magnitude and significance. Heart 2005;91;1380-1382.
Marcus F, MD, McKenna, WJ, Sherrill D et al. Diagnosis of Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia. Circulation. 2010;121:1533-1541
Maron BJ, Shirani J, Poliac LC, et al. Sudden death in young competitive athletes. Clinical, demographics,and pathological profiles. JAMA 1996;276:199–204
Corrado D, Pelliccia A, Bjørnstad H et al. Cardiovascular pre-participation screening of young competitive athletes for prevention of sudden death. Eur Heart J. 2005;26:516-2
Regular physical exercise reduces cardiac morbility and mortality, preventing atherosclerosis. In contrast, sudden death may occur in competition athletes, as a consequence of ventricular tachy-dysrhythmias in association with different cardiovascular situations, whether congenital or acquired. Particularly over the last decade, research has systematically dealt with the identification of the limits of the criteria of the athlete’s heart in order to allow the systematic outlining of the risk cardiovascular illnesses underlying sudden death (MS).
The cardiocirculatory modifications associated to the practice of exercise in aerobiosis are secondary to the increase of the consumption of oxygen by the muscular tissue, and are generally expressed by an increase in cardiac debit arising from the raising of the heart rate and of the systolic volume. In a more specific manner, among other factors, the type of sport is of crucial influence. Dynamic or isotonic exercise is associated to the reduction of peripheral resistances, to the increase in arterial pressure and to a circulatory pattern of volume overload. Yet static or isometric exercise accompanies an increase of peripheral resistance and of systodiastolic arterial pressure, setting up a pattern of pressure overload. Although the long distance race is close to the dynamic model and weight-lifting is paradigmatic of static exercise, most sports have mixed components, of differing importance.
The activity of regular exercise or sport is accompanied by electrophysiological alterations and modifications in ventricular remodelling which contribute towards maintaining the cardiac debit high and the parietal stress low. Thus, as a response to overload, one observes the increase in parietal thickness and of the left ventricular mass, which is most remarkable and has no ventricular dilation in isometric sports (concentric hypertrophy), while there is an increase in the dimensions of the cardiac chambers in the activities of the dynamic kind (eccentric hypertrophy) . (Studies with magnetic resonance have made it possible to state that physiological dilation is balanced out for both left and right ventricles . It should be stressed that in the process of conditioning the ventricular systolic function remains normal while the pattern of diastolic function, assessed by transmitral Doppler tissue flow, is normal or “supra-normal”. Recent studies have shown alterations in the myocardic deformation associated to sports of the static type, but their meaning has not been made clear. Adaptation by the autonomous nervous system to athletic conditioning is also a part of the physiological response to regular exercise, with a raising of the vagal tonus vagal and sympathetic inhibition, expressed as sinusal bradycardia and alterations in the auricular-ventricular conduction on the nodal level . The degree and nature of the response also depend on the sex, nature and degree of training and on genetic and ethnic factors .
The modifications described form the pattern of athlete’s heart, as a physiological response to continued physical training. In extreme situations the cardiac modifications may be close to those described for some myocardiopathies that are associated to risk of sudden death and are a counter-indication to competitive sport, with the differential diagnosis often being complex.
Sudden Death in the Athlete
Sudden death in an athlete is a rare but terrifying event, with values that vary according to the series, higher with age and in the male sex. A very well characterised series from the region of Veneto, in Italy, indicates an incidence of 2.1/100,000 athletes per year . Death appears in 80% of the cases during sports and in 20% after exercise, suggesting that this is the precipitating factor . In the older age group sudden death is more frequently associated to coronary atherosclerotic disease, through intense exercise and due to myocardial stroke or ischemic ventricular arrhythmia. In fact, if exercise has a preventive role for atherosclerosis in the incipient phase, it may have a deleterial effect if it is not efficiently controlled in the pre-clinical established disease. In the young athlete (=35 years old) an important number of cardiovascular studies is the substratum for cardiac sudden death by ventricular tachycardia/fibrillation.
Hypertrophic myocardiopathy, with a genetic base and which is characterised by hypertrophy, fibrosis and structural disarrangement of the ventricular myofibrillas forms over one third of the sudden death situations in the United States (Fig. 1). This situation may be confused with athlete’s heart, particularly when the thickness of the ventricular wall reaches 15-16 mm, a criterion that forms a grey zone . Arrhythmogenic myocardiopathy of the right ventricle, also a genetic disease that is expressed as dilation, dysfunction and fibrolipidic infiltration of the right ventricle (Fig. 2), was indicated as the substratum for sudden death in one quarter of the cases in the region of Veneto. Its diagnosis uses clinical criteria, ECG, genetics, imagiology (ecocardiography/magnetic resonance) . Other situations underlying sudden death include congenital coronary diseases, premature coronary disease, myocarditis, dilated myocardiopathy, conduction disturbances, Wolff-Parkinson-White or the canalopathies, of difficult diagnosis (congenital Short QT and Long QT syndromes, Brugada and catecolaminergical ventricular polymorphic tachycardia). The dissection of the aorta or non-cardiac etiologies may rarely form an etiological situation.
Prevention of Sudden Death by Pre-Participation Screening
Medical evaluation of the athletes allows identification of asymptomatic individuals with a risk of sudden death. The protocol is not universally established. In the United States only the clinical history is assessed, with a special emphasis on family history. Analysis of the efficiency of this screening shows it is not very sensitive and specific . In Italy the screening process is obligatory for all those who practice competitive sport. Besides a full clinical history, taken by sports doctors, it includes ECG as the single examination. In the cases of suspicion of cardiopathy other diagnostic methods are carried out ranging from ecocardiography to Holter monitoring, to ergometry or to magnetic resonance, to electrophysiological study and others, following a diagnostic algorhythm . This strategy has been efficient in reducing the incidence of sudden deaths from 3.6/100,000 in 1980 to 0.4/100,000 patients/year in 2004. Despite the economic impact of the screening strategies, their benefit is widely demonstrated in the results in Italy, the only country where preventive attitudes are legislated and are compulsory. However, the guidelines of the European Society of cardiology now recommend this strategy of assessing athletes.
Fig. 1. Hypertrophic myocardiopathy. Picture of the left ventricle obtained by magnetic showing septal hypertrophy with fibrosis
(in white, arrow).seta).
Fig. 2. Arrhythmogenic myocardiopathy of the left ventricle. Picture of dilation and aneurism (arrow) of the left ventricle, obtained by magnetic resonance.seta).
Ana G. Almeida
Associate Professor of Cardiology
University Clinic of Cardiology
Faculty of Medicine of the University of Lisbon
anagalmeida@gmail.com
REFERENCES
Fagard RH. Impact of different sports and training on cardiac structure and function. Cardiology Clinics 1997;15:397–412
Pelliccia A, Maron BJ, Culasso F, et al. Clinical significance of abnormal electrocardiographic patterns in trained athletes. Circulation 2000;102:278–84
Karjalainen J, Kujala HM, Stolt A, et al. Angiotensinogen gene M235T polymorphism predicts left ventricular hypertrophy in endurance athletes. J Am Coll Cardiol 1999;34:494: 9
Corrado D, Basso C, Rizzoli G, et al. Does sports activity enhance the risk of sudden death in adolescents and young adults? J Am Coll Cardiol 2003;42:1959–63
Corrado D, Maron BJ, Basso C, Pelliccia A, et al. Sudden cardiac death in athletes. In Gussac I, Antzelevitch C (eds.) Electrical diseases of the heart, 2008. London: Springer-Verlag, pp.911–23
Maron BJ. Distinguishing hypertrophic cardiomyopathy from athlete's heart: a clinical problem of increasing magnitude and significance. Heart 2005;91;1380-1382.
Marcus F, MD, McKenna, WJ, Sherrill D et al. Diagnosis of Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia. Circulation. 2010;121:1533-1541
Maron BJ, Shirani J, Poliac LC, et al. Sudden death in young competitive athletes. Clinical, demographics,and pathological profiles. JAMA 1996;276:199–204
Corrado D, Pelliccia A, Bjørnstad H et al. Cardiovascular pre-participation screening of young competitive athletes for prevention of sudden death. Eur Heart J. 2005;26:516-2
