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• W2070304234 abstract "HomeCirculationVol. 123, No. 23Athlete's Heart and Cardiovascular Care of the Athlete Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBAthlete's Heart and Cardiovascular Care of the AthleteScientific and Clinical Update Aaron L. Baggish, MD and Malissa J. Wood, MD Aaron L. BaggishAaron L. Baggish From the Division of Cardiology, Massachusetts General Hospital, Boston. Search for more papers by this author and Malissa J. WoodMalissa J. Wood From the Division of Cardiology, Massachusetts General Hospital, Boston. Search for more papers by this author Originally published14 Jun 2011https://doi.org/10.1161/CIRCULATIONAHA.110.981571Circulation. 2011;123:2723–2735“The physiologic capabilities of the heart are enormous, and in judging the effect of any undue exertion on it, we must not regard the murmurs of the irregularity alone, but must also consider carefully, the way in which the heart is doing its work, its strength, as shown by its ability to maintain proper arterial tension, and its recuperative power. As with other muscles, not size but quality tells in the long run.”1Eugene DarlingThe heart of the athlete has intrigued clinicians and scientists for more than a century. Early investigations in the late 1800s and early 1900s documented cardiac enlargement and bradyarrhythmias in individuals with above-normal exercise capacity and no attendant signs of cardiovascular disease. Since that time, scientific understanding of the association between sport participation and specific cardiac abnormalities has paralleled advances in cardiovascular diagnostic techniques. It is now well established that repetitive participation in vigorous physical exercise results in significant changes in myocardial structure and function. Recent increases in the popularity of recreational exercise and competitive athletics have led to a growing number of individuals exhibiting this phenomenon. This review provides an up-to-date summary of the science of cardiac remodeling in athletes and an overview of common clinical issues that are encountered in the cardiovascular care of the athlete.Historical Perspective: Past to PresentInitial reports describing cardiac enlargement in athletes date back to the late 1890s. In Europe, the Swedish clinician Henschen2 used the rudimentary yet elegant physical examination skills of auscultation and percussion to demonstrate increased cardiac dimensions in elite Nordic skiers. Similar observations were made during the same year by Eugene Darling1 of Harvard University in university rowers. In the early 1900s, Paul Dudley White3 studied radial pulse rate and pattern among Boston Marathon competitors, and was the first to report marked resting sinus bradycardia in long-distance runners.4 Early chest radiography work confirmed the physical examination findings of Darling and Henschen by showing global cardiac enlargement in trained athletes.5–7 The subsequent development of ECG enabled widespread study of electric activity in the heart of the trained athlete.8–14 In addition to the morphological patterns of cardiac hypertrophy, bradyarrhythmias15 and tachyarrhythmias16 were observed in healthy exercise-trained individuals. The development and rapid dissemination of 2-dimensional echocardiography led to important further advances in our understanding of the athlete's heart. Descriptions of ventricular chamber enlargement, myocardial hypertrophy, and atrial dilation have led to a more comprehensive understanding of the athlete's heart. Most recently, advanced echocardiographic techniques and magnetic resonance imaging have begun to clarify important functional adaptations that accompany previously reported structural characteristics of the athlete's heart.The significance of cardiac enlargement in athletes has been debated since the time Darling and Henschen made their initial observations. Although both investigators speculated that their findings represented beneficial adaptations to exercise, this view was not universally accepted. It was postulated as early as 1902 that cardiac enlargement in athletes is a form of overuse pathology, and that prolonged participation in sport could lead to premature cardiovascular system collapse.17 This line of thinking underscores the concept of the athlete's heart syndrome, a term often applied to the athletic patient who presents with subjective symptoms or an abnormal cardiovascular finding. This concept has resurfaced numerous times over the last 110 years of scientific inquiry despite the fact that there is no clear evidence to substantiate its validity. Importantly, a recent study of Olympic-caliber Italian athletes (n=114) demonstrated no deterioration in left ventricular (LV) function or occurrence of cardiovascular events over an extended period (8.6±3 years) of intense training.18 Although the debate is ongoing19 and more prospective, long-term studies are needed, the modern view of the athlete's heart implicates adaptive physiology, not preclinical disease.In the present era, participation in competitive sport and/or vigorous recreational exercise continues to gain in popularity in the United States and other countries. Factors such as the documented health benefits of regular physical exercise, the increasing availability of community-based athletic programs, and growing numbers of open-enrollment sport events (ie, community-based road-running races) underlie this popularity growth. In the face of the growing obesity epidemic, cardiovascular practitioners should be encouraged to support this trend both with individual patients and at the community level. However, the increasing interest in sport participation will likely be paralleled by increases in the number of people with features of athlete heart. Thus, the practicing cardiovascular clinician may find it increasingly important to possess a basic knowledge of this subject.Exercise-Induced Cardiac RemodelingOverview of Relevant PhysiologyNumerous superb reviews of clinically relevant exercise physiology are available20–22; thus, only key aspects relevant to cardiac remodeling are reviewed here. There is a direct relationship between exercise intensity (external work) and the body's demand for oxygen. This oxygen demand is met by increasing pulmonary oxygen uptake (Vo2). The cardiovascular system is responsible for transporting oxygen-rich blood from the lungs to the skeletal muscles, a process quantified as cardiac output (liters per minute). The Fick equation (cardiac output=Vo2×arterial-venous O2) /delta]) can be used to quantify the relationship between cardiac output and Vo2. In the healthy human, there is a direct and inviolate relationship between Vo2 and cardiac output.Cardiac output, the product of stroke volume and heart rate, may increase 5- to 6-fold during maximal exercise effort. Coordinated autonomic nervous system function, characterized by rapid and sustained parasympathetic withdrawal coupled with sympathetic activation, is required for this to occur. Heart rate in the athlete may range from <40 bpm at rest to >200 bpm in a young maximally exercising athlete. Heart rate increase is responsible for the majority of cardiac output augmentation during exercise. Maximal heart rate varies innately among individuals, decreases with age,23 and does not increase with exercise training.24In contrast, stroke volume both at rest and during exercise may increase significantly with prolonged exercise training. Cardiac chamber enlargement and the accompanying ability to generate a large stroke volume are direct results of exercise training and cardiovascular hallmarks of the endurance-trained athlete. Stroke volume rises during exercise as a result of increases in ventricular end-diastolic volume and, to a lesser degree, sympathetically mediated reduction in end-systolic volume (particularly during upright exercise).21 Left ventricular end-diastolic volume is determined by diastolic filling, a complex process that is affected by a variety of variables, including heart rate, intrinsic myocardial relaxation, ventricular compliance, ventricular filling pressures, atrial contraction, and extracardiac mechanical factors such as pericardial and pulmonary constraints. At the present time, to what degree each of these factors contributes to stroke volume augmentation during exercise remains uncertain.Hemodynamic conditions, specifically changes in cardiac output and peripheral vascular resistance, vary widely across sporting disciplines. Although some overlap exists, exercise activity can be segregated into 2 forms with defining hemodynamic differences. Isotonic exercise, further referred to as endurance exercise, involves sustained elevations in cardiac output, with normal or reduced peripheral vascular resistance. Such activity represents primarily a volume challenge for the heart that affects all 4 chambers. This form of exercise underlies activities such as long-distance running, cycling, rowing, and swimming. In contrast, isometric exercise, further referred to as strength training, involves activity characterized by increased peripheral vascular resistance and normal or only slightly elevated cardiac output. This increase in peripheral vascular resistance causes transient but potentially marked systolic hypertension and LV afterload. Strength training is the dominant form of exercise in activities such as weightlifting, track and field throwing events, and American-style football. Many sports, including popular team-based activities such as soccer, lacrosse, basketball, hockey, and field hockey, involve significant elements of both endurance and strength exercise. As discussed later, sport-specific hemodynamic conditions may play an important role in cardiac remodeling.The Left VentricleThe impact of exercise training on LV structure has been the topic of extensive study. Early studies with ECG demonstrated a high prevalence of increased cardiac voltage suggestive of LV enlargement in trained athletes.9,25 Subsequent work with 2-dimensional echocardiography confirmed underlying LV hypertrophy and dilation.26 Italian physician-scientists have contributed a great deal to our understanding of LV structure in athletes using data derived from their long-standing preparticipation screening program. Pelliccia et al27 reported echocardiographic LV end-diastolic cavity dimensions in a large group (n=1309) of Italian elite athletes. This cohort was made up predominantly of male athletes (73%) and included individuals from 38 different sports. Left ventricular end-diastolic diameters varied widely, from 38 to 66 mm in women (mean, 48 mm) and from 43 to 70 mm in men (mean, 55 mm). Importantly, LV end-diastolic diameter was ≥54 mm in 45% and >60 mm in 14% of the cohort. Markedly dilated LV chambers (>60 mm) were most common in athletes with higher body mass and those participating in endurance sports (cycling, cross-country skiing, and canoeing).Pelliccia et al28 have also reported echocardiographic measurements of LV wall thicknesses among 947 elite Italian athletes. Within this cohort, a small but significant percentage of athletes (1.7%) had LV wall thicknesses ≥13 mm, and all of these individuals had concomitant LV cavity dilation. Sharma et al29 also reported a low incidence (0.4%) of LV wall thickness >12 mm among 720 elite junior athletes and confirmed that increased LV wall thickness is associated with increased chamber size in young athletes. It must be emphasized that LV wall thickness in excess of 13 mm is a rare finding in healthy athletes. This finding should prompt consideration of pathological hypertrophy, and may serve as an indication for further diagnostic assessment. However, as reflected by the above data, a very small but significant number of healthy, highly trained individuals have wall thickness values in the 13- to 15-mm range. This finding may be particularly common among elite athletes who engage in the highest level of exercise training.30 Furthermore, it is has been consistently shown that the most marked LV hypertrophy occurs in athletes with relatively large body size, and those of Afro-Caribbean descent. As such, careful interpretation of LV hypertrophy in athletes, particularly with respect to differentiating adaptive from pathological hypertrophy, requires consideration of body size and ethnicity.The notion that endurance-based exercise and strength-based exercise lead to distinctly different changes in LV structure was first proposed by Morganroth et al in 1975.31 That study compared M-mode echocardiographic LV measurements in wrestlers (strength training), swimmers (endurance training), and sedentary control subjects and found significant differences across these 3 groups. Specifically, athletes exposed to strength training demonstrated concentric LV hypertrophy, whereas individuals exposed to endurance training demonstrated eccentric LV enlargement. This study led to the concept of sport-specific cardiac remodeling, often referred to as the Morganroth hypothesis. Although data have been presented that refute the concept of sport-specific LV remodeling,32–34 the majority of cross-sectional data and recent longitudinal work support Morganroth's original findings.35 In our experience, the magnitude of eccentric hypertrophy that results from endurance training is typically more pronounced than the concentric hypertrophy that accompanies strength training, although, rarely, extreme forms of both subtypes can be encountered. The interested reader is referred to a recent comprehensive review of this topic by Naylor and colleagues.36Exercise-induced adaptations in LV function have also been studied. Numerous investigators have examined resting LV systolic function in athletes using cross-sectional, sedentary control study designs.37–40 These studies and a large meta-analysis show that LV ejection fraction is generally normal among athletes,41 although at least 1 study of 147 cyclists participating in the Tour de France found that 17 (11%) had a calculated LV ejection fraction ≤52%.42 Such results suggest that healthy endurance athletes may occasionally demonstrate borderline or mildly reduced LV ejection fractions at rest. Recent advances in functional myocardial imaging, including tissue Doppler echocardiography and strain echocardiography, have also suggested that exercise training may lead to changes in LV systolic function that are not detected by assessment of a global index like LV ejection fraction.43–45 The importance of these findings with respect to our understanding of exercise physiology and for differentiating athletic from pathological remodeling is an area of active investigation.Left ventricular diastolic function has also been extensively evaluated in trained athletes. Most studies of diastolic function in athletes have used conventional 2-dimensional (transmitral) and tissue Doppler echocardiography. It is now well recognized that endurance exercise training leads to enhanced early diastolic LV filling as assessed by E-wave velocity and mitral annular/LV tissue velocities.30,46–50 It is likely that improved LV diastolic function, particularly the ability of the LV to relax briskly at high heart rates, is an essential mechanism of stroke volume preservation during exercise. There are sparse data examining diastolic function in strength-trained athletes, but a longitudinal study suggested that the concentric LV hypertrophy associated with strength training is accompanied by either unchanged or relative impairment of LV relaxation.35The majority of data characterizing LV structure and function in athletes come from cross-sectional studies in which participants are characterized at a single time point. This approach is popular because of its relative logistical ease, but it does not permit definitive conclusions about important issues, including the temporal nature, permanence/long-term implications, and dose-response relationships between exercise and cardiac remodeling. In contrast, longitudinal studies in which measurements are made serially and exercise exposure can be controlled, or at least accurately measured, provide an opportunity to address these areas of uncertainty. Representative prior longitudinal work is summarized in Table 1. Unfortunately, such studies constitute only a small fraction of the total body of literature. In our opinion, further longitudinal work is required to address many of the key remaining areas of uncertainty in this field.Table 1. Selected Studies Using a Longitudinal Study Design Documenting Significant Exercise-Induced Cardiac Remodeling (Training Studies) and Regression (Detraining Studies) in AthletesReferenceYearAthletes, nAthlete TypeExercise ExposurePrimary Findings*Training studies Ehsani et al5119788Swimmers (7 male, 1 female)Swimming for 9 wkIncreased LVMI (104 vs 109 g/m2) Wieling et al5219819Freshman rowers (all male)Rowing for 7 moIncreased LVIDd (51.5 vs 53.3 mm)14Senior rowers (all male)Rowing for 7 moIncreased LVIDd (56.1 vs 57.9 mm) Abergel et al42200437Cyclists (all male)Professional cycling for 3 yIncreased LVID (58.3±4.8 to 60.3±4.2 mm); decreased LVWT (11.8±1.2 to 10.8±1.2 mm) Naylor et al46200522Rowers (17 male, 5 female)Rowing for 6 moIncreased LVM (236±7 vs 249±9 g; P<0.05); increased early diastolic function duManoir et al53200710Rowers (all male)Rowing training for 10 wkIncreased LVMI (88±20 vs 103±22; P<0.05) associated with increased LVEDV and LVWT Baggish et al35200840Rowers (20 male, 20 female)Rowing for 90 dIncreased LVM (116±18 vs 130±19 g/m2) with increased LVEDV24Football (24 male)Football for 90 dIncreased LVM (115±14 vs 132±11 g/m2) with increased LVWT Baggish et al44200820Rowers (10 male, 10 female)Rowing for 90 dIncreased LV radial and longitudinal strain; decreased septal circumferential strain owing to concomitant RV dilation Weiner et al54201015Rowers (all male)Rowing for 90 dIncreased LV torsion and LV early diastolic untwisting rateDetraining studies Fagard et al55198312Cyclists (all male)Detraining for 12 wkDecreased IVS (12.3±0.4 vs 11.5±0.4)Decreased PWT (13.0±0.5 vs 11.8±0.6); LVIDd unchanged Pellicia et al56200240Mixed, elite (all male)Detraining for 12 wkDecreased LVWT by 15% (12.0±1.3 vs 10.1±0.8); decreased LVIDd by 7% (61.2±2.9 vs 57.2±3.1)LVMI indicates left ventricular mass index; LVIDd, left ventricular end-diastolic dimension; LVWT, left ventricular wall thickness; LVEDV, left ventricular volume; IVS, interventricular septum; and PWT, posterior wall thickness.*All findings reported have statistical significance of at least P<0.05.The Right VentricleExercise-induced cardiac remodeling is not confined to the LV. Endurance exercise requires both the LV and right ventricle (RV) to accept and eject relatively large quantities of blood. In the absence of significant shunting, both chambers must augment function to accomplish this task. Recent advances in noninvasive imaging have begun to clarify how the RV responds to the repeated challenges of exercise. An initial M-mode echocardiographic study demonstrated symmetrical RV and LV enlargement in a small (n=12) cohort of highly trained endurance athletes.57 Subsequently, Henriksen et al58 examined RV and LV cavity and wall measurements using M-mode and 2-dimensional echocardiography in 127 male elite endurance athletes. Compared with historical control subjects, endurance athletes demonstrated significantly larger RV cavities and a trend toward thicker RV free walls. In an elegant magnetic resonance imaging–based study, Scharhag et al59 recently confirmed that RV enlargement is common among endurance athletes. Data from this study suggest that RV enlargement parallels LV enlargement, supporting the concept of balanced, biventricular enlargement. A recent magnetic resonance imaging study in professional soccer players demonstrated similar findings.60The impact of strength training on the RV remains unclear because the limited available data are inconsistent. Perseghin et al61 compared RV and LV structure in endurance athletes (marathon runners), strength athletes (sprinters), and sedentary control subjects and found the largest RV volumes among the strength athletes. However, there were no significant difference between the RV dimensions in strength and endurance athletes after adjustment for body surface area. Right ventricular structure in collegiate endurance-trained (rowers) and strength-trained (American-style football players) athletes was recently assessed before and after 90 days of team-based exercise training.35 There was statistically significant RV dilation in the endurance athletes but no changes in RV architecture in the strength athletes. Further elucidation of how the RV responds to different forms of exercise and its contribution to exercise capacity is an important area for future work.The AortaThe aorta experiences a significant hemodynamic load during exercise. The nature of this load is dependent on sport type, with endurance activity causing high-volume aortic flow with modest systemic hypertension and strength activity resulting in normal-volume aortic flow with potentially profound systemic hypertension. It is logical to assume that such conditions should result in variable aortic remodeling in athletic individuals, and this premise has been the topic of several studies. Babaee Bigi and Aslani62 compared aortic dimensions in 100 elite strength-trained athletes with those in 128 age-matched control subjects. They reported significantly larger aortic dimensions at the valve annulus, sinuses of Valsalva, sinotubular junction, and proximal root in the strength-trained athletes. The largest dimensions were observed in those with the longest duration of exercise training. Similarly, D'Andrea et al63 used transthoracic echocardiography to measure aortic dimensions in 615 elite athletes (370 endurance-trained athletes and 245 strength-trained athletes; 410 men; mean age, 28.4±10.2 years; range, 18 to 40 years). These authors found that the aortic root diameter was significantly larger among strength-trained athletes. Vascular remodeling may also take in place in the descending abdominal aorta.64In contrast to the above work, Pelliccia et al65 recently reported aortic root dimensions in a heterogeneous group of 2317 Italian athletes and found the largest measurements in endurance-trained athletes, specifically swimmers and cyclists. Such contradictory data make definitive conclusions about the impact of sport-specific exercise training on aortic dimensions impossible. Of note, these and other studies66 have found that the ascending aortic root rarely exceeds the clinically accepted upper limits of normal (40 mm) in trained athletes. While we await further study, it seems reasonable to conclude that athletic training alone is not a common cause of marked aortic dilation.The Left AtriumNumerous authors have examined the left atrial structure in trained athletes. Hauser et al57 presented an early echocardiographic study demonstrating that a small group of endurance athletes (n=12) had larger left atria than sedentary control subjects. A similar early study documented left atrial enlargement in older individuals with a significant history of exercise training.67 Hoogsteen et al68 compared atrial dimensions in young competitive cyclists (age, 17±0.2 years; n=66) with those in older, presumably more experienced cyclists (29±2.6 years; n=35) and found larger dimensions in the older athletes. Pelliccia et al69 presented the largest data set of atrial measurements in athletes (n=1777) and demonstrated that left atrial enlargement (>40 mm in an anterior/posterior transthoracic echocardiographic view) was present in 20% of the athletes. Of note, few athletes with left atrial dilation in the Pelliccia et al series had clinical evidence of supraventricular arrhythmias.69 D'Andrea et al70 recently confirmed a high prevalence of left atrial enlargement in trained athletes and demonstrated an association with endurance exercise training.The Impact of Sex and EthnicityExercise-induced cardiac remodeling is similar in male and female athletes. However, available data suggest that female athletes exhibit quantitatively less physiological remodeling than their male counterparts.70–75 This appears to be true even when cardiac dimensions are corrected for the typically smaller female body size. Explanations for the sex-specific magnitude of remodeling remain elusive. Race is also an important determinant of remodeling, with black athletes tending to have thicker LV walls than white athletes. Basavarajaiah and colleagues75a recently studied a group of white and black athletes using echocardiographic imaging and found that nearly 20% of the black athletes had an LV wall thickness of at least 12 mm compared with 4% in white athletes. Importantly, 3% of black athletes in this cohort were found to have a wall thickness of >15 mm. Similarly, Rawlins et al75b studied ethnic/race-related differences in a group of 440 black and white female athletes using ECG and echocardiography. Black female athletes demonstrated significantly higher LV wall thickness and mass compared with the white women (in black athletes: LV wall thickness=9.2±1.2 mm and LV mass=187.2±42 g; in white athletes: LV wall thickness=8.6±1.2 mm and LV mass=172.3±42 g). Such anatomic differences are likely responsible for the increased prevalence of ECG abnormalities in black athletes, including LV hypertrophy, precordial T-wave inversions, and early repolarization.76Common Clinical Cardiovascular Issues in the Athletic PatientAlthough participation in sport and regular exercise promotes good health, athletes are not immune to cardiovascular symptoms and disease and thus represent an important population encountered in clinical practice. The athletic patient population is heterogeneous and comprises individuals spanning broad ranges of age, athletic talent, and performance goals. Athletes typically become patients in 1 of 2 ways. First, an abnormal value for one of the structural or function parameters discussed above may be detected in the asymptomatic individual. Such findings often raise concerns about potential underlying pathology, thereby prompting further assessment. Second, athletes may develop symptoms suggestive of cardiovascular disease during training or competition and thus seek or are referred for a symptom-driven evaluation.Cardiac Enlargement: Pathology Versus Physiological AdaptationThe phenotypic overlap between exercise-induced cardiac remodeling and pathological structural heart disease is widely appreciated. Cardiac structural abnormality of unclear origin and significance may be detected during preparticipation cardiovascular disease screening, routine health examinations, or evaluation of the athlete with symptoms. Extreme cases of exercise-induced ventricular remodeling may be difficult to differentiate from mild forms of hypertrophic cardiomyopathy, familial or acquired dilated cardiomyopathy, and arrhythmogenic RV cardiomyopathy. The clinical task of differentiating marked exercise-induced remodeling from these important forms of disease remains important, with implications including sport restriction, pharmacological therapy, and placement of an implantable cardiac defibrillator.The overlap between features of the athlete's heart and characteristics of cardiomyopathy, specifically hypertrophic cardiomyopathy, that may affect young athletes has been coined the Maron gray zone.77 A valuable schema for approaching the athletic patient with LV hypertrophy of unclear origin has been presented, and remains useful in clinical practice.78 It is noteworthy that this diagnostic approach was developed at a time when noninvasive cardiovascular imaging was in its infancy and, for the most part, restricted to basic 2-dimensional echocardiography. Recent advances in cardiovascular diagnostics have proven to be useful additions to these original criteria.Functional myocardial echocardiography, including tissue Doppler and speckle-tracking imaging, permits detailed and accurate assessment of myocardial function. Tissue Doppler imaging permits assessment of myocardial relaxation and contraction velocity. Across numerous studies, early diastolic relaxation velocity has been shown to be normal or increased in athletes with LV hypertrophy resulting from exercise-induced remodeling.79,80 In contrast, pathological forms of LV hypertrophy are typically associated with reduced early diastolic relaxation velocity and peak systolic tissue velocity.45,81–83 Tissue strain and strain rate may also provide useful insight into the origin of LV hypertrophy in athletes.84,85Cardiac magnetic resonance imaging has similarly emerged as an invaluable tool for the evaluation of the athlete with indeterminate cardiac enlargement. Cardiac magnetic resonance allows highly accurate assessment of myocardial thickness, chamber volumes, tissue composition, extracardiac anatomy, and cardiac magnetic resonance–derived reference values in athletes have been published.86 Importantly, the use of gadolinium contrast with delayed imaging provides information about the presence and location of myocardial fibrosis. Recent data document myocardial fibrosis patterns that are relatively specific to certain cardiomyopathies and highlight the utility of cardiac magnetic resonance for the assessment of indeterminate cardiac enlargement in the athlete.87,88 At the present time, we use cardiac magnetic resonance in athletes with either indeterminate echocardiographic imaging or clinical features that suggest a diagnosis that may not be definitively assessed by echocardiography (ie, myocarditis). The interested re" @default.
• W2070304234 created "2016-06-24" @default.
• W2070304234 creator A5029838858 @default.
• W2070304234 creator A5077949191 @default.
• W2070304234 date "2011-06-14" @default.
• W2070304234 modified "2023-10-11" @default.
• W2070304234 title "Athlete's Heart and Cardiovascular Care of the Athlete" @default.
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