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Correspondence: Address to Thijs M.H. Eijsvogels, PhD, Department of Physiology (392), Radboud University Medical Center, PO Box 9101, 6500 HB Nijmegen, The Netherlands.
Department of Physiology, Radboud University Medical Center, Nijmegen, The NetherlandsResearch Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UKDivision of Cardiology, Hartford Hospital, Hartford, CT
Myocardial fibrosis (MF) is a common phenomenon in the late stages of diverse cardiac diseases and is a predictive factor for sudden cardiac death. Myocardial fibrosis detected by magnetic resonance imaging has also been reported in athletes. Regular exercise improves cardiovascular health, but there may be a limit of benefit in the exercise dose-response relationship. Intense exercise training could induce pathologic cardiac remodeling, ultimately leading to MF, but the clinical implications of MF in athletes are unknown. For this comprehensive review, we performed a systematic search of the PubMed and MEDLINE databases up to June 2016. Key Medical Subject Headings terms and keywords pertaining to MF and exercise (training) were included. Articles were included if they represented primary MF data in athletes. We identified 65 athletes with MF from 19 case studies/series and 14 athletic population studies. Myocardial fibrosis in athletes was predominantly identified in the intraventricular septum and where the right ventricle joins the septum. Although the underlying mechanisms are unknown, we summarize the evidence for genetic predisposition, silent myocarditis, pulmonary artery pressure overload, and prolonged exercise-induced repetitive micro-injury as contributors to the development of MF in athletes. We also discuss the clinical implications and potential treatment strategies of MF in athletes.
Habitual physical activity is known to reduce the risk of future cardiovascular morbidity and mortality. Several studies exploring the relationship between physical activity and cardiovascular health have reported a curvilinear association. However, emerging evidence suggests that cardiac maladaptations may occur in a few endurance athletes who perform exercise at the upper end of the physical activity continuum. Among other observations (ie, enhanced coronary artery calcification, cardiac dysfunction, cardiac biomarker release, and arrhythmias), evidence of myocardial fibrosis (MF) has been reported in case reports and athletic population studies.
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Typically, MF is observed in cardiac patients and is a predictive factor for adverse cardiac outcome, such as sudden cardiac death. Whether the development of MF in athletes is related to their exercise training and competition regimens or is secondary to (subclinical) cardiovascular disease is key because this provides essential insight into the underlying mechanisms.
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Characterization of the phenotype of MF is important to allow early identification of athletes at risk. Furthermore, the pattern, location, and quantification of MF may importantly drive the choice of specific treatment strategies and lifestyle advice.
Cardiac remodeling is a common adaptation in trained athletes that consists of increased left ventricular (LV) and right ventricular (RV) dimensions and atrial cavity size and is associated with normal systolic and diastolic function.
Systematic review and meta-analysis of training mode, imaging modality and body size influences on the morphology and function of the male athlete's heart.
but myocardial fibrosis (MF) has been detected in endurance athletes by cardiac magnetic resonance imaging (CMR) using late gadolinium enhancement (LGE).
T1 and T2 mapping for early diagnosis of dilated non-ischaemic cardiomyopathy in middle-aged patients and differentiation from normal physiological adaptation.
Correlation between ECG abnormalities and cardiac parameters in highly trained asymptomatic male endurance athletes: evaluation using cardiac magnetic resonance imaging.
Myocardial fibrosis is defined by a significant increase in the collagen volume of myocardial tissue. It is a complex process that involves all components of the myocardial tissue and can be triggered by tissue injury from myocardial ischemia (hypoxia), inflammation, and hypertensive overload.
which increases LV end-diastolic and left atrial pressures. In animal models and patient studies, MF is also associated with reduced ventricular systolic function.
Ventricular arrhythmias in hypertensive left ventricular hypertrophy: relationship to coronary artery disease, left ventricular dysfunction, and myocardial fibrosis.
Incidence and prognostic implication of unrecognized myocardial scar characterized by cardiac magnetic resonance in diabetic patients without clinical evidence of myocardial infarction.
making the relationship between lifelong endurance exercise and the development of MF unclear. Furthermore, the clinical implications of MF in athletes are unknown. This systematic review summarizes the available data on the prevalence of MF in physically active individuals to identify predictors and the potential mechanism(s) of MF development and its clinical implications.
Methods
MF Assessment
Myocardial fibrosis can be determined by microscopic examination of tissue samples or by CMR. Myocardial tissue is obtained in vivo by transvenous endomyocardial biopsy of the RV. Fibrillar collagen can then be quantified under polarized light after Picrosirius red
staining. Using CMR to assess LGE, a sign of MF, is preferred for assessment of focal MF because it is readily available, is noninvasive, and has the capacity to assess all the cardiac chambers. Alternatively, CMR-based contrast-enhanced T1 mapping can be used to assess diffuse MF.
We performed a systematic search of peer-reviewed studies that examined MF in athletes using cardiac biopsy or CMR. The literature was searched using the PubMed and MEDLINE databases up to June 1, 2016. Key Medical Subject Headings terms and keywords were included pertaining to MF (delayed [gadolinium] enhancement, pathological late gadolinium enhancement, myocardial late gadolinium enhancement, abnormal late gadolinium enhancement, fibrosis, myocardium, myocardial fibrosis, papillary muscles/pathology, ventricular dysplasia, and ventricular torsion) and exercise training (exercise, athletes, sports, sport, motor activity, marathon, triathlon, bicycling, swimming, physical endurance, marathon running, sports medicine, and exercise-induced).
Selection of Studies
The selection process consisted of review of the titles, abstracts, and full texts of articles by two authors (F.R.S. and T.M.H.E.), who later met to reach mutual consensus. The inclusion criteria were (1) fibrosis established by validated techniques and (2) a study population consisting of athletes, defined as “individuals who are proficient in sports, have routinely performed exercise training for an extended period of time and participate in sporting events.” The only exclusion criteria was underlying (genetic) cardiovascular disease, such as hypertrophic cardiomyopathy or arrhythmogenic RV cardiomyopathy.
Results
The systematic search yielded 33 studies: 19 case reports/series using biopsy (n=17) and CMR (n=2) to determine MF and 14 studies in athletic populations using CMR to determine MF (Figure 1).
Figure 1Flowchart of the search strategy to determine the prevalence of myocardial fibrosis (MF) in athletes. The following Medical Subject Headings keywords were used in the literature search: delayed enhancement, pathological late gadolinium enhancement, myocardial late gadolinium enhancement, abnormal late gadolinium enhancement, fibrosis, myocardium, myocardial fibrosis, papillary muscles/pathology, ventricular dysplasia, ventricular torsion, exercise, athletes, sports, sport, motor activity, marathon, triathlon, bicycling, swimming, physical endurance, marathon running, sports medicine, and exercise-induced.
Exercise-induced right ventricular dysplasia/cardiomyopathy: an emerging condition distinct from arrhythmogenic right ventricular dysplasia/cardiomyopathy.
Athletes ranged in age from 13 to 73 years at MF diagnosis, and 76% of the population was male. Although the sex and age of 6 athletes was not reported,
High prevalence of right ventricular involvement in endurance athletes with ventricular arrhythmias: role of an electrophysiologic study in risk stratification.
Myocardial disarray, fibrosis, fatty infiltration, mononuclear cell infiltration of the left-sided bundle of His, and fibrosis of the right bundle branch; patchy fibrosis of the left side of the septum
Basketball player (n=1) Soccer players (n=2) Volleyball player (n=1) Water-skier (n=1)
Not specified
17-23
60% male
Fibrosis prevailing in the RV with occasional focus of cellular necrosis (basketball player) Focal nonspecific fibrosis (soccer player) Diffuse, nonspecific fibrosis (soccer player) Myocarditis with fibrosis largely prevailing in the RV (volleyball player) Mild focal increase of the interstitial fibrous tissue, suggesting active myocarditis (water-skier)
Biopsy (minor arrhythmias or echocardiographic abnormalities)
Rated officially as a first-class runner; middle and long distances Not specified
22 20
100% male
Scar tissue (foci of connective and granulation tissue) in the posterior wall of the LV and interventricular septum Foci of connective tissue in the LV and interventricular septum
High prevalence of right ventricular involvement in endurance athletes with ventricular arrhythmias: role of an electrophysiologic study in risk stratification.
There were wide swaths of MF consistent with areas of old healed infarction, as well as areas of recent infarction; other areas in the heart showed myocardial fatty infiltration, fibrosis, and marked myofibrillary disarray
Running for 20 y, completed multiple marathons, personal best 2 h and 30 min
57
Male
Fibrosis throughout both chambers, predominating in the LV; widespread replacement fibrosis in the lateral and posterior ventricular walls, and interstitial fibrosis in the inner layer of the myocardium
Exercise-induced right ventricular dysplasia/cardiomyopathy: an emerging condition distinct from arrhythmogenic right ventricular dysplasia/cardiomyopathy.
After running 1460 km and ascending >2600 m the run was ended; in support of the event, after a 3-d rest, the individual cycled an additional 1580 km in 9 d ascending another 1190 m
46
Male
At the inferior insertion of the RV and in the interventricular septum that may represent subtle inflammation secondary to a combined exercise and altitude effect
Cyclists (n=5) Football player (n=1) Basketball player (n=1)
≥6 h/wk for ≥5 y
19-32
86% male
LGE predominantly in the lateral wall; mean ± SD size of 20.3±7.7 g Subepicardial (cyclist, football player, basketball player) Transmural patches (cyclist) Intramural patches (cyclists) Likely to reflect chronic scarring
CMR (pathologic T-wave inversions on ECG (n=4) or ventricular arrhythmias (n=3)
CMR = cardiac magnetic resonance imaging; ECG = electrocardiogram; LGE = late gadolinium enhancement; LV = left ventricle; RV = right ventricle.
The existence of MF was also assessed by CMR in athletic populations (Table 2). A total of 509 endurance exercise athletes were examined; 7 studies confirmed the presence of MF in athletes, and 7 studies did not. Overall, 89% of the population was male, and MF was reported in 30 of the 509 athletes (5.9%). Interestingly, lifetime exercise exposure (1-100 completed marathons) and age (26-72 years) varied substantially across participants, but most reports occurred in long-term endurance athletes.
Table 2Prevalence and Patterns of Myocardial Fibrosis (MF) in Athletic Populations Using CMR
Mean ± SD of 43±6 y of competitive exercise training No exercise training Mean ± SD of 18±7 y of competitive exercise training
57±6 60±5 31±5
100% male
50 0 0
1. Septal and lateral wall 2. Epicardial lateral wall 3. Basal and mid insertion point 4. Inferior insertion point mid and apical 5. Insertion point inferior mid/apical 6. Inferior insertion point
Athletes: 42% involving the subendocardial layer and partial transmural spreading; 58% atypical patchy to streaky subepicardial to midmyocardial hyperenhancement, which may represent interstitial fibrosis or myocardial fiber disarray for various potential reasons Controls: 50% CAD pattern; 50% non-CAD pattern
T1 and T2 mapping for early diagnosis of dilated non-ischaemic cardiomyopathy in middle-aged patients and differentiation from normal physiological adaptation.
Mean ± SD of 47±7 miles/wk ≥3 marathons in the past 2 y
55±4
84% male
8
Anterior wall of the LV myocardium in subendocardial distribution before running the marathon, with concomitant evidence of obstructive LAD artery disease
Correlation between ECG abnormalities and cardiac parameters in highly trained asymptomatic male endurance athletes: evaluation using cardiac magnetic resonance imaging.
High prevalence of right ventricular involvement in endurance athletes with ventricular arrhythmias: role of an electrophysiologic study in risk stratification.
Reproducibility and clinical significance of exercise-induced increases in cardiac troponins and N-terminal pro brain natriuretic peptide in endurance athletes.
Mountain bike marathon cyclists (n=15) Marathon runners (n=5)
Training history in endurance exercise of a mean ± SD of 7±3 y and trained a mean ± SD of 9±4 h/wk
36±7
100% male
0
Not applicable
a CAD = coronary artery disease; CMR = cardiac magnetic resonance imaging; LAD = left anterior descending; LGE = late gadolinium enhancement; LV = left ventricle; RV = right ventricle.
b Studies are arranged from highest to lowest MF prevalence.
The pattern of MF in athletes determined by microscopic examination varies (Table 1), and this likely represents different causes. Fourteen of the 35 athletes with MF (40%) included in the case reports/series demonstrated a nonspecific LGE pattern, and the remaining athletes demonstrated an ischemic (n=7, 20%), myocarditic (n=7, 20%), or hypertrophic (n=1, 3%) MF pattern; the pattern was not specified in 6 athletes (17%) (Figure 2).
Figure 2The prevalence of the pattern of myocardial fibrosis (MF) found in athletes in case reports/series and athletic population studies.
A subendocardial pattern, typically seen after ischemic myocardial injury because the subendocardium is the region most vulnerable to reduced coronary blood flow, was observed in 8 of 30 athletes with MF (27%).
T1 and T2 mapping for early diagnosis of dilated non-ischaemic cardiomyopathy in middle-aged patients and differentiation from normal physiological adaptation.
Correlation between ECG abnormalities and cardiac parameters in highly trained asymptomatic male endurance athletes: evaluation using cardiac magnetic resonance imaging.
The location of MF determined by biopsy (case studies/series) and CMR-LGE (athletic population studies) varies substantially (Figure 3). La Gerche et al
reported that MF was confined to the interventricular septum, frequently where the RV attaches to the septum (the hinge points). Overall, a significant proportion of MF in athletes is found in the septum (19 of 65, 29%)
T1 and T2 mapping for early diagnosis of dilated non-ischaemic cardiomyopathy in middle-aged patients and differentiation from normal physiological adaptation.
Some have speculated that the distention of the RV during endurance exercise due to an acute increase in RV work with exercise may be responsible for this interventricular scar pattern.
Figure 3The frequency of the location of myocardial fibrosis (MF) reported in case studies/series and athletic population studies. In 10 athletes (5 in case series
The quantification of MF is poorly reported: only 3 case reports and 1 CMR study describe the extent of fibrosis. The volume of the scar in a biopsy taken from a runner confirmed that MF was present in 2.9% of the LV and 3.5% of the interventricular septum.
reinforced the heterogeneity of the percentage of LGE-positive myocardium (range, 0.5%-17.8%) in German marathon runners. Also, these authors found that the median percentage of MF was comparable between runners with a subendocardial LGE pattern (0.9%), runners with a nonspecific pattern (1.2%), and physically inactive controls (2.2%). Last, the mean ± SD volume of the LGE region in the study by Schnell et al
was 20.3±7.7 g, which was the equivalent of 12%±4.8% of the LV mass.
Discussion
The present review reveals that the phenotype of MF in athletes demonstrates large variance in patterns, location, and quantification. Nonetheless, a nonspecific LGE pattern, location in the RV or septum, and representing 1% to 3% of the myocardium seem to be the most common descriptors used for MF typically found in athletes by magnetic resonance imaging. The phenotype of MF in athletes differs from that in the general population, and this difference may provide insight into the underlying mechanisms and clinical prognosis of MF in assumingly healthy athletes.
MF in Athletes vs Controls
The prevalence of MF varied from 0% to 50% in often small-scale athlete populations. Only 2 studies compared MF prevalence between athletes and age- and sex-matched physically inactive controls.
observed MF in 6 of 12 lifelong veteran endurance athletes but not in any of 20 sedentary peers. Although both studies reported a higher prevalence of MF in athletes vs physically inactive controls, the presence of MF in these control groups was lower compared with recent observations in the general population. In a large American cohort study of nonathletes (mean ± SD age, 68±9 years), MF was found in 146 of 1840 participants (7.9%).
report an even higher prevalence of unknown MF (17.0% and 19.8%, respectively). These findings highlight the need for additional high-quality studies comparing the prevalence and extent of MF in large populations of physically active and inactive individuals. Future studies should consider the amount and intensity of exercise training, as well as the lifelong exercise exposure, to test the hypothesis that MF prevalence differs between athletes and the general population.
Focal vs Diffuse MF
The CMR studies assessing MF in athletes included predominantly LGE measurements. Although CMR-LGE is a validated technique to assess quantification of focal MF, it does not provide information about the presence of diffuse MF. This may lead to underestimating the true prevalence of MF in athletes and may limit the generalizability of these findings. Nevertheless, 2 recent studies used T1 and T2 mapping to assess (diffuse) MF in athletes.
T1 and T2 mapping for early diagnosis of dilated non-ischaemic cardiomyopathy in middle-aged patients and differentiation from normal physiological adaptation.
In a Scottish study, no difference in native T1, T2 relaxation time and extracellular volume was observed between athletes (n=21, ≥6 h/wk of exercise training) and controls (n=21).
T1 and T2 mapping for early diagnosis of dilated non-ischaemic cardiomyopathy in middle-aged patients and differentiation from normal physiological adaptation.
In contrast, significantly higher native T1 values of the LV and interventricular septum were found in Turkish athletes (≥6 h/wk intense exercise training) compared with age- and sex-matched controls (<3 h/wk moderate exercise). Moreover, athletes reporting at least 5 years of exercise training had higher T1 values, indicating more diffuse fibrosis compared with athletes exercising for less than 5 years (P<.05).
These findings suggest a higher prevalence of diffuse MF in Turkish athletes vs controls. Apart from the age difference between Scottish (mean ± SD age, 46±11 years) and Turkish (mean ± SD age, 25±3 years) athletes, there is no clear explanation for the conflicting outcomes. We, therefore, recommend that future studies include measurements of T1 relaxation times before and after contrast administration to determine the myocardial extracellular volume fraction and to quantify diffuse MF in addition to LGE-based assessment of focal MF. Also, the use of free-breathing, motion-corrected, averaged LGE CMR measurements may improve image quality of the RV.
Use of these novel imaging techniques should further improve our understanding of the development, progression, and clinical interpretation of MF in athletes.
Factors Associated With MF
Several studies identified factors that are associated with the presence of MF in athletes. La Gerche et al
reported that athletes with LGE had participated in endurance exercise longer (mean ± SD, 20±16 years) than athletes without MF (mean ± SD, 8±6 years; P=.043). Similarly, Wilson et al
reported that LGE was related to the years of training (P<.001) and the number of completed competitive marathons (P<.001) or ultra-endurance marathons (>50 miles) (P=.007). Möhlenkamp et al
reported an association between the number of completed marathons and LGE (P=.02). Evidence from case reports/series confirms that athletes diagnosed as having MF demonstrate high doses of exercise for many years (Table 1). For example, an athlete trained 10 h/wk, including 50 km of running and 1 to 2 hours of mountain biking,
found that the prevalence of MF was the highest (50%) in veteran endurance athletes (mean ± SD age, 57±6 years) who had been involved in lifelong competitive training for a mean ± SD of 43±6 years. Studies including predominantly younger participants or less-trained individuals generally fail to find MF.
Evidence of MF in athletic populations is exclusively based on observational studies, which do not provide insight into potential underlying mechanisms. However, we summarize the available evidence for 4 different pathways based on patient characteristics, location and patterns of MF, and identified predictors.
Genetic Predisposition
Ten case reports describe the presence of MF in 28 young athletes (≤30 years old). Their young age raises the question whether genetic predisposition contributes to MF development. Hypertrophic cardiomyopathy is the most common genetic heart disease
Characteristics and clinical significance of late gadolinium enhancement by contrast-enhanced magnetic resonance imaging in patients with hypertrophic cardiomyopathy.
Mutations in genes coding for sarcomere proteins, Z-disk or calcium-handling proteins, are responsible for the phenotype of hypertrophic cardiomyopathy.
However, variability can be so striking in individuals with the same genetic defect that little, if any, relationship can be established between mutations and phenotype, clinical course, and patient outcome. Similarly, genetic factors may contribute to the variability of MF presentations in athletes.
Silent Myocarditis
The results of 5 biopsy studies and 3 CMR-LGE studies suggest that myocarditis is responsible for LGE and that this is probably true in some (n=10) but not all (n=65) athletes. Late gadolinium enhancement has high specificity for the detection of injury in myocarditis but variable sensitivity to detect active or chronic inflammation.
This might be due to limited areas of necrotic myocytes that cannot be visualized because of limited pixel size in CMR images compared with larger regions of scarring in ischemic necrosis. Myocarditis is defined as inflammatory cellular infiltrate, whereas associated myocyte necrosis may be present on stained heart tissue sections.
Myocarditis usually results from infections with viruses such as coxsackievirus B3, adenoviruses, and parvovirus B19 but may also result from other pathogens, such as the protozoan Trypanosoma cruzi (Chagas disease), toxic or hypersensitivity drug reactions (anticonvulsants, antibiotics, and antipsychotics), giant cell myocarditis, or sarcoidosis.
Mice were infected with coxsackievirus to induce myocarditis and then were divided into 4 groups: group 1 received immunosuppression with daily doses of cyclosporine and an antithymocyte monoclonal antibody, group 2 performed daily swimming exericise, group 3 received both interventions, and group 4 served as controls. After 21 days, mortality rates were highest in the exercise-only group (group 2).
Hence, it is possible that continued exercise training accelerates myocardial damage and MF during a silent myocarditis.
Pulmonary Artery Pressure Overload
The volume of LGE is typically small and confined to the septum or RV insertion points in 48% of athletes diagnosed as having MF by magnetic resonance imaging LGE. This may result from local mechanical stress due to prolonged exercise. Interestingly, MF in this cardiac location is also observed in patients with pulmonary arterial hypertension.
Late gadolinium enhancement was present at a similar anatomical location in adults whose RV was forced to produce systemic pressures after atrial redirection surgery for transposition of the great vessels.
Late gadolinium enhancement cardiovascular magnetic resonance of the systemic right ventricle in adults with previous atrial redirection surgery for transposition of the great arteries.
Late gadolinium enhancement cardiovascular magnetic resonance of the systemic right ventricle in adults with previous atrial redirection surgery for transposition of the great arteries.
Exercise produces a greater relative increase in pulmonic than aortic systolic pressure, resulting in an increase in wall stress of 125% vs 4% for the RV and LV, respectively.
The thinner wall of the RV may facilitate the progression from increased wall stress to cardiomyocyte damage more than in the LV. Although echocardiography studies show that acute exercise-induced changes in RV structure and function fully recover within days,
chronic structural changes from repetitive prolonged exercise are possible. Therefore, MF in athletes may result from long-term endurance exercise training and competition and the associated repetitive exercise-induced elevations in pulmonary artery pressures.
Repetitive Microdamage
Cardiac troponin I and T are the standard biomarkers used to serologically identify myocardial damage. Many studies have reported increases in cardiac troponin levels after prolonged exercise.
but they may represent microdamage to cardiomyocytes. Accordingly, repetitive exposure to high-intensity endurance exercise–induced cardiac microdamage, evidenced by minor troponin level elevations, could lead to MF development after lifelong exercise training, as observed in veteran athletes.
Incidence and prognostic implication of unrecognized myocardial scar characterized by cardiac magnetic resonance in diabetic patients without clinical evidence of myocardial infarction.
Gadolinium cardiovascular magnetic resonance predicts reversible myocardial dysfunction and remodeling in patients with heart failure undergoing beta-blocker therapy.
Gender differences in survival in patients with severe left ventricular dysfunction despite similar extent of myocardial scar measured on cardiac magnetic resonance.
Impact of unrecognized myocardial scar detected by cardiac magnetic resonance imaging on event-free survival in patients presenting with signs or symptoms of coronary artery disease.
However, the impact of MF on cardiovascular health has not been carefully studied in athletes. Three of 12 German marathon runners with LGE (25%) required revascularization during a mean ± SD of 21±3 months of follow-up compared with 1 of 90 runners (1%) without LGE (P<.001).
Half of the runners with MF, however, had an LGE pattern suggestive of ischemic myocardial injury. The increased risk of MF on adverse outcomes persisted during a mean ± SD of 74±12 months of follow-up.
Runners with coronary events had a higher prevalence of LGE (57%) compared with peers without coronary events (8%; P=.003), despite comparable mean ± SD 10-year Framingham Risk Scores (7.9%±2.3% vs 7.0%±3.7%).
The presence of LGE in this cohort was also associated with higher coronary artery calcification scores (median Agatston coronary artery calcium scores, 192 vs 26; P=.0046),
demonstrating that the increased incidence of cardiovascular events in some runners with LGE is due to atherosclerosis and previous infarction. Other studies in other patients do not support atherosclerosis and previous infarction as the cause of the LGE. Although the German findings suggest a worse prognosis in athletes with MF, it must be emphasized that these data are derived from a single cohort. Nevertheless, athletes with LGE patterns consistent with coronary artery disease and previous infarction or those with evidence of active myocardial inflammation should be pharmacologically treated to reduce their risk of an acute cardiac event and to treat their myocarditis, respectively.
The prognostic significance of nonspecific MF patterns seen in athletes is unknown. There is no evidence that athletes with this pattern should be restricted from exercise. Additional clinical testing should be recommended based on the individual’s symptoms and clinical profile. Myocardial fibrosis detected by LGE in cardiac studies of asymptomatic athletes performed for other nonclinical reasons should be treated as an incidental finding and not pursued.
The impact of lifelong exercise training on cardiovascular health is under debate.
Million Women Study Collaborators Frequent physical activity may not reduce vascular disease risk as much as moderate activity: large prospective study of women in the United Kingdom.
Nevertheless, data from CMR athletic population studies suggest that some long-term endurance athletes develop MF.
Conclusion
Myocardial fibrosis has been reported in some lifelong endurance athletes. The pattern of LGE is heterogeneous, which may represent different causation and could contribute to the difference in MF locations between case studies/series and athletic population studies. In a few of these athletes, CMR-detected LGE is consistent with coronary artery disease and previous infarction and seems to be associated with increased risk of cardiovascular events. Other middle-aged and older athletes demonstrate LGE largely confined to the interventricular septum, often near the hinge points between the RV and the septum. This pattern seems more common in long-term endurance athletes and may represent the effect of repetitive myocardial microtrauma or repetitive dilatation of the RV with exercise. Athletes with underlying cardiovascular disease should receive pharmacological treatment to reduce the risk of secondary events. The significance of nonspecific MF is largely unknown, and future studies investigating the functional and clinical consequences of MF in athletes are warranted.
Systematic review and meta-analysis of training mode, imaging modality and body size influences on the morphology and function of the male athlete's heart.
T1 and T2 mapping for early diagnosis of dilated non-ischaemic cardiomyopathy in middle-aged patients and differentiation from normal physiological adaptation.
Correlation between ECG abnormalities and cardiac parameters in highly trained asymptomatic male endurance athletes: evaluation using cardiac magnetic resonance imaging.
Ventricular arrhythmias in hypertensive left ventricular hypertrophy: relationship to coronary artery disease, left ventricular dysfunction, and myocardial fibrosis.
Incidence and prognostic implication of unrecognized myocardial scar characterized by cardiac magnetic resonance in diabetic patients without clinical evidence of myocardial infarction.
High prevalence of right ventricular involvement in endurance athletes with ventricular arrhythmias: role of an electrophysiologic study in risk stratification.
Exercise-induced right ventricular dysplasia/cardiomyopathy: an emerging condition distinct from arrhythmogenic right ventricular dysplasia/cardiomyopathy.
Reproducibility and clinical significance of exercise-induced increases in cardiac troponins and N-terminal pro brain natriuretic peptide in endurance athletes.
Characteristics and clinical significance of late gadolinium enhancement by contrast-enhanced magnetic resonance imaging in patients with hypertrophic cardiomyopathy.
Late gadolinium enhancement cardiovascular magnetic resonance of the systemic right ventricle in adults with previous atrial redirection surgery for transposition of the great arteries.
Gadolinium cardiovascular magnetic resonance predicts reversible myocardial dysfunction and remodeling in patients with heart failure undergoing beta-blocker therapy.
Gender differences in survival in patients with severe left ventricular dysfunction despite similar extent of myocardial scar measured on cardiac magnetic resonance.
Impact of unrecognized myocardial scar detected by cardiac magnetic resonance imaging on event-free survival in patients presenting with signs or symptoms of coronary artery disease.
Grant Support: This study was supported by Marie Sklodowska-Curie Fellowship grant 655502 (T.M.H.E) from the European Commission; Rubicon grant 825.12.016 from the Netherlands Organisation for Scientific Research (T.M.H.E.) ; and a grant from the Radboud Institute for Health Sciences (V.L.A).
Potential Competing Interests: Dr Thompson has received research grants from Aventis, Regeneron, Sanofi, and Pfizer; has served as a consultant for Aventis, Regeneron, Merck, Genomas, Abbvie, Sanofi, and Pfizer; has received speaker honoraria from Regeneron, Sanofi, Amgen, Aventis, and Merck; and owns stock in General Electric, JA Wiley Publishing, Johnson & Johnson, Abbvie, Abbott, Medtronic, and Cryolife.
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