Introduction At the pandemic's beginning, significant concern has risen about the prevalence of myocardial involvement after SARS‐CoV‐2 infection. We assessed the cardiovascular burden of SARS‐CoV‐2 in a large cohort of athletes and identified factors that might affect the disease course. We included 633 athletes in our study on whom we performed extensive cardiology examinations after recovering from SARS‐CoV‐2 infection. More than half of the athletes ( n = 322) returned for a follow‐up examination median of 107 days after the commencement of their infection. Results Troponin T positivity was as low as 1.4% of the athletes, where the subsequently performed examinations did not show definitive, ongoing myocardial injury. Altogether, 31% of the athletes' rapid training rebuild was hindered by persistent or reoccurring symptoms. Female athletes reported a higher prevalence of return to play (RTP) symptoms than their male counterparts (34% vs. 19%, p = 0.005). The development of long COVID symptoms was independently predicted by increasing age and acute symptoms' severity in a multiple regression model (AUC 0.75, CI 0.685–0.801). Athletes presenting with either or both cough and ferritin levels higher than >150 μg/L had a 4.1x (CI 1.78–9.6, p = 0.001) higher odds ratio of developing persistent symptoms. Conclusion While SARS‐CoV‐2 rarely affects the myocardium in athletes, about one in three of them experience symptoms beyond the acute phase. Identifying those athletes with a predisposition to developing long‐standing symptoms may aid clinicians and trainers in finding the optimal return‐to‐play timing and training load rebuild pace.
Prolonged and intensive exercise induces remodeling of all four cardiac chambers, a physiological process which is coined as the “athlete’s heart”. This cardiac adaptation, however, shows overlapping features with non-ischemic cardiomyopathies, such as dilated, arrhythmogenic and hypertrophic cardiomyopathy, also associated with athlete’s sudden cardiac death. Cardiac magnetic resonance (CMR) is a well-suited, highly reproducible imaging modality that can help differentiate athlete’s heart from cardiomyopathy. CMR allows accurate characterization of the morphology and function of cardiac chambers, providing full coverage of the ventricles. Moreover, it permits an in-depth understanding of the myocardial changes through specific techniques such as mapping or late gadolinium enhancement. In this narrative review, we will focus on the certainties and uncertainties of the role of CMR in sports cardiology. The main aspects of physiological adaptation due to regular and intensive sports activity and the application of CMR in highly trained athletes will be summarized.
Funding Acknowledgements Type of funding sources: Other. Main funding source(s): This study was financed by the Ministry of Innovation and Technology NRDI Office within the framework of the Artificial Intelligence National Laboratory Program. LS is supported by the EACVI Research Grant 2021. Introduction Cardiac adaptation due to regular and intense exercise is a well-known phenomenon. Cardiac magnetic resonance (CMR) imaging is a well suited, highly reproducible technique that has a vital role in differentiating physiological adaptation and pathological alterations. Native T1 and T2 mapping enable the quantitative assessment of tissue characteristics without the administration of contrast material. These techniques are increasingly used in studies aiming to consider subtle differences. However, the sex-and training-dependence of native T1 and T2 mapping values remains incompletely understood. Purpose We aimed to describe the differences in native T1 and T2 mapping among healthy athletes and less active individuals. Methods We enrolled healthy elite athletes (n=88, 56 male, 25±5 years) and healthy volunteers (n=82, 46 male, 25±3 years) to undergo CMR examinations at our Centre. Healthy elite athletes performed high sports activity levels (>10 hours/week) and competed nationally or internationally. Sex- and age-matched healthy volunteers engaged in ≤6 hours/week of sports activity. Standardized CMR protocol included short- and long-axis cine images covering the entire left (LV) and right (RV) ventricle and native T1 and T2 mapping in basal, midventricular and apical slices. Results Athletes had consistently higher LV and RV volumes and mass indexes compared to healthy volunteers (p<.001 for all). Native T1 mapping was lower in athletes than in the control group (T1: 954±24 ms vs 970±23 ms; p <.001). T1 mapping showed a moderately strong negative correlation to markers of cardiac adaptation, including LV mass, end-diastolic volume and stroke volume indexes (p<.001 for all). Moreover, we found a negative correlation between native T1 and training hours (Rho: -0.302; p<.001). On the other hand, native T2 mapping showed no difference between athletes and less active controls. Furthermore, T2 correlated with LV shape features but not with training hours. We found that mapping values differed between sexes, both in the athletic and control groups. Females showed slightly higher values compared to their male counterparts (T2: 46±2 vs 43±2; p<.001). Finally, native T1 mapping was associated with training hours and sex in our multiple linear regression model, adjusted for age, resting heart rate, body mass index, body surface area and LVM (p<.001). While T2 mapping was associated only with sex considering the same covariates. Conclusion Our study demonstrates the importance of sex-matched controls in CMR studies evaluating mapping parameters. Moreover, the consideration of exercise load seems paramount in the case of T1 mapping.
Arrhythmogenic cardiomyopathy (ACM) is a genetic heart muscle disease, structurally characterized by progressive fibro‐fatty replacement of the normal myocardium and clinically by ventricular arrhythmias (VAs). Predominantly thanks to the use of cardiac magnetic resonance, we have learnt that the spectrum of the disease encompasses not only the classical right ventricular phenotype, but also biventricular and left dominant variants. Sport activity contributes to the phenotypic expression and progression of ACM and may trigger life‐threatening VAs and sudden cardiac death (SCD). We conducted a review of the literature about ACM and its implications in Sport Cardiology and summarized the main findings in this topic. Early identification of affected athletes through preparticipation screening (PPS) is fundamental but, while classical right‐ventricular or biventricular phenotypes are usually suspected because of electrocardiogram (ECG) and echocardiographic abnormalities, variants with predominant left ventricular involvement are often characterized by normal ECG and unremarkable echocardiography. Usually the only manifestations of such variants are exercise‐induced VAs and for this reason exercise testing may empower the diagnostic yield of the PPS. Patients with ACM are not eligible to competitive sports activity, but low‐to‐moderate intensity physical activity under medical supervision is possible in most cases.
Introduction Sudden cardiac death (SCD) is the leading cause of death in athletes occurring usually during intensive training. Cardiac magnetic resonance (CMR) is a reliable technique to assess ventricular volumes and function. Furthermore, it provides tissue-specific information and has a crucial role in detecting structural myocardial diseases. Aim We aimed to investigate the prevalence of myocardial structural heart diseases and the etiology of sudden cardiac death in highly trained athletes and their outcome during follow-up. Method We examined athletes (training ≥6 hours/week) who underwent CMR due to suspected structural myocardial disease at Semmelweis University Heart and Vascular Center between 2009 and 2019. Cine movie images and late gadolinium enhanced (LGE) images were performed. Athletes with structural myocardial alterations were followed for the endpoint of all-cause-mortality. Results CMR was performed on a total of 338 athletes (280 male, 24±11 age). The indications for CMR were as follows: aborted sudden cardiac death/sustained ventricular tachycardia (SVT) (4%), ECG alterations (36%), echocardiographic alterations (32%), positive family history of SCD or cardiomyopathies (CMP) (3%), and patients' complaints, e.g. palpitation, syncope, dyspnoea, chest complaints (25%). CMR confirmed structural myocardial disease in 82 athletes with the following distribution: 20 hypertrophic (HCM), 10 arrhythmogenic (AC), 8 dilated (DCM), and 7 non-compact (NCCMP) CMP. The CMR images of three patients indicated Fabry disease. We found post-myocardial infarction scars in 7 cases, and atypical non-ischemic scars in 28 athletes. Besides pathological conditions, we identified minor alterations in 58 patients (51 male, 25±12 age) such as: increased trabeculation, nonspecific LGE in left ventricular insertion point and myocardial crypts. Among athletes examined after aborted sudden cardiac death or SVT we found structural heart disease in 11 males and one female: AC (n=7), HCM (n=1), NCCMP (n=1) and atypical non-ischemic scars (n=3, in two patients the localisation was lateral subepicardial) were diagnosed. During the median follow up of five years one patient died in whom CMR showed lateral scar formation and only mildly reduced left ventricular ejection fraction (50%). Conclusions The most common structural alteration was non-ischaemic scar, the most common CMP was HCM, and the leading cause of sudden cardiac death or SVT in our competitive athletes was AC and lateral subepicardial scar formation. LGE pattern in various cardiomyopathies Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Project no. NVKP_16-1-2016-0017 has been implemented with the support provided from the National Research, Development and Innovation Fund of Hungary, financed under the NVKP_16 funding scheme. This project was supported by a grant from the National Research, Development and Innovation Office (NKFIH) of Hungary (K 120277).
Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Project no. TKP2021-NKTA-46 has been implemented with the support provided by the Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund, financed under the TKP2021-NKTA funding scheme. This project was also supported by a grant from the National Research, Development, and Innovation Office (NKFIH) of Hungary (K135076 to BM). Introduction Feature tracking strain analysis using cardiac magnetic resonance (CMR) imaging enables the appreciation of complex mechanics of the athlete’s heart without adding extra sequences and increasing image acquisition time. Purpose We evaluated the associations of the left (LA) and right atrial (RA) functional and strain parameters with sports activity and demographic characteristics in a large cohort of competitive athletes. We compared the athlete’s biatrial remodelling with healthy, sex-matched control subjects. Methods We performed a retrospective analysis on native CMR cine images acquired between 2009 and 2021. Standard two-chamber and four-chamber long-axis cine movies were analyzed using Medis Suite software. We excluded images with foreshortening or apparent planning flaw. Subjects were categorized into four groups based on their weekly training loads (<6 hours, 6-10 hours, 11-20 hours and 21< hours). Results We performed CMR on 510 subjects, of which 375 were highly trained athletes (median age 20 ys, IQR 16-25; 244 male). A group of 135 healthy volunteers [median (mdn) age 25 ys, IQR 23-28, 64 male] served as controls. Left atrial global longitudinal strain (GLS) was lower (p=.002) in athletes (mdn 41%) than in controls (mdn 43%), whereas RA GLS showed a more pronounced decrease (mdn 32% vs 43%, p<.0001). Between male athletes and controls, LA global circumferential strain [(GCS), mdn 40% vs 47%, p=.0001], LA conduit (mdn 26% vs 28%, p=.025), RA GLS (mdn 31% vs 38%, p<.0001), RA GCS (mdn 17% vs 20%, p=.024), RA booster (mdn 10% vs 9%, p<.001) and RA conduit (mdn 21% vs 24%, p=.001) strain values showed a difference. Between female athletes and controls, RA GLS (mdn 34% vs 44%, p<.0001), RA GCS (mdn 19% vs 29%, p<.001), RA booster (mdn 9% vs 13%, p=.006), and RA conduit (mdn 25% vs 32%, p<.001) were significantly different, while LA strain values were comparable. We found a significant difference between male and female athletes in terms of LA GLS (mdn 39%, vs 43%, p=.0001), LA GCS (mdn 40% vs 42%, p=.01) and LA conduit strain (mdn 26% vs 29%, p<.001). Regarding the right atrium, GLS (mdn 31% vs 34%, p=.047) and conduit strain (mdn 21% vs 25%, p=.004) were significantly lower in male athletes. LA GLS only differed between the lowest and highest training volumes (p=0.048). LA GCS was higher in the least trained group (p<.001) than in the other three categories. Interestingly, the LA end-diastolic volume index was less (r=0.13, p=0.008) correlated to weekly training volume than the left ventricular end-diastolic volume index (r=0.51, p<.0001). Conclusion The atrial adaptation of the athlete’s heart shows distinct mechanic properties, which are further stratified with exercise level and sex. The RA seems to be more prone to increasing exercise load than the LA. Sophisticated atrial function characterization by strain analysis might provide novel insight into healthy sports adaptation.
Az aritmogén cardiomyopathia (ACM) diagnózisa leggyakrabban fizikai terheléssel összefüggő palpitáció vagy syncope, hirtelen szívhalál, illetve jobb kamrai eredetű ritmuszavarok esetén merül fel. A jobb kamrai dominanciájú ACM diagnózisa a 2010-ben módosított Task Force kritériumokon alapul, ami azonban a mindkét kamrát érintő, illetve bal kamrai dominanciájú ACM esetén sokszor nem segíti a diagnózist. Ezekben az esetekben kiemelt szerepe van a kontrasztanyag adásával végzett szív-mágnesesrezonancia- (MR) vizsgálatnak, továbbá a genetikai vizsgálatnak. Két beteg esetét ismertetjük, amikor a klinikai tünetek, vagy a Task Force kritériumok nem voltak ACM-re típusosak. Az 58 éves nőbeteg kivizsgálása szívelégtelenség miatt kezdődött. Szívultrahang-vizsgálat során tág jobb kamra, csökkent jobbkamra-funkció, jelentős tricuspidalis regurgitáció és enyhén emelkedett pulmonalis nyomás igazolódott. Szív-MR-vizsgálattal emelkedett jobb kamrai volumenek, jelentősen csökkent jobb kamrai ejekciós frakció, mindkét kamrát érintő falmozgászavarok és kiterjedt noniszkémiás kontraszthalmozás ábrázolódott, amely alapján felmerült kardiális sarcoidosis, illetve kétkamrás ACM diagnózisa. FDG PET-CT-vizsgálat sarcoidosisra típusos miokardiális dúsulást nem igazolt. Genetikai vizsgálat a Desmoglein 2 gén patogén mutációját igazolta, így kétkamrás érintettségű ACM diagnózisát állítottuk fel. Az 56 éves férfi beteget nyugalomban bekövetkezett eszméletvesztés miatt vizsgáltuk. Koronarográfia ép koszorúsereket igazolt. Telemetriás monitorozással nem tartós kamrai tachycardiát észleltek, elektrofiziológiai vizsgálat során kamrai tachycardiát lehetett kiváltani. Szív-MR-vizsgálat enyhén csökkent bal kamrai ejekciós frakciót, enyhén emelkedett bal kamrai volumeneket igazolt normál jobb kamrai paraméterek mellett. A septumban midmiokardiálisan a T1 súlyozott és zsírelnyomásos felvételek, illetve az alacsony T1-mapping érték alapján zsíros átépülés, továbbá az inferior fal mentén szubepi-midmiokardiális fibrózisnak megfelelő kontraszthalmozás ábrázolódott. Az atípusos MR-kép alapján felmerült bal kamrai ACM, amit a genetikai vizsgálattal felfedezett Desmoplakin gén patogén mutációja igazolt. Eseteink rámutatnak arra, hogy ACM kétkamrás, illetve bal kamrai dominanciájú formáinak diagnózisában kiemelkedő szerepe lehet a szív-MR-nek és a genetikai vizsgálatnak.
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