Assessment of left atrial-left ventricular-arterial coupling in amateur marathon runners using three-dimensional speckle-tracking echocardiography

Introduction

Marathon running has gained significant popularity as both a recreational activity and a health promotion strategy. With the increasing number of amateur participants, considerable attention has focused on its cardiac implications (1). Current evidence suggests that regular moderate exercise confers cardiovascular benefits, whereas sustained high-intensity training may elevate cardiovascular risk (2,3). Historically, prolonged vigorous physical exertion—particularly among athletes—has been associated with structural cardiac adaptations, including chamber enlargement and ventricular wall thickening, a phenomenon termed the “athlete’s heart” (4), which is considered a physiologic and efficient adaptation to chronic intensive exercise (5).

While previous studies have demonstrated cardiac remodeling primarily involving the right and left ventricles (6) in amateur marathon runners, data about left atrial (LA) involvement are limited. This is pertinent as emerging evidence from heart failure-centered studies suggest that LA changes can be associated with the progression of heart failure and atrial fibrillation (7).

Left ventricular (LV) ejection into the arterial system depends on the dynamic regulation of preload, afterload, and myocardial contractility. Optimal LV-arterial coupling is essential for normal cardiovascular function (8). Beyond LV-arterial interactions, the left ventricle is hemodynamically coupled with the left atrium. The LA modulates LV filling and cardiovascular performance through its reservoir, conduit, and booster pump functions. Consequently, the integrated left atrial-left ventricular-arterial (LA-LV-arterial) system interaction may be regarded as a key determinant of overall cardiovascular performance. Recent studies indicate that the left atrial stiffness index (LASI) serves as a biomarker reflecting both LA stiffness and LA-LV coupling (9). Furthermore, arterial stiffness is recognized as a critical determinant of cardiovascular events.

Conventional two-dimensional speckle-tracking echocardiography (2D-STE) is limited in assessing LA volume and function due to LA geometric complexity and angle dependency. In contrast, three-dimensional speckle-tracking echocardiography (3D-STE) enables direct visualization of the three-dimensional LA anatomy, providing superior quantification of LA volumetric dynamics and strain patterns throughout the cardiac cycle. As an advanced echocardiographic modality integrating real-time 3D imaging with speckle-tracking algorithms, 3D-STE permits accurate and quantitative assessment of myocardial deformation and chamber volumetry. Our previous investigation demonstrated significant impairment in all LA functional phases—reservoir, conduit, and booster pump functions—among amateur marathon runners, with more pronounced abnormalities observed in amateur ultramarathoners (race distance ≥50 km) (10). The core objectives of this research are: (I) to evaluate the cardio-arterial coupling status in a specific population; (II) to analyze the functional correlation between internal cardiac structures; (III) to investigate the relationship between cardiac structure and vascular characteristics; and (IV) to identify the characteristics of exercise-induced cardiac adaptation. These objectives provide pathophysiological insights to inform clinical evaluation of athlete’s heart syndrome. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1699/rc).

Methods

Study population

Between February 2024 and February 2025, volunteer amateur marathon runners were consecutively recruited for this study, the cohort comprised:45 ultramarathon athletes (UM group, race distance ≥50 km) and 48 classic marathon runners (M group, race distance <50 km). Additionally, 40 healthy volunteers undergoing routine health examinations at the Affiliated Hospital of Hangzhou Normal University served as controls. All participants underwent comprehensive anthropometric and hemodynamic assessments, including height, weight, blood pressure, body mass index (BMI), body surface area (BSA), and weekly running distance. Inclusion criteria for Marathon Runners: (I) non-professional status: amateur runners without athletic scholarships or professional training contracts; exclusion of strength-trained athletes and those with a history of congenital heart disease, hypertension, valvular heart disease, diabetes mellitus, kidney disease, or other systemic diseases; (II) ultramarathon athletes must have completed ≥1 official ultramarathon event (≥50 km) within 3 months preceding echocardiography. Classic marathon runners must have completed either ≥1 full marathon (42.195 km), or ≥2 half-marathons (21.0975 km) within the same period; (III) a running frequency of ≥3 times per week, with a distance ≥10 km per run, and sustained running training for more than 1 year; (IV) no strenuous exercise within 72 hours before the examination.

Control group inclusion criteria: healthy volunteers who were non-habitual exercisers, engaged in no strength training, and maintained minimal activity levels (≤1 hour per session, ≤1 session weekly). Exclusion criteria: (I) pre-existing cardiometabolic disorders, congenital heart disease, hypertension, diabetes mellitus, valvulopathy, renal impairment, or active malignancy; (II) history of regular strength-oriented training.

The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Scientific Research Ethics Committee of the Affiliated Hospital of Hangzhou Normal University (No. 2025[E2]-KS-180), and informed consent was obtained from all participants.

Analysis by 2D echocardiography

The GE Vivid E95 ultrasound diagnostic system, equipped with a 4V cardiac probe (frequency range: 1.5–4.0 MHz) and built-in analysis software, was used. Subjects were positioned in the left lateral decubitus position while synchronously recording electrocardiograms. In the parasternal long-axis view of the left ventricle, the following parameters were measured: left atrial diameter (LAd), left ventricular end-diastolic diameter (LVEDd). The apical four-chamber view was used to record the peak early diastolic velocity of the mitral valve orifice (E) and the peak early diastolic velocity of the lateral mitral annulus (e′), and the E/e′ ratio was then calculated.

Strain analysis by 3D-STE

A 4V transducer was used to acquire real-time full-volume images of 3 cardiac cycles in the apical four-chamber view. The four-dimensional left ventricular quantification (4D-LVQ) software function was applied to automatically identify the LV endocardial surface, generate a three-dimensional (3D) model of the left ventricle, and obtain LV end-diastolic volume (LVEDV), LV end-systolic volume (LVESV), and LV ejection fraction (LVEF). Additionally, the four-dimensional left atrial quantification (4D-LAQ) software function was utilized to automatically recognize the LA endocardial surface, create a 3D model of the left atrium, and acquire LA volumes—including minimal volume (LAVmin), maximal volume (LAVmax), pre-atrial contraction volume (LAVpreA), and maximal volume index (LAVImax)—as well as LA strain parameters, including reservoir strain (LASr), conduit strain (LAScd), and contractile strain (LASct). LA volume parameters were used to calculate the LA expansion index (LAEI) as [(LAVmax − LAVmin)/LAVmin], LA passive ejection fraction (LApEF) as [(LAVmax − LAVpreA)/LAVmax], and LA active ejection fraction (LAaEF) as [(LAVpreA − LAVmin)/LAVpreA]. LASI was defined as the ratio of E/e′ to LASr. LV-arterial coupling was defined as the ratio of pulse wave velocity (PWV) to LV global longitudinal strain (GLS), i.e., PWV/GLS.

Statistical analysis

Statistical analyses were performed using SPSS 26.0 (IBM Corp, Armonk, NY, USA) and GraphPad Prism 9 (GraphPad Software, San Diego, CA, USA). Normality was tested for continuous variables. Normally distributed data were expressed as mean ± standard deviation and compared using one-way analysis of variance (ANOVA) with LSD t-test for pairwise comparisons. Non-normally distributed data were presented as median with interquartile range (IQR) and compared using the Kruskal-Wallis H test, with the Mann-Whitney U test for pairwise comparisons. Pearson correlation analysis was used for normally distributed bivariate data, while Spearman correlation analysis was applied otherwise. Multiple linear regression analysis was performed to identify independent factors influencing LA-LV-arterial coupling parameters in amateur marathon runners. Intra-class correlation coefficients (ICCs) were used to assess inter- and intra-observer reproducibility. A two-sided P value <0.05 was considered statistically significant.

Results

Clinical and conventional echocardiographic characteristics

A total of 45 amateur ultramarathon runners (UM group), 48 amateur classic marathon runners (M group), with a mean age of 38.27±5.61 years. and 40 healthy controls (with a mean age of 36.30±5.59 years) were enrolled in this study, with no missing data. Demographic and conventional echocardiographic parameters of the participants are summarized in Tables 1,2. No significant differences were observed among the three groups in terms of age, BMI, systolic blood pressure, diastolic blood pressure, or BSA (all P>0.05). However, heart rate was significantly lower in the amateur marathon runners compared to the control group (P<0.05), with the UM group exhibiting a further reduction relative to the M group (P<0.05). As expected, the weekly running volume was greater in the UM group than in the M group (P<0.05). Regarding cardiac structural parameters, LAd, LVEDd, LVEDV, and LVESV were significantly increased in both marathon groups compared to the control group (all P<0.05), and these values were more pronounced in the UM group than in the M group (P<0.05). In contrast, no significant differences were found in LVEF or E/e′ among the groups (P>0.05; Tables 1,2).

Cardiac strains and LA-LV-arterial coupling parameters

Measurements of cardiac strains and coupling parameters are detailed in Table 3 and Figure 1. Compared with the control group, amateur marathon runners demonstrated significantly increased left atrial volumes (LAVs)—including LAVmin, LAVmax, LAVpreA, and LAVImax—as well as higher PWV (all P<0.05). These parameters were further elevated in the UM group compared to the M group (P<0.05). Conversely, LA functional parameters—namely LAEF, LApEF, LAaEF, LASr, LAScd, and LASct—were significantly reduced in the runner groups relative to controls (all P<0.05), though no significant differences were observed between the UM and M groups (P>0.05). The left atrial expansion index (LAEI) was also significantly higher in marathon runners than in controls (P<0.05). Notably, the LASI was significantly elevated in the marathon runners compared to the control group (P<0.05). Furthermore, both GLS (absolute value) and the PWV/GLS ratio were significantly higher in the UM group than in both the M and control groups (P<0.05), whereas the M group values for these parameters were comparable to those of the control group (P>0.05).

Figure 1 UM group (A), M group (B) and control group (C): analysis diagrams of left atrial volume-strain. M group, marathon runners (running distance of <50 km); UM group, ultramarathon runners (running distance of ≥50 km). LAEF, left atrial total ejection fraction; LAScd, left atrial strain conduit; LAScd-c, conduit circumferential strain; LASct, left atrial strain contractile; LASct-c, left atrial contraction circumferential strain; LASr, left atrial strain reservoir; LASr-c, LA reservoir circumferential strain; LAVImax, left atrial maximal volume index; LAVmax, left atrial maximal volume; LAVmin, left atrial minimum volume; LAVpreA, left atrial pre-systolic volume.

Correlation analysis

Results of the correlation analysis are presented in Table 4 and Figure 2. A significant negative correlation was observed between the LASI and left atrial ejection fraction (LAEF). Similarly, the PWV/GLS ratio showed significant negative correlations with LAVs (LAVmin, LAVmax, LAVpreA, LAVImax) and average weekly running mileage. Furthermore, multivariate linear regression analysis identified weekly running mileage as an independent predictor for both LASI and PWV/GLS in amateur marathon runners (P<0.001; Table 5).

Figure 2 Correlation of LASI with LAEF and PWV/GLS with LAVmin, LAVmax, LAVImax, LAVpreA, average weekly mileage. M group, marathon runners (running distance of <50 km); UM group, ultramarathon runners (running distance of ≥50 km). LAEF, left atrial total ejection fraction; LASI, left atrial stiffness index; LAVImax, left atrial maximal volume index; LAVmax, left atrial maximal volume; LAVmin, left atrial minimum volume; LAVpreA, left atrial pre-systolic volume; PWV/GLS, pulse wave velocity to left ventricular global longitudinal strain.

Reproducibility of echocardiographic measurements

The intra- and inter-observer reproducibility of key echocardiographic measurements was assessed using ICCs, with the results detailed in Figure 3. For intra-observer variability, the ICCs for LAVmin, LAVmax, LVEDV, LVESV, and GLS were 0.859, 0.877, 0.876, 0.834, and 0.814, respectively. Regarding inter-observer variability, the corresponding ICCs for the same parameters were 0.755, 0.810, 0.784, 0.799, and 0.776, respectively.

Figure 3 Bland-Altman analysis of LAVmin and LAVmax. LAVmax, left atrial maximal volume; LAVmin, left atrial minimum volume; SD, standard deviation.

Discussion

This study primarily evaluated LA-LV-arterial coupling in amateur marathon runners and its correlation with LA and LV parameters, aiming to elucidate the relationship between cardiac remodeling and arterial stiffness. Our key findings are: (I) structural parameters of the left ventricle and left atrium (LAd, LVEDd, LVEDV, LVESV, LAVmin, LAVmax, LAVpreA, LAVImax) were significantly higher in amateur marathon runners than in controls, with the UM group showing more pronounced changes than the M group; (II) LA functional parameters (LAEF, LApEF, LAaEF, LASr, LAScd, LASct) were significantly lower in runners than in controls. LASI was significantly higher, and the PWV/GLS ratio was significantly greater in the UM group compared to both the M and control groups; (III) LASI correlated negatively with LAEF, while PWV/GLS correlated negatively with LAVmin, LAVmax, LAVpreA, LAVImax, and average weekly mileage. Multivariate linear regression analysis identified weekly running mileage as an independent predictor of both LASI and PWV/GLS. In amateur marathon runners engaged in long-term high-intensity aerobic training, atrial and ventricular remodeling is characterized by increased LA and LV diameters, along with enlarged LVEDV and LVESV. The left atrium, an active organ regulating LV filling via its reservoir, conduit, and contractile functions (11), plays a crucial role in overall cardiac performance. In this study, LAVmax, LAVmin, LAVpreA, and LAVImax were significantly larger in runners, who also exhibited lower resting heart rates, consistent with the characteristics of endurance athletes possessing good cardiac reserve (12,13). Gabrielli et al. (14) similarly found significantly increased LA volume in amateur ultramarathon athletes, more evident in high-level performers. Thus, all LA volume indices were larger in the UM group than in the M group. These remodeling changes may represent a physiological adaptation to volume overload, facilitating greater stroke volume and cardiac output. However, chronic repetitive stretching may lead to adverse structural changes in some individuals (15,16). The LA strain parameters (LASr, LAScd, LASct), representing myocardial deformation during reservoir, conduit, and contractile functions, were significantly lower in runners, likely due to LA myocardial fiber remodeling reducing deformation capacity. Relevant studies indicate that LA strain parameters can detect LA myocardial abnormalities earlier and more sensitively than volume parameters alone (17). The LAEF, LAaEF, and LApEF, derived from 3D-STE volume measurements, represent the LA’s three major functions. In this study, despite abstaining from strenuous exercise for 72 hours prior to examination, the runners’ persistent daily training likely contributed to the observed significant reductions in LAEF, LAaEF, and LApEF, indicating impaired reservoir, conduit, and contractile functions, consistent with previous findings (10). LA reservoir strain is a key parameter for assessing LA compliance and a sensitive predictor of early LA dysfunction (18), LV diastolic dysfunction (19), and atrial fibrillation recurrence (20). ESC guidelines note that LASI can aid in atrial fibrillation risk stratification. Populations engaged in long-term high-intensity endurance exercise may face increased risks of cardiovascular disease (CVD) and arterial stiffness (21). LASI, a novel index combining E/e′ (reflecting LV filling pressure) and LASr (reflecting LA reservoir function), serves as an indicator of both LA function/compliance and LA-LV coupling. LV ejection into the arterial system depends on preload, afterload, and contractility. PWV is a common measure of arterial elasticity, while GLS assesses LV myocardial contractile function. The PWV/GLS index quantifies the matching state between arterial afterload and LV contractility, serving as a vital tool for evaluating cardiovascular coupling. Our results showed that LASI was significantly higher in runners than in controls, and the PWV/GLS ratio was significantly higher in the UM group. This may be attributed to long-term endurance exercise increasing pro-inflammatory markers and altering endothelial function. Increased blood flow and shear stress to meet oxygen demands can initially promote arterial dilation via nitric oxide (NO) release (22). In addition, laminar shear stress can induce the activation of phosphatidylinositol 3-kinase (PI3K) and extracellular signal-regulated kinase (ERK) pathways, directly promoting the expression of endothelial nitric oxide synthase (eNOS) and the production of NO, thereby leading to arterial dilation. However, long-term training may reduce NO bioavailability due to reactive oxygen species (ROS), potentially increasing arterial stiffness. Studies indicate that ultramarathon participants exhibit increased resting arterial stiffness compared to age-matched amateur athletes (21). Thus, LASI is elevated in amateur marathoners. Furthermore, poor ventriculo-arterial coupling is recognized as a cause of decreased cardiac performance during high-intensity exercise (23), aligning with our findings. The relatively poor LA-LV-arterial coupling observed after high-intensity training reflects a subclinical decline in LA and LV physiological adaptation alongside increased arterial stiffness, suggesting that long-term endurance athletes, especially ultramarathoners, may face higher cardiovascular risk.This study found that in amateur runners, LAVmin, LAVmax, LAVpreA, LAVImax, and average weekly mileage correlated with PWV/GLS, while LAEF correlated with LASI. The LA significantly influences LV filling through its reservoir (collecting pulmonary venous flow during LV systole), conduit (passive emptying during early diastole), booster pump (contributing 15–30% of LV filling in late diastole), and suction functions (24,25). Consequently, larger LA volumes were associated with higher PWV/GLS. Greater weekly running mileage correlated with higher PWV and PWV/GLS. Impaired LV-vascular coupling, reflecting early LA damage and remodeling, is a recognized cause of reduced cardiac performance during maximal exercise (26). Thus, LAEF, LAaEF, and LApEF were significantly reduced in the runners. Multivariate linear regression confirmed weekly running mileage as an independent predictor of LASI and PWV/GLS. Multiple studies have confirmed that marathon athletes exhibit increased atherosclerosis and arterial stiffness due to extensive aerobic training (27,28), potentially related to oxidative stress and inflammation during endurance running (29,30).

Limitations

There are several limitations in this study. It is a small-sample study, with most participants being male, which may affect gender-specific responses; LA-LV-arterial coupling might also be associated with the menstrual cycle. Secondly, the study lacked long-term follow-up on the prognosis of these athletes. Additionally, it did not compare LA and LV parameters pre- and post-exercise. However, it is expected that LA-LV-arterial coupling would gradually normalize with sufficient rest. Future follow-up studies are warranted to improve the diagnostic model’s efficacy.

Conclusions

A growing body of evidence indicates that extremely high-volume aerobic exercise may be associated with a decline in cardiac physiological adaptation. As participation in such events continues to rise, a better understanding of the impact of ultra-endurance exercise on cardiac health is needed. After long-term high-intensity endurance exercise, amateur marathon runners exhibit varying degrees of impairment in LA and LV structure and function. Elevated LASI and PWV/GLS ratios are early signs of abnormal LA-LV-arterial coupling. 3D-STE can sensitively identify these subclinical changes, providing valuable clinical information for evaluating heart-vascular interactions in this population.

Acknowledgments

The authors would like to thank the Affiliated Hospital of Hangzhou Normal University, Hangzhou Normal University and Hangzhou Institute of Sports Medicine for Marathon for their help and support.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1699/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1699/dss

Funding: This project was funded by the Medical and Health Research Program of Zhejiang Province (No. 2024KY1341) and the Chun’an County Medical and Health Science and Technology Project (No. 2025CAYY024).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1699/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Scientific Research Ethics Committee of the Affiliated Hospital of Hangzhou Normal University (No. 2025[E2]-KS-180), and informed consent was obtained from all participants.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. D’Silva A, Bhuva AN, van Zalen J, Bastiaenen R, Abdel-Gadir A, Jones S, Nadarajan N, Menacho Medina KD, Ye Y, Augusto J, Treibel TA, Rosmini S, Ramlall M, Scully PR, Torlasco C, Willis J, Finocchiaro G, Papatheodorou E, Dhutia H, Cole D, Chis Ster I, Hughes AD, Sharma R, Manisty C, Lloyd G, Moon JC, Sharma S. Cardiovascular Remodeling Experienced by Real-World, Unsupervised, Young Novice Marathon Runners. Front Physiol 2020;11:232. [Crossref] [PubMed]
2. Pelliccia A, Sharma S, Gati S, Bäck M, Börjesson M, Caselli S, Collet JP, Corrado D, Drezner JA, Halle M, Hansen D, Heidbuchel H, Myers J, Niebauer J, Papadakis M, Piepoli MF, Prescott E, Roos-Hesselink JW, Graham Stuart A, Taylor RS, Thompson PD, Tiberi M, Vanhees L, Wilhelm MESC Scientific Document Group. 2020 ESC Guidelines on sports cardiology and exercise in patients with cardiovascular disease. Eur Heart J 2021;42:17-96. Erratum in: Eur Heart J 2021;42:548-549.
3. Nystoriak MA, Bhatnagar A. Cardiovascular Effects and Benefits of Exercise. Front Cardiovasc Med 2018;5:135. [Crossref] [PubMed]
4. Predel HG. Marathon run: cardiovascular adaptation and cardiovascular risk. Eur Heart J 2014;35:3091-8. [Crossref] [PubMed]
5. La Gerche A, Burns AT, D’Hooge J, Macisaac AI, Heidbüchel H, Prior DL. Exercise strain rate imaging demonstrates normal right ventricular contractile reserve and clarifies ambiguous resting measures in endurance athletes. J Am Soc Echocardiogr 2012;25:253-262.e1. [Crossref] [PubMed]
6. Guo C, Zhang H, Yang C, Hu P, Li M, Ma H, Ma Y, Gao F. Assessment of left ventricular systolic function using a non-invasive index of myocardial work in amateur marathon runners. Quant Imaging Med Surg 2024;14:9394-9406. [Crossref] [PubMed]
7. Qing J, Mao WW, Zhang Y. Real time three-dimensional echocardiography evaluation of left atrial function in chronic heart failure patients with preserved ejection fraction. Chinese Journal of Ultrasound Medicine 2021;37:418-421.
8. Little WC, Pu M. Left ventricular-arterial coupling. J Am Soc Echocardiogr 2009;22:1246-8. [Crossref] [PubMed]
9. Sun Q, Pan Y, Zhao Y, Liu Y, Jiang Y. Association of Nighttime Systolic Blood Pressure With Left Atrial-Left Ventricular-Arterial Coupling in Hypertension. Front Cardiovasc Med 2022;9:814756. [Crossref] [PubMed]
10. Chen L, Li B, Yang CX, Long LM, Zhang HB, Ma Y. Evaluation of left atrial structural and functional changes in amateur ultra-marathon athletes by threedimensional speckle tracking echocardiography. Chinese Journal of Ultrasonography 2024;34:122-128.
11. Zeng T, Chu TS, Zhang XJ, Xing Y, Li HX, Wu M, Zhu HH. Real time three-dimensional echocardiography evaluation of left atrial volume and functional changes in patients with ankylosing spondylitis. Chinese Journal of Ultrasound Medicine 2024;40:418-422.
12. Mont L, Tamborero D, Elosua R, Molina I, Coll-Vinent B, Sitges M, Vidal B, Scalise A, Tejeira A, Berruezo A, Brugada J. Physical activity, height, and left atrial size are independent risk factors for lone atrial fibrillation in middle-aged healthy individuals. Europace 2008;10:15-20. [Crossref] [PubMed]
13. Wang SQ, Lv WG, Chang Y. Effects of marathon on the heart:physiological adaptation and potential risks. China SportScienceand Technology 2020;56:9-21.
14. Gabrielli L, Herrera S, Contreras-Briceño F, Vega J, Ocaranza MP, Yáñez F, Fernández R, Saavedra R, Sitges M, García L, Chiong M, Lavandero S, Castro PF. Increased active phase atrial contraction is related to marathon runner performance. Eur J Appl Physiol 2018;118:1931-9. [Crossref] [PubMed]
15. Pluim BM, Zwinderman AH, van der Laarse A, van der Wall EE. The athlete’s heart. A meta-analysis of cardiac structure and function. Circulation 2000;101:336-44. [Crossref] [PubMed]
16. Maron BJ, Pelliccia A. The heart of trained athletes: cardiac remodeling and the risks of sports, including sudden death. Circulation 2006;114:1633-44. [Crossref] [PubMed]
17. Gao F, Yuan JJ, Liu YL, Zhang XJ, Tian J, Zhu LM, Zhu HH. Study of left atrial volume and function by real-time three-dimensional echocardiography between hyperthyroidism and hyperthyroid heart disease . Chinese Journal of Ultrasonography 2021;30:764-771.
18. Singh A, Medvedofsky D, Mediratta A, Balaney B, Kruse E, Ciszek B, Shah AP, Blair JE, Maffessanti F, Addetia K, Mor-Avi V, Lang RM. Peak left atrial strain as a single measure for the non-invasive assessment of left ventricular filling pressures. Int J Cardiovasc Imaging 2019;35:23-32. [Crossref] [PubMed]
19. Abid L, Charfeddine S, Kammoun S. Relationship of left atrial global peak systolic strain with left ventricular diastolic dysfunction and brain natriuretic peptide level in end-stage renal disease patients with preserved left ventricular ejection fraction. J Echocardiogr 2016;14:71-8. [Crossref] [PubMed]
20. Anagnostopoulos I, Kousta M, Kossyvakis C, Lakka E, Paraskevaidis NT, Schizas N, Deftereos S, Giannopoulos G. The role of left atrial peak systolic strain in atrial fibrillation recurrence after catheter ablation. A systematic review and meta-analysis. Acta Cardiol 2022;77:536-44. [Crossref] [PubMed]
21. Burr JF, Drury CT, Phillips AA, Ivey A, Ku J, Warburton DE. Long-term ultra-marathon running and arterial compliance. J Sci Med Sport 2014;17:322-5. [Crossref] [PubMed]
22. Jee H, Jin Y. Effects of prolonged endurance exercise on vascular endothelial and inflammation markers. J Sports Sci Med 2012;11:719-26.
23. Najjar SS, Schulman SP, Gerstenblith G, Fleg JL, Kass DA, O’Connor F, Becker LC, Lakatta EG. Age and gender affect ventricular-vascular coupling during aerobic exercise. J Am Coll Cardiol 2004;44:611-7. [Crossref] [PubMed]
24. Hoit BD. Assessing atrial mechanical remodeling and its consequences. Circulation 2005;112:304-6. [Crossref] [PubMed]
25. Mor-Avi V, Lang RM, Badano LP, Belohlavek M, Cardim NM, Derumeaux G, Galderisi M, Marwick T, Nagueh SF, Sengupta PP, Sicari R, Smiseth OA, Smulevitz B, Takeuchi M, Thomas JD, Vannan M, Voigt JU, Zamorano JL. Current and evolving echocardiographic techniques for the quantitative evaluation of cardiac mechanics: ASE/EAE consensus statement on methodology and indications endorsed by the Japanese Society of Echocardiography. J Am Soc Echocardiogr 2011;24:277-313. [Crossref] [PubMed]
26. Miyachi M, Kawano H, Sugawara J, Takahashi K, Hayashi K, Yamazaki K, Tabata I, Tanaka H. Unfavorable effects of resistance training on central arterial compliance: a randomized intervention study. Circulation 2004;110:2858-63. [Crossref] [PubMed]
27. Kroger K, Lehmann N, Rappaport L, Perrey M, Sorokin A, Budde T, Heusch G, Jockel KH, Thompson PD, Erbel R, Mohlenkamp S. Carotid and periph- eral atherosclerosis in male marathon runners. Med Sci Sports Exerc 2010;43:1142-1147. [Crossref] [PubMed]
28. Vlachopoulos C, Kardara D, Anastasakis A, Baou K, Terentes-Printzios D, Tousoulis D, Stefanadis C. Arterial stiffness and wave reflections in marathon runners. Am J Hypertens 2010;23:974-9. [Crossref] [PubMed]
29. Knez WL, Coombes JS, Jenkins DG. Ultra-endurance exercise and oxidative damage : implications for cardiovascular health. Sports Med 2006;36:429-41. [Crossref] [PubMed]
30. Nickel KJ, Acree LS, Gardner AW. Effects of a single bout of exercise on arterial compliance in older adults. Angiology 2011;62:33-7. [Crossref] [PubMed]