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. 2019 Sep;12(9):e009417.
doi: 10.1161/CIRCIMAGING.119.009417. Epub 2019 Sep 11.

Regression of Left Ventricular Mass in Athletes Undergoing Complete Detraining Is Mediated by Decrease in Intracellular but Not Extracellular Compartments

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Regression of Left Ventricular Mass in Athletes Undergoing Complete Detraining Is Mediated by Decrease in Intracellular but Not Extracellular Compartments

Peter P Swoboda et al. Circ Cardiovasc Imaging. 2019 Sep.

Erratum in

Abstract

Background: Athletic cardiac remodeling can occasionally be difficult to differentiate from pathological hypertrophy. Detraining is a commonly used diagnostic test to identify physiological hypertrophy, which can be diagnosed if hypertrophy regresses. We aimed to establish whether athletic cardiac remodeling assessed by cardiovascular magnetic resonance is mediated by changes in intracellular or extracellular compartments and whether this occurs by 1 or 3 months of detraining.

Methods: Twenty-eight athletes about to embark on a period of forced detraining due to incidental limb bone fracture underwent clinical assessment, ECG, and contrast-enhanced cardiovascular magnetic resonance within a week of their injury and then 1 month and 3 months later.

Results: After 1 month of detraining, there was reduction in left ventricular (LV) mass (130±28 to 121±25 g; P<0.0001), increase in native T1 (1225±30 to 1239±30 ms; P=0.02), and extracellular volume fraction (24.5±2.3% to 26.0±2.6%; P=0.0007) with no further changes by 3 months. The decrease in LV mass was mediated by a decrease in intracellular compartment volume (94±22 to 85±19 mL; P<0.0001) with no significant change in the extracellular compartment volume. High LV mass index, low native T1, and low extracellular volume fraction at baseline were all predictive of regression in LV mass in the first month.

Conclusions: Regression of athletic LV hypertrophy can be detected after just 1 month of complete detraining and is mediated by a decrease in the intracellular myocardial compartment with no change in the extracellular compartment. Further studies are needed in athletes with overt and pathological hypertrophy to establish whether native T1 and extracellular volume fraction may complement electrocardiography, echocardiography, cardiopulmonary exercise testing, and genetic testing in predicting the outcome of detraining.

Keywords: athletes; hypertrophy; magnetic resonance imaging; sports.

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Figures

Figure 1.
Figure 1.
Change in cardiac morphology on detraining. Change in left ventricular (LV) and right ventricular (RV) end-diastolic volume (EDV), end-diastolic volume index (EDVI), ejection fraction (EF), and mass after 1 and 3 months of detraining.
Figure 2.
Figure 2.
Native T1 and extracellular volume (ECV) fraction maps before and after 1 month of detraining. Native T1 (above) and ECV (below) maps from a rugby player before and after 1 month of detraining. During this period, native T1 increased from 1160 to 1213 ms, ECV increased from 19.5% to 23.3%, and left ventricular mass decreased from 186 to 164 g.
Figure 3.
Figure 3.
Change in cardiac compartment volumes on complete detraining. Individual participant data showing volumes of intracellular (red) and extracellular (blue) compartments at baseline and then after 1 and 3 months of detraining.

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References

    1. Maron BJ, Pelliccia A. The heart of trained athletes: cardiac remodeling and the risks of sports, including sudden death. Circulation. 2006;114:1633–1644. doi: 10.1161/CIRCULATIONAHA.106.613562 - PubMed
    1. Pelliccia A, Maron BJ, Spataro A, Proschan MA, Spirito P. The upper limit of physiologic cardiac hypertrophy in highly trained elite athletes. N Engl J Med. 1991;324:295–301. doi: 10.1056/NEJM199101313240504 - PubMed
    1. McDiarmid AK, Swoboda PP, Erhayiem B, Lancaster RE, Lyall GK, Broadbent DA, Dobson LE, Musa TA, Ripley DP, Garg P, Greenwood JP, Ferguson C, Plein S. Athletic cardiac adaptation in males is a consequence of elevated myocyte mass. Circ Cardiovasc Imaging. 2016;9:e003579 doi: 10.1161/CIRCIMAGING.115.003579 - PMC - PubMed
    1. Treibel TA, Kozor R, Menacho K, Castelletti S, Bulluck H, Rosmini S, Nordin S, Maestrini V, Fontana M, Moon JC. Left ventricular hypertrophy revisited: cell and matrix expansion have disease-specific relationships. Circulation. 2017;136:2519–2521. doi: 10.1161/CIRCULATIONAHA.117.029895 - PubMed
    1. Swoboda PP, McDiarmid AK, Erhayiem B, Broadbent DA, Dobson LE, Garg P, Ferguson C, Page SP, Greenwood JP, Plein S. Assessing myocardial extracellular volume by T1 mapping to distinguish hypertrophic cardiomyopathy from Athlete’s Heart. J Am Coll Cardiol. 2016;67:2189–2190. doi: 10.1016/j.jacc.2016.02.054 - PubMed

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