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Reduced Ejection Fraction in Elite Endurance Athletes
Quick Takes
- Among elite endurance athletes from sports principally involving aerobic conditioning, approximately one in six had reduced LVEF and/or RVEF.
- Reduced EF was associated with a higher burden of ventricular premature beats, lower LV global longitudinal strain, and a higher polygenic risk score for indexed LV end-systolic volume previously associated with dilated cardiomyopathy.
- It remains to be determined whether it makes sense to use imaging and/or genetic screening of endurance athletes in an attempt to mitigate what is still an unclear clinical risk.
Study Questions:
What is the prevalence, what is the genetic predisposition, and what are the clinical consequences of reduced left (LVEF) and/or right ventricular ejection fraction (RVEF) among endurance athletes?
Methods:
Young endurance athletes from sports principally involving aerobic conditioning and competing at a national or international level were recruited from elite training programs and underwent comprehensive cardiac phenotyping and genetic testing. Those with reduced EF using cardiac magnetic resonance imaging (defined as LVEF <50%, RVEF <45%, or both) were compared with athletes with normal EF. A validated polygenic risk score for indexed LV end-systolic volume (LVESVi-PRS), previously associated with dilated cardiomyopathy, was assessed. Clinical events were recorded over a mean of 4.4 years.
Results:
Of 281 elite endurance athletes (22 ± 8 years, 79.7% male) undergoing comprehensive assessment, 44 (15.7%) had reduced EF (LVEF in 12 [4.3%], RVEF in 14 [5.0%], both in 18 [6.4%]). Reduced EF was associated with a higher burden of ventricular premature beats (13.6% vs. 3.8% with >100 ventricular premature beats/24 hours, p = 0.008) and lower LV global longitudinal strain (–17 ± 2% vs. –19 ± 2%, p < 0.001). Athletes with reduced EF had a higher mean LVESVi-PRS (0.57 ± 0.13 vs. 0.51 ± 0.14, p = 0.009), with athletes in the top decile of LVESVi-PRS having an 11-fold increase in the likelihood of reduced EF compared with those in the bottom decile (p = 0.034). Male sex and higher LVESVi-PRS were the only significant predictors of reduced EF in a multivariate analysis that included age and fitness. During follow-up, no athletes developed symptomatic heart failure or arrhythmias. Two athletes died, one from trauma and one from sudden cardiac death, the latter having a reduced RVEF and a LVESVi-PRS >95%.
Conclusions:
Reduced EF was seen in approximately one in six elite endurance athletes and was related to genetic predisposition in addition to exercise training. The authors conclude that genetic and imaging markers might help identify endurance athletes in whom scrutiny about long-term clinical outcomes may be appropriate.
Perspective:
Habitual intense endurance exercise is associated with adaptive cardiac changes including chamber dilation and reduced measures of ventricular systolic function (“athlete’s heart”), but also an increased prevalence of myocardial fibrosis and arrhythmias. This study found that approximately one in six elite endurance athletes had reduced EF; with an association between reduced EF and reduced LV strain, increased ventricular premature beats, and a higher measure of a LVESVi -PRS associated with dilated cardiomyopathy. These data suggest that differences in genetic predisposition might, at least in part, account for variability in cardiac dilation and LVEF and RVEF among different athletes exposed to similar exercise burdens. It remains to be determined whether it makes sense to use imaging and/or genetic screening of endurance athletes in an attempt to mitigate what is still an unclear clinical risk.
Clinical Topics: Cardiovascular Care Team, Diabetes and Cardiometabolic Disease, Heart Failure and Cardiomyopathies, Prevention, Sports and Exercise Cardiology, Exercise
Keywords: Athletes, Cardiomyopathy, Dilated, Endurance Training
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