In many endurance athletes, increased left ventricular (LV) size, a mildly reduced left ventricular ejection fraction (LVEF), and lower resting heart rate develop as an adaptation to strenuous exercise. These non-pathological changes are termed as ‘athlete’s heart’, a term first used in the medical literature in 1953, although the first description of athletes with enlarged hearts dates back to the late 19th century. However, there is a fine line between athlete’s heart and true systolic dysfunction and pathological cardiomyopathy. Many professional athletes are diagnosed with cardiac pathology while still competing at the highest levels, while many others have died during games or competitions, or shortly after that, mostly due to dilated cardiomyopathy leading to sudden cardiac arrest. These findings have challenged the notion that excellent exercise capacity excludes pathological cardiomyopathy.

In an interesting study published recently in the European Heart Journal – Cardiovascular Imaging, Claessen and colleagues use real-time cardiac magnetic resonance imaging during exercise (ex-CMR) to distinguish between healthy endurance athletes (EA-healthy), patients with mild dilated cardiomyopathy (DCM), and athletes with known LV dysfunction and fibrosis (EA-fibrosis). The authors hypothesized that preserved exercise capacity does not exclude pathological damage and that LV contractile reserve is a reliable tool to differentiate between pathological and physiological remodeling. The subjects’ age, BMI, and weight was similar in all groups. EA-healthy and DCM subjects had a resting LVEF < 52%, and as expected, healthy athletes had a greater exercise capacity than DCM patients. EA-fibrosis subjects, all high-level former athletes diagnosed with LV fibrosis while still competing, had superior exercise capacity compared to both EA-healthy and DCM subjects, despite having significant LV pathology confirmed by imaging. The key difference was in the LV contractile reserve; both DCM and EA-fibrosis subjects had diminished augmentation of LVEF and contractility during exercise compared to healthy athletes, and a cutoff value of Δ11.2% differentiated these subjects.

The study showed that LV contractile reserve measured during exercise can be a useful diagnostic tool to distinguish athlete’s heart (or even benign physiological remodeling in non-athletes) from pathological LV remodeling. Exercise capacity alone did not exclude pathology, and it is possible that peripheral factors may play a role in preserving exercise performance despite a reduced LV augmentation and contractility, as seen in high-level retired athletes with known LV hypertrophy or ventricular arrhythmias. In addition, the study demonstrated abnormalities beyond LV; in both DCM and EA-fibrosis subjects the augmentation of right ventricular ejection fraction was also diminished during exercise. This study can have implications for individuals at risk of developing DCM, and may help to better dissect the fine line between DCM and athlete’s heart.

Reference:
Claessen, Guido, et al. “Exercise cardiac magnetic resonance to differentiate athlete’s heart from structural heart disease.” European Heart Journal-Cardiovascular Imaging (2018).