Myocardial Fibrosis in Young and Veteran Athletes: Evidence from a Systematic Review of the Current Literature

Abstract

Background: Exercise is associated with several cardiac adaptations that can enhance one's cardiac output and allow one to sustain a higher level of oxygen demand for prolonged periods. However, adverse cardiac remodelling, such as myocardial fibrosis, has been identified in athletes engaging in long-term endurance exercise. Cardiac magnetic resonance (CMR) imaging is considered the noninvasive gold standard for its detection and quantification. This review seeks to highlight factors that contribute to the development of myocardial fibrosis in athletes and provide insights into the assessment and interpretation of myocardial fibrosis in athletes. Methods: A literature search was performed using the PubMed/Medline database and Google Scholar for publications that assessed myocardial fibrosis in athletes using CMR. Results: A total of 21 studies involving 1642 endurance athletes were included in the analysis, and myocardial fibrosis was found in 378 of 1595 athletes. A higher prevalence was seen in athletes with cardiac remodelling compared to control subjects (23.7 vs. 3.3%, p < 0.001). Similarly, we found that young endurance athletes had a significantly higher prevalence than veteran athletes (27.7 vs. 19.9%, p < 0.001), while male and female athletes were similar (19.7 vs. 16.4%, p = 0.207). Major myocardial fibrosis (nonischaemic and ischaemic patterns) was predominately observed in veteran athletes, particularly in males and infrequently in young athletes. The right ventricular insertion point was the most common fibrosis location, occurring in the majority of female (96%) and young athletes (84%). Myocardial native T1 values were significantly lower in athletes at 1.5 T (p < 0.001) and 3 T (p = 0.004), although they had similar extracellular volume values to those of control groups. Conclusions: The development of myocardial fibrosis in athletes appears to be a multifactorial process, with genetics, hormones, the exercise dose, and an adverse cardiovascular risk profile playing key roles. Major myocardial fibrosis is not a benign finding and warrants a comprehensive evaluation and follow-up regarding potential cardiac disease.

Keywords: T1 mapping; cardiac magnetic resonance imaging; endurance athlete; late gadolinium enhancement; myocardial fibrosis.

Figure 1

Flow chart of the literature selection.

Figure 2

Patterns and locations of LGE in athletic populations consisting of major (nonischaemic in 23.4% and ischaemic in 7.6% of cases) and minor MF (RV insertion points in 69% of cases).

Figure 3

MF patterns and locations characterised by the athletes’ age and sex (A) Ischaemic patterns, (B) Nonischaemic patterns, (C) Non-specific patterns).

Figure 4

(A) T1 mapping with native T1 (1126 ± 46 ms) and (B) post-contrast T1 (490 ± 38 ms) images (ECV 22.9%) (ShMOLLI 3T) in a 24-year-old male runner.

Figure 5

LGE of the inferior RV insertion point in a young male triathlete.

Figure 6

(A) Subepicardial scar in a 20-year-old female swimmer with VA (arrhythmogenic cardiomyopathy—gene elusive). (B) Mid-myocardial and subepicardial LGE in a 31-year-old male triathlete presenting with ventricular ectopy and chest pain (arrhythmogenic cardiomyopathy—desmin gene variant). (C) Mid-myocardial and subepicardial LGE in a 51-year-old male runner with previous reports of chest pain and raised inflammatory markers (prior myocarditis).

Figure 7

(A) Subendocardial LGE in the RCA territory in a 60-year-old asymptomatic male cyclist; and (B) Transmural LGE in a 76-year-old male marathon runner presenting with anterior T-wave inversion on electrocardiogram (possible links to coronary ischaemia, focal emboli, or coronary spasm).