Assessment of left ventricular systolic function by non-invasive pressure-strain loop area in young male strength athletes

The concept of “athlete’s heart”, including physiological adaptation and pathological changes both in cardiac morphology and function after prolonged and intensive exercise, was firstly raised by the end of nineteenth century [1‐3]. To date, a growing number of reports on sudden cardiac death (SCD) of athletes caused by long-standing practice has made it imperative to screen athletes for the prevention of SCD [4, 5]. With the wide application of echocardiography and the continuous development of new ultrasonic technology, studies on the athletes’ hearts are getting more thorough, making it play a pivotal role in detecting and monitoring the subclinical changes of athletes’ cardiac morphology and function in time [6].

As a new parameter taking both deformation and afterload of left ventricular (LV) into account, myocardial work (MW) potentially could provide more reliable value to myocardial function assessment than that of strain only [7]. Russell et al. [8] has demonstrated the effectiveness of the non-invasive method to evaluate LVMW, via combining LV strain data by two-dimensional speckle tracking echocardiography (2D-STE) with non-invasive estimated LV pressure curves from brachial artery and correlated well with invasive measurements [9]. The clinical values of this new approach have potential in predicting response to cardiac resynchronization therapy and assessing myocardial contractility in hypertension and dilated cardiomyopathy [10, 11].

The purpose of this study aimed to: (i) describe the basic echocardiography characteristics of LV in the hearts of the athletes and (ii) explore the possibility of LVMW parameters to evaluate myocardial function among the athletes.

As is known to all that moderate exercise not only benefits to reduce the risk of developing cardiovascular disease but also promotes physical and mental health [16]. Nevertheless, more haste less speed. As repeated professional and systematic training, athletes’ hearts would undergo chambers dilatation, ventricular wall thickening, capacity enlargement, arrhythmia and more seriously, SCD following [17, 18]. Therefore, it seemed clinically significant that every effort would be made to distinguish physiological adaptation from pathological abnormality of athletes’ hearts as soon as possible in case of putting the athletes at risk [4, 17, 19]. Heart changes depended on the type of exercises [20]. In this study, structural and capacity parameters of LV were increased in the athlete group with RWT (0.42 ± 0.01, P<0.001) exceeding the reference value (RWT >0.42) and LVMI (99.88 ± 11.76, P<0.001) remaining within standard range. All of these suggested that concentric remodeling of LV in athletes was displayed after recurrent exercise, which was well consistent with previous researches [6, 17].

After prolonged exercise, the augment of RWT and the dropping of capillary density in strength athletes would lead to increased regional myocardial oxygen consumption and insufficient blood supply to myocardium [16, 21]. Moreover, given the complicated three-layer structure of myocardium, microvascular dysfunction and myocardial fibrosis were more likely to occur in the endocardium due to low compliance and high oxygen expenditure of the vascular which led to limited ability to dilate blood vessels and store blood [22, 23]. The description of these changes has led to a more comprehensive understanding of reduced longitudinal strain of LV, as well as the decrease of GWI and GCW that could be supposed to reflect LV performance and mechanics globally [11]. In this study, compared with the control group, the reduction in GWI and GCW in the athlete group was not statistically significant, but suggested that the myocardial metabolism was decreased and LV systolic function was impaired to some extent. LV remodeling can lead to abnormal electrophysiology of the myocardium, resulting in conduction disorders of myocardial cells, and reducing the effectiveness of coordinated contraction of the myocardium. Significantly, increased PSD in the athlete group draw attention to the points that the systolic synchronization of LV had been destroyed and nonuniformity of ventricular wall motion would reduce the mechanical efficiency during cardiac ejection [14]. In addition, the strength athletes were characterized by high LV afterload which would lead to the increased of LV stiffness. Eventually, result in more energy loss expressed as increased GWW and reduced GWE.

Previous studies have demonstrated that the reduction of GLS in athletes was an early sign of LV dysfunction [6]. However, in this study, compared with the control group, the athlete group shew increased GWW and reduced GWE, while EF and GLS having no statistical differences. The above results illustrated that subclinical changes in LV systolic function have occurred in athletes and MW indexes were more sensitive to provide early diagnosis value for LV performance among athletes [24]. According to the ROC analysis about LVMW parameters, GWE (AUC = 0.733) was considered of being the best predictor of LV systolic function in athletes and superior to GLS (AUC = 0.627) which was principally limited by the defect of being load-dependent and might lead to errors in judging LV performance [25].

In summary, this study revealed that the athletes after long-term intensive training not only generated LV concentric remodeling, but also developed subtle subclinical changes in LV contractility performed by increased GWW and decreased GWE. Compared with the conventional echocardiographic indicators, the MW derived from novel non-invasive PSL was a promising tool to evaluate progressive changes of LV performance and produce incremental practical significance to detect myocardial function abnormalities of LV in order to prevent athletes from being SCD in the early stage.