Multiparametric ultrasound approach for early detection of cardiac dysfunction: ready for the clinical arena?

This editorial refers to ‘Biventricular dysfunction and lung congestion in athletes on anabolic androgenic steroids: a speckle tracking and stress lung echocardiography analysis’, by A. D'Andrea et al., pp. 1928–1938.

Anabolic-androgenic steroids (AAS), synthetic derivatives of testosterone, stimulate cellular protein synthesis and have been abused by athletes since the middle of the last century for their ability to increase muscle mass and improve athletic performance.¹

The real effects of the chronic consumption of AAS on cardiovascular structures are subjects of debate. Previous experimental in vitro and in vivo studies have demonstrated the adverse effects of AAS on the cardiovascular system, such as increased collagen synthesis, aberrant myocardial myofibrils, and reduced ventricular compliance. Indeed, AAS can lead to ventricular hypertrophy and a disproportionate increase in the connective tissue content.^1,2 However, few studies examined the real prevalence of AAS abuse in competitive body-builders (37.5–66.7% of top-level athletes). Considering myocardial function studies using speckle-tracking echocardiography (STE) analyses, few papers on small numbers AAS abusers have been published so far, documenting subtle cardiac impairment.^3,4 STE represents a useful technique providing non-Doppler, relatively angle-independent measurement of myocardial deformation and cardiac chambers systolic and diastolic dynamics, and it is particularly suited for the detection of subclinical dysfunctions which are not detectable by standard echocardiography.⁵ Also, beyond the global assessment of myocardial and atrial function, segmental STE deformation measures have shown limited but definite evidence of providing information on the underlying tissue.⁶ Modern software packages allow a fast, reproducible (intra- and inter-operator) evaluation of deformation parameters for the left ventricle, left atrium, and, more recently, right ventricle (possibly right atrium), with an already established inter-vendor consistency.⁷

In this issue of the Journal, D'Andrea et al.⁸ used a multiparametric echocardiographic approach combining standard Doppler echocardiography, STE, and lung ultrasound at rest and during exercise stress echocardiography (ESE) to detect right ventricular (RV) and left ventricular (LV) dysfunction in competitive bodybuilders abusing AAS.

They compared 115 top-level body-builders, including 65 AAS users for at least 5 years and 50 anabolic-free athletes, to 50 age- and sex-matched healthy sedentary controls. Standard Doppler echocardiography, STE analysis, and lung ultrasound at rest and peak supine-bicycle ESE were performed, paired with cardiopulmonary exercise testing (CPET). Athletes showed increased LV mass index, wall thickness, and RV diameters compared with controls, whereas LV ejection fraction was comparable between groups. Left atrial volume index, LV and RV strain, and LV E/e′ were significantly higher in AAS users. Also, users showed more echocardiographic signs of congestion during stress. The number of weeks of AAS use per year emerged as an independent determinant of resting RV lateral wall peak systolic two-dimensional strain, a functional parameter showing a close association with VO2 peak during ESE, with a strong incremental value concerning clinical and standard echocardiographic data. The authors concluded that in athletes abusing steroids, STE analysis helps detecting impaired RV systolic deformation, closely associated with reduced functional capacity and pulmonary congestion during exercise.

Most of the previous reports identified the possible effects of AAS abuse, mainly on LV regional myocardial function in power athletes.⁹ Only a single previous report analysed RV myocardial function in athletes abusing AAS.⁴ The results of the present study demonstrate the incremental value of STE for the assessment of RV and LV myocardial function in power athletes abusing AAS, with higher sensitivity than other ultrasound techniques. Intriguingly, and of novelty in the field, despite the absence of manifest RV global systolic dysfunction, RV regional strain measurements were impaired in users compared with non-users and healthy sedentary controls, predicting functional capacity during ESE and vulnerability to pulmonary congestion in users, not apparent in resting evaluation.

Despite some considerable limitations (cross-sectional data; no histological determination of cardiac structure; no cardiac magnetic resonance imaging (MRI) data; no urine or serum measurements of drugs, which could have been appealing to show a correlation between serum concentrations and strain parameters; self-reported information about the intake of steroids; potential training-related influences) the paper is intriguing from several points beyond the specific topic of AAS abuse. First of all, it remarks the cost-effectiveness and sensibility of STE in detecting subtle myocardial alterations, both in left and right chambers, potentially reflecting tissue impairment. In this respect, MRI studies would add some helpful information, although at higher costs and accessibility. Although with some technical limitations, a further potential aid, progressively overcome by advanced technology, would derive from 3D echocardiographic imaging. The feasibility of the proposed multiparametric stress-echocardiography evaluation fosters this approach for a deeper understanding and functional characterization/phenotyping of patients. In particular, lung ultrasound during ESE has been demonstrated once again a clinically relevant tool to detect, together with RV hemodynamic indices, latent congestion, and to evaluate, at initial stages of exercise, diastolic function.¹⁰ Similarly, the combination of CPET-ESE provides interesting information on the patho-physiological relation between CPET functional indicators and structural/haemodynamic data on ESE. Complementing this information with cardiac biomarkers would be a powerful tool for the clinician to phenotype different physiological (athletes) or pathological (heart failure; valvular heart disease; pulmonary hypertension) settings.¹¹

In conclusion, a profound revision of exercise physiology in light of advanced non-invasive echocardiographic techniques and a modern vision of exercise echocardiography could offer the chances to better characterize (also at the tissue level) and clarify physiological and pathological changes in different clinical settings. Cardiovascular imaging (and Sports Medicine) community should address these issues in standardized protocols, aiming at prospective and large samples clinical datasets, thus providing univocal bodies of evidence, especially in the emerging field of CPET-ESE.

Conflict of interest: none declared.

The opinions expressed in this article are not necessarily those of the Editors of the European Journal of Preventive Cardiology or of the European Society of Cardiology.

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