Exercise-induced left-ventricular hypertrabeculation in athlete's heart

Left ventricular non-compaction (LVNC) is a cardiomyopathy characterized by increased LV trabeculation and intertrabecular recesses, associated with progressive LV dilatation, systolic and diastolic impairment, life-threatening arrhythmias, and thromboembolic events [1,2]. Implementation of cardiac imaging techniques (e.g., echocardiography) in the cardiovascular screening has revealed increased LV trabeculation in a large, unsuspected prevalence of competitive athletes, with a morphologic pattern fulfilling the conventional echocardiographic criteria for LVNC [3]

Cardiac benefits after alcohol withdrawal

Numerous studies demonstrated that a chronic consumption of alcohol is directly related to alcoholic cardiomyopathy (ACM), which is a specific dilated cardiomyopathy

Training-induced right ventricular remodelling in pre-adolescent endurance athletes: The athlete's heart in children

Aims Little is known about the adaptation of the right ventricle (RV) to endurance exercise in children. The aim of this study was to assess the effects of 5 months of intensive training on RV morphology and function in preadolescent endurance athletes. Methods Ninety-four children were evaluated in this study. Fifty-seven male competitive swimmers (aged 10.8 ± 0.2 years) were evaluated before (baseline) and after 5 months of the training (peak-training), and compared to 37 age- and sex-matched non-athlete children evaluated at baseline and after 5 months of natural growth. All subjects were asymptomatic, with negative family history for cardiomyopathies. Results At baseline no differences were found between athletes and controls for indexed RV outflow tract (RVOT) (18.5 ± 2.7 vs. 16.8 ± 5.0 mm/m2, p = 0.18) and RV basal end-diastolic diameter (EDD) (24.9 ± 4.1 vs. 23.6 ± 3.0 mm/m2, p = 0.15). After 5 months, indexed RVOT and RV basal EDD significantly increased in athletes (20.2 ± 2.9 mm/m2 and 25.4 ± 3.3 mm/m2, p < 0.0001 vs. baseline) while no differences were observed in controls (p = 0.84 and p = 0.25). Despite the increase in RV size, RV function remained normal in athletes, with no changes in RV fractional area change (p = 0.97), s′ value (p = 0.22), and RV longitudinal strain (p = 0.28). Conclusions Endurance training influences the growing heart of male preadolescent athletes with an addictive increase in RV dimensions, with a preserved RV function. Therefore, in children engaged in endurance sports the increase in RV size associated with normal RV function represents a physiological expression of the athlete's heart and should not be misinterpreted as an expression of incipient RV cardiomyopathy. © 2017 Elsevier B.V

Right ventricular remodelling induced by exercise training in competitive athletes

Aims Conflicting evidence exists concerning right ventricular (RV) morphological and functional remodelling in trained athletes, with a very few longitudinal data prospectively investigating the RV changes. The aim of this study was to assess the morphological and functional RV changes occurring during the competitive season in young athletes engaged in the most popular team sports. Methods and results Twenty-nine top-level athletes (age: 20.9 ± 6.7 years), practicing basketball and volleyball, were evaluated at pre-season, mid-season, and end-season time-points, using tissue Doppler imaging and 2D speckle-tracking echocardiography. RV basal and mid-cavity end-diastolic diameters (EDDs; overall P = 0.011 and P < 0.0001, respectively), and RV diastolic area (overall P < 0.0001) increased during the season. Conversely, RV outflow tract did not vary (overall P = 0.96). During the season, no significant differences were observed in RV diastolic functional indexes and in RV fractional area change (overall P = 0.35). Global RV longitudinal strain did not significantly change (overall P = 0.52), although apical longitudinal strain significantly increased (overall P = 0.017). In association, left ventricular (LV) volume and mass increased during the season (overall P = 0.007). On multivariate analysis, LV mass was the only independent predictor of RVEDD at pre-season (β = 0.69, P < 0.0001) and at end-season (β = 0.82, P < 0.0001). Conclusions Right ventricular chamber size increases during the competitive season in top-level athletes, with no significant changes in the outflow tract. RV morphological adaptation in top-level athletes practicing team sports is not associated with a reduction in RV function or in myocardial deformation and occurs in close association with changes on the left ventricle, suggesting a physiological remodelling of the right ventricle

Increased left atrial size is associated with reduced atrial stiffness and preserved reservoir function in athlete's heart

Left atrial (LA) fibrosis with increased stiffness has been assumed to be the substrates for occurrence of atrial arrhythmias in athletes. However, this hypothesis has not yet been confirmed in humans. Aim of this study was, therefore, to assess LA remodeling and stiffness in competitive athletes. 150 competitive athletes and 90 age and sex-matched sedentary subjects were analyzed by speckle-tracking echocardiography to measure peak atrial longitudinal strain (PALS) and peak atrial contraction strain (PACS). LA stiffness was determined using E/e' ratio in conjunction with PALS. Left ventricular (LV) stiffness was also calculated. LA volume index was greater in athletes as compared with controls (24.6 ± 7.3 vs. 18.4 ± 7.8 mL/m(2), p < .0001). LA PALS, LA PACS, and E/e' ratio were lower in athletes in comparison with controls (p < .05, p ≤ .001, and p < .0001, respectively). Despite greater LA size, competitive athletes had lower LA stiffness as compared with controls (0.13 ± 0.04 vs. 0.16 ± 0.06, p ≤ .001). In addition, LV stiffness was lower in athletes (0.84 ± 0.27 vs. 1.07 ± 0.46, p ≤ .001). The only independent predictor of LA stiffness was LV stiffness (β = 0.46, p < .0001), while the only independent predictor of LA volume index was LV end-systolic volume index (β = 0.25, p = .002). Competitive athletes showed greater LA size associated with lower stiffness as compared with controls. Thus, LA remodeling in the context of the athlete's heart is not associated with increased LA stiffness. These findings support the benign nature of LA remodeling in athletes, occurring as a physiological adaptation to exercise conditioning

Training-induced dynamic changes in left atrial reservoir, conduit, and active volumes in professional soccer players

Purpose: Although left atrial (LA) enlargement is a recognized component of athlete’s heart, dynamic cavity changes occurring during the training period remain to be elucidated. We aimed to investigate the adaptive changes of LA reservoir, conduit, and active volumes in elite athletes vs. controls and their response to different training loads. Methods: LA maximum, pre-P, and minimum volumes were assessed in 26 top-level athletes and 23 controls. In athletes, LA volumes were measured at pre-, mid-, end-training, and post-detraining time points using conventional 2D echocardiography. Results: Athletes had larger maximum (27.5 ± 3.2 vs. 20.3 ± 5.8 mL/m2, p = 0.001), pre-P (11.5 ± 0.9 vs. 9.8 ± 2.2 mL/m2, p = 0.001), and minimum (6.6 ± 0.9 vs. 5.0 ± 1.2 mL/m2, p 2, p 2, p < 0.05, respectively), while active emptying volume was similar (p = 0.74). During training, LA maximum (p < 0.0001), pre-P (p < 0.0001), minimum (p < 0.0001), total (p < 0.005), and passive (p < 0.05) emptying volume indices progressively increased, while active emptying volume (p = 0.10) and E/e′ ratio (p = 0.32) remained unchanged. After detraining, LA volume measurements were not different from pre-training ones. End-training left ventricular mass index was the only independent predictor of the respective maximum LA volume (β = 0.74, p < 0.005). Conclusions: Top-level athletes exhibit a dynamic morphological and functional LA remodeling, induced by training, with an increase in reservoir and conduit volumes, but stable active volume. LA remodeling is closely associated with left ventricular adaptation to exercise and both completely regress after detraining

Heart transplantation and anti‐HLA antibodY: myocardial dysfunction and prognosis ‐ HeartLAy study

Abstract Aims The presence of anti‐human leucocyte antigen (HLA) antibodies has been implicated in a higher incidence of complications as well as mortality rate in heart transplantation. The aim of the study was to identify through non‐invasive parameters early signs of myocardial dysfunction in the presence of anti‐HLA antibodies but without evidence of antibody‐mediated rejection (AMR) and its possible prognostic impact. Methods and results A total of 113 heart‐transplanted patients without acute cellular rejection (ACR) and AMR or cardiac allograft vasculopathy (CAV) were prospectively enrolled and divided into two groups [‘HLA+’ (50 patients) and ‘HLA−’ (63 patients)], based on the presence of anti‐HLA antibodies. Each patient was followed for 2 years after the enrolment, recording episodes of AMR, ACR, CAV, and mortality. Clinical characteristics were similar between the two groups. Among laboratory data, N‐terminal pro‐B‐type natriuretic peptide and high‐sensitivity cardiac troponin values were significantly higher in the presence of anti‐HLA antibodies (P < 0.001 and P = 0.003, respectively). The echocardiographic parameters that showed a statistically significant difference between the two groups were deceleration time of E wave (DecT E, P < 0.001), left ventricular global longitudinal strain (P < 0.001), tricuspid annular plane systolic excursion (P = 0.011), tricuspid S′ wave (P = 0.002), and free wall right ventricular longitudinal strain (fwRVLS, P = 0.027), whereas left atrial strain did not differ significantly (P = 0.408). Univariate analysis showed that anti‐HLA antibodies were associated with the development of CAV at both 1 and 2 year follow‐up [odds ratio (OR) 11.90, 95% confidence interval (CI) 1.43–90.79, P = 0.022 and OR 3.37, 95% CI 1.78–9.67, P = 0.024, respectively]. Bivariate analysis demonstrated that both fwRVLS and DecT E were predictors of CAV development independently from HLA status. Conclusions The presence of circulating anti‐HLA antibodies is correlated with a mild cardiac dysfunction, even in the absence of AMR, and CAV development. Interestingly, reduced values of DecT E and fwRVLS were predictors of future development of CAV, independently from anti‐HLA antibody

Electromechanical delay by speckle-tracking echocardiography: A novel tool to distinguish between Brugada syndrome and isolated right bundle branch block

Background: The electrocardiographic (ECG) definition of Brugada syndrome (BS) can be challenging because benign ECG abnormalities, such as right bundle branch block (RBBB), may mimic pathological ECG characteristics of BrS. However, although myocardial delay and deformation can be quantified by advanced imaging, it has not yet been used to differentiate between BrS and RBBB. The aim of this study was to characterize the electro-mechanical behavior of the heart of patients with type-1 BrS and isolated complete RBBB in order to differentiate these conditions. Methods: In this two-center study, 66 subjects were analyzed by standard and speckle-tracking echocardiography (STE): 22 type-1 BrS, 24 isolated complete RBBB, and 20 healthy subjects. The participants were not treated by any drug potentially influencing myocardial conduction. Results: Standard echocardiographic parameters did not differ among the groups. The greatest right ventricular (RV) mechanical dispersion was found in RBBB. Mean absolute deviations (MADs) of time-to-peak longitudinal strain calculated for each left ventricular (LV) region were greater in patients with RBBB as compared to BrS (p &lt; .01). No differences were found between BrS and controls (p = .36). MADs in the basal segments in RBBB group were greater than MADs found in BrS group and controls (37.3 ms vs. 26.7 ms and 29.0 ms, respectively, p &lt; .05). The greatest differences were found in the antero-septal, anterior, lateral, and infero-septal basal segments. Conclusions: Advanced echocardiographic techniques may help to differentiate between BrS and RBBB. Indeed, STE allows to identify an electro-mechanical conduction delay in RBBB patients that is not found in patients affected by type-1 BrS. Keywords: Brugada pattern; Channelopathy; Deformation; Mechanical dispersion; Strain. Copyright © 2020. Published by Elsevier B.V