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BACKGROUND: Athlete’s heart is a term describing the cardiovascular effects of long-term conditioning among highly trained athletes. It is a variation of normal standards. DESIGN AND SETTING: Case series study at the cardiology division of a public university hospital. METHODS: We studied 14 visually handicapped paralympic athletes (8 men) in the national judo team. They were 26.3 ± 6.4 years old, with body mass index 25 ± 14, and had been practicing judo for 9.2 ± 7.9 years. Clinical evaluations, electrocardiograms, exercise testing and echocardiograms were performed by independent observers. RESULTS: Signs of athlete’s heart were found in all athletes, comprising left ventricular hypertrophy (5 cases), sinus bradycardia (5), T-wave juvenile pattern (3), T wave juvenile pattern (3), left atrial hypertrophy (2) and increased left ventricular volume (9 cases; 62.22 ± 6.46 ml/m2). There were very strong correlations between left ventricular mass/body surface and endurance time (r: 0.91) and estimated peak oxygen uptake (r: 0.8). The correlations between left ventricular internal diastolic dimension and endurance time (r: 0.91) and estimated peak oxygen uptake (r: 0.8) were strong. Despite increased left ventricular dimensions (4 cases), atrial dimensions (1) and relative wall thickness (4), all athletes had normal left ventricular mass/body surface (89.98 ± 21.93 g/m²). The exercise testing was normal: exercise duration 706 ± 45 seconds and estimated peak oxygen uptake 62.70 ± 9.99 mlO2/min. CONCLUSIONS: Signs of athlete’s heart were seen frequently in the paralympic judo team. These demonstrated the presence of mild cardiac adaptations to training.

Exercise-associated benefits on the cardiovascular systems are well established. Although exercise-associated sudden cardiac death is rare, most deaths in young athletes are due to hereditary or congenital cardiac diseases. Athletic adaptation itself is associated with several structural changes that overlap those observed in individuals with cardiomyopathies, often leading to dilemmas for the clinician regarding life-changing decisions including advice against competitive sports participation. Cardiac magnetic resonance plays an increasingly important role in helping to establish an accurate diagnosis in these individuals. This review highlights the role of cardiac magnetic resonance in differentiating physiological adaptation in athletes from pathology.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an important cause of sudden cardiac death (SCD) in youth and athletes. In the last decade, several studies focused on right ventricular (RV) remodeling in athletes and revealed that features of the physiological adaptation of the right heart to training, such as RV dilation, may overlap with those of ARVC. Therefore, a careful multiparametric evaluation is required for differential diagnosis in order to avoid false diagnosis of ARVC or, in contrast, fail to identify the risk of causing SCD. This review summarizes physiological adaptation of the RV to exercise and describes features that could help distinguishing between athlete’s heart and ARVC.

Sudden cardiac death (SCD) is the nontraumatic death, due to loss of heart function that occurs suddenly and unexpectedly within 6 hours of a previously normal state of health. It is related to intense competitive sports promoting ventricular tachycardia (VT)/ventricular fibrillation (VF) in the presence of underlying abnormal substrate. A serial evaluation of cardiac physiologic changes taking place during training will allow the better understanding of athlete's heart and will facilitate its discrimination from other grey-zone cardiomyopathies. According to the ESC recommendations, a pre-participation evaluation should include medical history, physical examination as well as a 12-lead electrocardiogram (ECG). Additional tests, such as echocardiography, 24-hours Holter monitoring, stress testing and cardiovascular magnetic resonance (CMR) should be requested upon positive findings at the initial evaluation. Cardiovascular magnetic resonance can be of great value in the differential diagnosis between various cardiomyopathies including hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), left ventricle noncompaction cardiomyopathy (LVNC) and athlete's heart. This is due to its great versatility that can provide reliable and reproducible anatomical, functional and tissue characterization information, which are operator and acoustic window independent.

ObjectiveTo identify electrocardiographic findings, especially deep Q and S waves in lead III, that differentiate athletes from patients with hypertrophic cardiomyopathy (HCM).MethodsDigital ECGs of athletes and patients with HCM followed at the Stanford Center for Inherited Cardiovascular Disease were studied retrospectively. All patients with HCM had an echocardiogram performed. A multivariable logistic regression model was used to calculate ORs for various demographic and ECG characteristics. Linear regression was used to correlate ECG characteristics with echocardiogram findings.ResultsWe studied 1124 athletes and 240 patients with HCM. The average Q+S wave amplitude in lead III (IIIQ+S) was significantly higher in patients with HCM compared with athletes (0.71±0.69 mV vs 0.21±0.17 mV, pQ+S directly correlated with interventricular septal (IVS) thickness on echocardiography (ρ=0.45, pQ+S values remained independently associated with HCM compared with athletes (OR=4.2 per 0.5 mV, pQ+S remained associated with HCM. The addition of IIIQ+S>1.0 mV as an abnormal finding to the International Criteria for athletic ECG interpretation improved sensitivity from 64.2% to 70.4%, with a minimal decrease in specificity.ConclusionLarge Q and S waves in lead III distinguished athletes from patients with HCM, independent of axis and well-known ECG markers associated with HCM. The correlation between IVS thickness in patients with HCM and IIIQ+S suggests a partial explanation for this association.

Cardiomyopathies are a group of heterogeneous myocardial diseases that are frequently inherited and are a recognised cause of premature sudden cardiac death in young individuals. Incomplete expressions of disease and the overlap with the physiological cardiac manifestations of regular intensive exercise create diagnostic challenges in young athletes and military recruits. Early identification is important because sudden death in the absence of prodromal symptoms is a common presentation, and there are several therapeutic strategies to minimise this risk. This paper examines the classification and clinical features of cardiomyopathies with specific reference to a military population and provides a detailed account of the optimum strategy for diagnosis, indications for specialist referral and specific guidance on the occupational significance of cardiomyopathy. A 27-year-old Lance Corporal Signaller presents to his Regimental medical officer (RMO) after feeling ‘light-headed’ following an 8 mile unloaded run. While waiting to see the RMO, the medical sergeant records a 12-lead ECG. The ECG is reviewed by the RMO immediately prior to the consultation and shows voltage criteria for left ventricular (LV) hypertrophy and inverted T-waves in II, III, aVF and V1–V3 (Figure 1). This Lance Corporal is a unit physical training instructor and engages in >10 h of aerobic exercise per week. He is a non-smoker and does not have any significant medical history.

Cardiorespiratory fitness is a strong predictor of cardiovascular (CV) disease and all-cause mortality, with increases in cardiorespiratory fitness associated with corresponding decreases in CV disease risk. The effects of exercise upon the myocardium and vascular system are dependent upon the frequency, intensity and duration of the exercise itself. Following a prolonged period (≥6 months) of regular intensive exercise in previously untrained individuals, resting and submaximal exercising heart rates are typically 5-20 beats lower, with an increase in stroke volume of ∼20% and enhanced myocardial contractility. Structurally, all four heart chambers increase in volume with mild increases in wall thickness, resulting in greater cardiac mass due to increased myocardial cell size. With this in mind, the present paper aims to review the basic science behind the CV benefits of exercise. Attention will be paid to understanding (1) the relationship between exercise and cardiac remodelling; (2) the cardiac cellular and molecular adaptations in response to exercise, including the examination of molecular mechanisms of physiological cardiac growth and applying these mechanisms to identify new therapeutic targets to prevent or reverse pathological remodelling and heart failure; and (3) vascular adaptations in response to exercise. Finally, this review will briefly examine how to optimise the CV benefits of exercise by considering how much and how intense exercise should be.

Contractile function is considered to be precisely measurable only by invasive hemodynamics. We aimed to correlate strain values measured by speckle-tracking echocardiography (STE) with sensitive contractility parameters of pressure-volume (P-V) analysis in a rat model of exercise-induced left ventricular (LV) hypertrophy. LV hypertrophy was induced in rats by swim training and was compared with untrained controls. Echocardiography was performed using a 13-MHz linear transducer to obtain LV long- and short-axis recordings for STE analysis (GE EchoPAC). Global longitudinal (GLS) and circumferential strain (GCS) and longitudinal (LSr) and circumferential systolic strain rate (CSr) were measured. LV P-V analysis was performed using a pressure-conductance microcatheter, and load-independent contractility indices [slope of the end-systolic P-V relationship (ESPVR), preload recruitable stroke work (PRSW), and maximal dP/d t-end-diastolic volume relationship (dP/d tmax-EDV)] were calculated. Trained rats had increased LV mass index (trained vs. control; 2.76 ± 0.07 vs. 2.14 ± 0.05 g/kg, P < 0.001). P-V loop-derived contractility parameters were significantly improved in the trained group (ESPVR: 3.58 ± 0.22 vs. 2.51 ± 0.11 mmHg/μl; PRSW: 131 ± 4 vs. 104 ± 2 mmHg, P < 0.01). Strain and strain rate parameters were also supernormal in trained rats (GLS: −18.8 ± 0.3 vs. −15.8 ± 0.4%; LSr: −5.0 ± 0.2 vs. −4.1 ± 0.1 Hz; GCS: −18.9 ± 0.8 vs. −14.9 ± 0.6%; CSr: −4.9 ± 0.2 vs. −3.8 ± 0.2 Hz, P < 0.01). ESPVR correlated with GLS ( r = −0.71) and LSr ( r = −0.53) and robustly with GCS ( r = −0.83) and CSr ( r = −0.75, all P < 0.05). PRSW was strongly related to GLS ( r = −0.64) and LSr ( r = −0.71, both P < 0.01). STE can be a feasible and useful method for animal experiments. In our rat model, strain and strain rate parameters closely reflected the improvement in intrinsic contractile function induced by exercise training.

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/m2, p

NanoUPLC/MSE was used to verify the effects of 8 weeks of low (SHR-LIT = 4) and high (SHR-HIT = 4) intensity training over the left ventricle proteome of hypertensive rats (SHR-C = 4). Training enhanced the aerobic capacity and reduced the systolic blood pressure in all exercised rats. NanoUPLC/MSE identified 250 proteins, with 233 in common to all groups and 16 exclusive to SHR-C, 2 to SHR-LIT, and 2 to the SHR-HIT. Cardiac hypertrophy related proteins appeared only in SHR-C. The SHR-LIT enhanced the abundance of 30 proteins and diminished 6, while SHR-HIT enhanced the abundance of 39 proteins and reduced other 7. The levels of metabolic (β and γ-enolase, adenine phosphoribosultransferase, and cytochrome b-c1), myofibril (myosin light chain 4, tropomyosin α and β-chain), and transporter proteins (hemoglobin, serum albumin, and hemopexin) were increased by both intensities. Transcription regulator and histone variants were enhanced by SHR-LIT and SHR-HIT respectively. SHR-LIT reduced the concentration of myosin binding protein C, while desmin and membrane voltage dependent anion selective channel protein-3 were reduced only by SHR-HIT. In addition, polyubiquitin B and C, and transcription regulators decreased in both intensities. Exercise also increased the concentration of anti-oxidant proteins, peroxiredozin-6 and glutathione peroxidase-1. Biological significance Pathologic left ventricle hypertrophy if one of the major outcomes of hypertension being a strong predictor of heart failure. Among the various risk factors for cardiovascular disorders, arterial hypertension is responsible for the highest rates of mortality worldwide. In this way, this present study contribute to the understanding of the molecular mechanisms involved in the attenuation of hypertension and the regression of pathological cardiac hypertrophy induced by exercise training.

AT1 receptor (AT1R) blockade prevents physiological cardiac hypertrophy induced by resistance training. Also, our group showed that a single bout of resistance exercise (RE) activates the AKT/mTOR which was also inhibited by AT1R blocker. Here, we investigated whether IGF1-receptor (IGF1-R) and MAPKs were also activated after a single bout of RE. Wistar rats were divided into Sedentary (Sed), Sedentary treated with losartan (Sed+LOS), Exercise (EX), and Exercise treated with losartan (EX+LOS). Cardiac tissue was obtained 5 and 30 min after 4 sets of 12 repetitions of squat exercise (80 % 1RM). We demonstrated that a single bout of RE did not induce IGF1-R tyrosine phosphorylation. ERK1/2 and P38 phosphorylation levels were elevated in the EX 5min and EX 30min groups however, only ERK1/2 was inhibited by losartan treatment (AT1R blocker). Next, we showed that β-arrestin-2 expression increased 28 % in trained animals compared to sedentary group. Altogether, our results demonstrate that AT1R, but not IGF1-R, may exert the hypertrophic cardiac stimulus RE-induced. Also, activation of AKT/mTOR and ERK1/2 pathways may occur through the β-arrestin-dependent pathway.

Arrhythmogenic right ventricular (RV) remodeling has been reported in response to regular training, but it remains unclear how exercise intensity affects the presence and extent of such remodeling. We aimed to assess the relationship between RV remodeling and exercise load in a long-term endurance training model. Wistar rats were conditioned to run at moderate (MOD; 45 min, 30 cm/s) or intense (INT; 60 min, 60 cm/s) workloads for 16 wk; sedentary rats served as controls. Cardiac remodeling was assessed with standard echocardiographic and tissue Doppler techniques, sensor-tip pressure catheters, and pressure-volume loop analyses. After MOD training, both ventricles similarly dilated (~16%); the RV apical segment deformation, but not the basal segment deformation, was increased [apical strain rate (SR): −2.9 ± 0.5 vs. −3.3 ± 0.6 s−1, SED vs. MOD]. INT training prompted marked RV dilatation (~26%) but did not further dilate the left ventricle (LV). A reduction in both RV segments' deformation in INT rats (apical SR: −3.3 ± 0.6 vs. −3.0 ± 0.4 s−1 and basal SR: −3.3 ± 0.7 vs. −2.7 ± 0.6 s−1, MOD vs. INT) led to decreased global contractile function (maximal rate of rise of LV pressure: 2.53 ± 0.15 vs. 2.17 ± 0.116 mmHg/ms, MOD vs. INT). Echocardiography and hemodynamics consistently pointed to impaired RV diastolic function in INT rats. LV systolic and diastolic functions remained unchanged in all groups. In conclusion, we showed a biphasic, unbalanced RV remodeling response with increasing doses of exercise: physiological adaptation after MOD training turns adverse with INT training, involving disproportionate RV dilatation, decreased contractility, and impaired diastolic function. Our findings support the existence of an exercise load threshold beyond which cardiac remodeling becomes maladaptive. NEW & NOTEWORTHY Exercise promotes left ventricular eccentric hypertrophy with no changes in systolic or diastolic function in healthy rats. Conversely, right ventricular adaptation to physical activity follows a biphasic, dose-dependent, and segmentary pattern. Moderate exercise promotes a mild systolic function enhancement at the right ventricular apex and more intense exercise impairs systolic and diastolic function.

The last few decades have seen substantial growth in the populations of competitive athletes and highly active people (CAHAP). Although vigorous physical exercise is an effective way to reduce the risk of cardiovascular (CV) disease, CAHAP remain susceptible to inherited and acquired CV disease, and may be most at risk for adverse CV outcomes during intense physical activity. Traditionally, multidisciplinary teams comprising athletic trainers, physical therapists, primary care sports medicine physicians, and orthopedic surgeons have provided clinical care for CAHAP. However, there is increasing recognition that a care team including qualified CV specialists optimizes care delivery for CAHAP. In recognition of the increasing demand for CV specialists competent in the care of CAHAP, the American College of Cardiology has recently established a Sports and Exercise Council. An important primary objective of this council is to define the essential skills necessary to practice effective sports cardiology.

Pathologic forms of left ventricular hypertrophy (LVH) are associated with impaired myocardial metabolic efficiency (MME), the ratio of myocardial work to oxygen consumption (MVO2), which may serve as a key mechanistic link between LVH and the development of heart failure syndromes [(1,2)][1]. At

The aim of this study was to assess the early electrocardiogram (ECG) changes induced by physical training in preadolescent elite footballers. This study included 94 preadolescent highly trained male footballers (FG) competing in Serbian Football League (minimum of 7 training hours/week) and 47 age-matched healthy male controls (less than 2 training hours/week) (CG). They were screened by ECG and echocardiography at a tertiary referral cardio center. Sokolow–Lyon index was used as a voltage electrocardiographic criterion for left ventricular hypertrophy diagnosis. Characteristic ECG intervals and voltage were compared and reference range was given for preadolescent footballers. Highly significant differences between FG and CG were registered in all ECG parameters: P-wave voltage (p p p 1–2 + R V5–6 (p p p p p p p > 0.05). During 6-year follow-up period, there was no adverse cardiac event in these footballers. None of them expressed pathological ECG changes. Benign ECG changes are presented in the early stage of athlete’s heart remodeling, but they are not related to pathological ECG changes and they should be regarded as ECG pattern of LV remodeling.

The number of recreational/non-elite athletes participating in marathons is increasing, but data regarding impact of endurance exercise on cardiovascular health are conflicting. This study evaluated 79 recreational athletes of the 2016 Barcelona Marathon (72% men; mean age 39 ± 6 years; 71% ≥35 years). Blood samples were collected at baseline (24–48 h before the race), immediately after the race (1–2 h after the race), and 48-h post-race. Amino-terminal pro-B type natriuretic peptide (NT-proBNP, a marker of myocardial strain), ST2 (a marker of extracellular matrix remodeling and fibrosis, inflammation, and myocardial strain), and high-sensitivity troponin T (hs-TnT, a marker of myocyte stress/injury) were assayed. The median (interquartile range, IQR) years of training was 7 (5–11) years and median (IQR) weekly training hours was 6 (5–8) h/week, respectively. The median (IQR) race time (h:min:s) was 3:32:44 (3:18:50–3:51:46). Echocardiographic indices were within normal ranges. Immediately after the race, blood concentration of the three cardiac biomarkers increased significantly, with 1.3-, 1.6-, and 16-fold increases in NT-proBNP, ST2, and hs-TnT, respectively. We found an inverse relationship between weekly training hours and increased ST2 (p = 0.007), and a direct relationship between race time and increased hs-TnT (p < 0.001) and ST2 (p = 0.05). Our findings indicate that preparation for and participation in marathon running may affect multiple pathways affecting the cardiovascular system. More data and long-term follow-up studies in non-elite and elite athletes are needed.

Pathological cardiac hypertrophy may be associated with reduced expression of glucose transporter 4 (GLUT4) in contrast to exercise-induced cardiac hypertrophy, where GLUT4 levels are increased. However, mice with cardiac-specific deletion of GLUT4 (G4H−/−) have normal cardiac function in the unstressed state. This study tested the hypothesis that cardiac GLUT4 is required for myocardial adaptations to hemodynamic demands. G4H−/−and control littermates were subjected to either a pathological model of left ventricular pressure overload [transverse aortic constriction (TAC)] or a physiological model of endurance exercise (swim training). As predicted after TAC, G4H−/−mice developed significantly greater hypertrophy and more severe contractile dysfunction. Somewhat surprisingly, after exercise training, G4H−/−mice developed increased fibrosis and apoptosis that was associated with dephosphorylation of the prosurvival kinase Akt in concert with an increase in protein levels of the upstream phosphatase protein phosphatase 2A (PP2A). Exercise has been shown to decrease levels of ceramide; G4H−/−hearts failed to decrease myocardial ceramide in response to exercise. Furthermore, G4H−/−hearts have reduced levels of the transcriptional coactivator peroxisome proliferator-activated receptor-γ coactivator-1, lower carnitine palmitoyl-transferase activity, and reduced hydroxyacyl-CoA dehydrogenase activity. These basal changes may also contribute to the impaired ability of G4H−/−hearts to adapt to hemodynamic stresses. In conclusion, GLUT4 is required for the maintenance of cardiac structure and function in response to physiological or pathological processes that increase energy demands, in part through secondary changes in mitochondrial metabolism and cellular stress survival pathways such as Akt.NEW & NOTEWORTHY Glucose transporter 4 (GLUT4) is required for myocardial adaptations to exercise, and its absence accelerates heart dysfunction after pressure overload. The requirement for GLUT4 may extend beyond glucose uptake to include defects in mitochondrial metabolism and survival signaling pathways that develop in its absence. Therefore, GLUT4 is critical for responses to hemodynamic stresses.

Background: The significance and spectrum of reduced right ventricular (RV) deformation, reported in endurance athletes, is unclear. Purpose: to comprehensively analyze the cardiac performance at rest of athletes, especially focusing on integrating RV size and deformation to unravel the underlying triggers of this ventricular remodelling. Methods: 100 professional male athletes and 50 sedentary healthy males of similar age were prospectively studied. Conventional echocardiographic parameters of all 4 chambers were obtained, as well as 2D echo-derived strain (2DSE) in the left (LV) and in the RV free wall with separate additional analysis of the RV basal and apical segments. Results: Left and right-sided dimensions were larger in athletes than in controls, but with a disproportionate RA enlargement. RV global strain was lower in sportsmen (-26.8 ± 2.8 vs -28.5 ± 3.4%, p

Aerobic exercise confers sustainable protection against cardiac hypertrophy and heart failure (HF). Nitric oxide synthase (NOS) and nitric oxide (NO) are known to play an important role in exercise-mediated cardioprotection, but the mechanism of NOS/NO stimulation during exercise remains unclear. The aim of this study is to determine the role of β3-adrenergic receptors (β3-ARs), NOS activation, and NO metabolites (nitrite and nitrosothiols) in the sustained cardioprotective effects of aerobic exercise. An HF model was constructed by transverse aortic constriction (TAC). Animals were treated with either moderate aerobic exercise by swimming for 9 weeks and/or the β3-AR-specific inhibitor SR59230A at 0.1 mg/kg/hour one day after TAC operation. Myocardial fibrosis, myocyte size, plasma catecholamine (CA) level, cardiac function and geometry were assessed using Masson’s trichrome staining, FITC-labeled wheat germ agglutinin staining, enzyme-linked immuno sorbent assay (ELISA) and echocardiography, respectively. Western blot analysis was performed to elucidate the expression of target proteins. The concentration of myocardial NO production was evaluated using the nitrate reductase method. Myocardial oxidative stress was assessed by detecting the concentration of myocardial super oxidative dismutase (SOD), malonyldialdehyde (MDA), and reactive oxygen species (ROS). Aerobic exercise training improved dilated left ventricular function and partially attenuated the degree of cardiac hypertrophy and fibrosis in TAC mice. Moreover, the increased expression of β3-AR, activation of neuronal NOS (nNOS), and production of NO were detected after aerobic exercise training in TAC mice. However, selective inhibition of β3-AR by SR59230A abolished the upregulation and activation of nNOS induced NO production. Furthermore, aerobic exercise training decreased the myocardial ROS and MDA contents and increased myocardial levels of SOD; both effects were partially attenuated by SR59230A. Our study suggested that aerobic exercise training could improve cardiac systolic function and alleviate LV chamber dilation, cardiac fibrosis and hypertrophy in HF mice. The mechanism responsible for the protective effects of aerobic exercise is associated with the activation of the β3-AR-nNOS-NO pathway.

Exercise-induced physiological cardiac hypertrophy is generally considered to be a type of adaptive change after exercise training and is beneficial for cardiovascular diseases. This study aims at investigating exercise-regulated microRNAs (miRNAs) and their potential biological pathways. Here, we collected 23 miRNAs from 8 published studies. MirPath v.3 from the DIANA tools website was used to execute the analysis, and TargetScan was used to predict the target genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses were performed to identify potential pathways and functional annotations associated with exercise-induced physiological cardiac hypertrophy. Various miRNA targets and molecular pathways, such as Fatty acid elongation, Arrhythmogenic right ventricular cardiomyopathy (ARVC), and ECM-receptor interaction, were identified. This study could prompt the understanding of the regulatory mechanisms underlying exercise-induced physiological cardiac hypertrophy.

Left ventricular hypertrophy (LVH) develops in response to a variety of physical, genetic, and biochemical stimuli and represents the early stage of ventricular remodeling. In patients with LVH, subclinical left ventricular (LV) dysfunction despite normal ejection fraction (EF) may be present before the onset of symptoms, which portends a dismal prognosis. Strain measurement with two-dimensional speckle tracking echocardiography (STE) represents a highly reproducible and accurate alternative to LVEF determination. The present review focuses on current available evidence that supports the incremental value of STE in the diagnostic and prognostic workup of LVH. When assessing the components of LV contraction, STE has an incremental value in differentiating between primary and secondary LVH and in the differential diagnosis with storage diseases. In addition, STE provides unique information for the stratification of patients with LVH, enabling to detect intrinsic myocardial dysfunction before LVEF reduction.

Cardiovascular physiologic remodeling associated with athleticism may mimic many of the features of genetic and acquired heart disease. The most pervasive dilemma is distinguishing between normal and abnormal physiologic remodeling in an athlete's heart. Imaging examinations, such as magnetic resonance imaging and computed tomography, which focus predominantly on anatomy, and electrocardiography, which monitors electrical components, do not simultaneously evaluate cardiac anatomy and physiology. Despite nonlinear anatomic and electrical remodeling, the athlete's heart retains normal or supernormal myocyte function, whereas a diseased heart has various degrees of pathophysiology. Echocardiography is the only cost-effective, validated imaging modality that is widely available and capable of simultaneously quantifying variable anatomic and physiologic features. Doppler echocardiography substantially redefines the understanding of normal remodeling from preemergent and overt disease.

Physical activity is a potent therapy for both the prevention and treatment of cardiovascular disease. Exercise appears to most benefit people who are the least active. There is some evidence to suggest that a curvilinear relationship exists between exercise and survival, whereby beyond an optimal level of fitness, the principle of diminishing returns applies. Indeed, some go further in suggesting that there is evidence that extreme athletic training may be harmful in some individuals. The incidence of sudden cardiac death in athletes is greater than in matched, nonathletic counterparts, and this finding is driven by the provocation of an underlying cardiac abnormality by strenuous exertion. The task of detecting pathological myocardial substrate in athletes is made difficult by physiological adaptations to exercise that can mimic the appearance of cardiomyopathies and ion channelopathies in some individuals. This article details the clinical evaluation of the athlete with reference limits for cardiac physiological remodeling and discusses the diagnostic dilemmas that arise.

Vitamin D (25(OH)D) deficiency has associations with bowl/colon cancer, arthritis, diabetes, and cardiovascular disease. Many athletes are vitamin D deficient, yet no studies have examined the association between 25(OH)D status and cardiac structure and function in healthy athletes.A total of 506 national-level athletes [football (50%), handball (23%), volleyball (16%), and basketball (11%)] and 244 control participants presented for precompetition medical assessment. Controls were healthy individuals registered with a sporting federation undertaking2 h of exercise per week.All individuals undertook a physical examination, 12-lead electrocardiogram, echocardiogram, and serum 25(OH)D evaluation.From 506 athletes and 244 controls, 23 and 12.3% demonstrated 25(OH)D sufficiency (30 ng/ml), 30 and 23.4% insufficiency (20-30 ng/ml), 37.2 and 48.8% deficiency (10-20 ng/ml), and 11 and 15.6% severe deficiency (10 ng/ml). Severely 25(OH)D-deficient athletes present significantly (p 0.05) smaller aortic root and left atria diameters, intraventricular septum diameter (IVSd), left ventricular diameter during diastole (LVIDd), left ventricular mass (LVM), left ventricular volume during diastole (LVvolD), and right atrial (RA) area than insufficient and sufficient athletes. Furthermore, following logarithmic transformation adjusting 25(OH)D for age, body surface area, ethnicity, and athletic participation, positive associations were observed between 25(OH)D and IVSd, LVIDd, posterior wall thickness during diastole, LVM, and LVvolD in athletes but not in the control participants.Severely 25(OH)D-deficient athletes present significantly smaller cardiac structural parameters than insufficient and sufficient athletes. Future research should investigate the precise mechanism(s) causing cardiac hypertrophy with increases in serum 25(OH)D in healthy athletes.

Regular physical activity over a long period of time increases the output of the cardiovascular system. That leads to development of a normal (physiological) athlete's heart. Bradycardia, cardiac hypertrophy, and arterial hypotension are three major characteristics of a normal athlete's heart. Changes in parameters of cardiovascular system and features of heart remodeling are determined by type, frequency, and duration of a physical activity. Excessive levels of physical activity could result in development of a pathologic athlete's heart, negatively affect hearts metabolism, and increase the risk of both atherosclerosis and myocardial infarction. Autopsy studies have shown that atherosclerosis, which leads to development of an ischemic heart disease, is often found in both young and elderly athletes. 56% of sudden deaths in all athletes were due to cardiovascular problems. Reports of ischemic heart disease in athletes of all ages have increased over the past few years. Echocardiographic features and clinical outcomes of stable angina and myocardial infarction in retired professional athletes are not well studied. Further studies are needed to improve diagnosis, prevention, treatment, and rehabilitation in elite athletes with ischemic heart disease.

Background— Recent reports have suggested that long-term, intensive physical training may be associated with adverse cardiovascular effects, including the development of myocardial fibrosis. However, the dose–response association of different levels of lifelong physical activity on myocardial fibrosis has not been evaluated. Methods and Results— Seniors free of major chronic illnesses were recruited from predefined populations based on the consistent documentation of stable physical activity over >25 years and were classified into 4 groups by the number of sessions/week of aerobic activities ≥30 minutes: sedentary (group 1), Conclusions— A lifelong history of consistent physical activity, regardless of dose ranging from sedentary to competitive marathon running, was not associated with the development of focal myocardial fibrosis.

Purpose To investigate determinants of right ventricular (RV) function in competitive athletes by a combined assessment of speckle tracking (STE) and real time 3D echocardiography (RT3DE). Methods Right ventricular function of 40 top-level rowers was compared to 43 sedentary normal controls by standard Doppler echocardiography, RT3DE, and STE. RV diameters and wall thickness, tricuspid annular plane systolic excursion (TAPSE), tricuspid E/A ratio, and pulsed tissue Doppler of lateral tricuspid annulus were analyzed. RV volumes, ejection fraction (EF), and stroke volume (SV) were determined. RV global longitudinal strain (GLS) (average of 6 regions), septal strain (average of 3 septal regions, septal longitudinal strain [SLS]), and lateral strain (average of 3 lateral regions, lateral longitudinal strain [LLS]) were estimated by STE. Results The 2 groups were comparable for age, body mass index, and blood pressure, but heart rate was lower in rowers. RV diameters were larger and TAPSE, tricuspid E/A ratio, and tissue Doppler-derived s′ and e′ velocities were higher in rowers. By RT3DE, RV end-diastolic volume (EDV) and end-systolic volume were greater in rowers (both P

Hypertrophic cardiomyopathy is a hereditary, not uncommon cardiac disease, which is associated with asymmetric thickening and hypertrophy of the interventricular septum unrelated to hemodynamic reasons. Despite hypertrophic cardiomyopathy is considered to be a disorder of the heart muscle, several associated vascular alterations have been described. The aim of the present review is to summarize vascular functional alterations in hypertrophic cardiomyopathy.A hypertrophiás cardiomyopathia genetikailag öröklődő, nem túl ritka kardiológiai megbetegedés, amely legtöbbször az interventricularis septum hemodinamikai okokkal nem magyarázható aszimmetrikus megvastagodásával, hypertrophiájával jár együtt. Annak ellenére, hogy a hypertrophiás cardiomyopathiát a szívizomzat betegségének tartjuk, számos tanulmány igazolta a kórképpel együtt járó vascularis eltéréseket. Jelen összefoglaló tanulmány célja annak bemutatása, hogy milyen vascularis funkcionális eltérések ismertek hypertrophiás cardiomyopathia fennállása esetén. Orv. Hetil., 2013, 154(47), 1851–1857.