Left Ventricular Hypertrophy In Athletes Research Articles

Left ventricular hypertrophy in athletes, a case-control analysis of interindividual variability

BackgroundA variability in cardiac remodeling is observed in athletes regardless of age, sex, body size and sport participated. We sought to investigate whether other individual characteristics could affect the extent of Left ventricular hypertrophy (LVH). MethodsFrom 2120 consecutive Olympic athletes, those with LVH (defined as LV Wall thickness ≥ 13 mm) were matched 1:1 by age, gender, body surface area and type of sport with non-LVH Athletes. Clinical and Echocardiographic variables were compared. Results48 athletes with LVH (2.3%) and 48 matched non-LVH athletes were identified. LVH Athletes had higher body weight (90 ± 18 vs 81 ± 11Kg; p = 0.006) body mass index (26 ± 2 vs 24 ± 2 Kg/m2; p < 0.001) and body fat percentage (15 ± 7% vs 12 ± 4%; p = 0.016) compared to non-LVH Athletes. They also had higher systolic (123 ± 1 vs 116 ± 11 mmHg; p = 0.002) and diastolic blood pressure (76 ± 8 vs 71 ± 9 mmHg; p = 0.002). On exercise testing, LVH Athletes reached a lower index workload (3.7 ± 0.9 vs 4.1 ± 0.8 W/Kg; p = 0.013) and a higher peak diastolic blood pressure (79 ± 10 vs 74 ± 11 mmHg; p = 0.012) than those without LVH. Binary logistic regression analysis showed that diastolic blood pressure (OR 1.052; 95% CI from 1.011 to 1.130; p = 0.020) and BMI (OR 1.220; 95% CI from 1.016 to 1.465; p = 0.033) had the strongest association with LVH as categorical variable. ConclusionsOur study showed that increased blood pressure at rest and during exercise, together with larger body weight, body mass and fat percentage are associated with a higher degree of LVH, which is not associated with a greater physical performance and therefore possibly disproportionate to the sport activity.

Differentiation between physiological sport adaptation and hypertrophic cardiomyopathy in highly trained athletes using cardiac magnetic resonance

Abstract Differentiation between hypertrophic cardiomyopathy (HCM) patients and healthy athletes (HA) is a common clinical conundrum. We aimed to analyze cardiac magnetic resonance (CMR) characteristics of HA, sedentary HCM and athletic HCM patients and to determine CMR parameters which can help to diagnose HCM in athletes. Male sedentary HCM patients with slightly elevated maximal end-diastolic wall thickness (EDWT 13–18 mm, n=40, 47.6±14.7y) and HA (n=30, 27.5±5.6y) were consecutively enrolled. Additionally, athletes with HCM were enrolled (n=16, 29.6±13.4 y), where a comprehensive investigation confirmed the diagnosis of HCM. We determined conventional CMR parameters (left ventricular (LV) ejection fraction (EF), end-diastolic (EDVi) and end-systolic volume index, mass index (Mi)), derived parameters such as EDWT/LVEDVi, LVM/LVEDV ratio and strain parameters such as global longitudinal (GLS), radial (GRS) and circumferential strain (GCS), SD of peak LS and CS using feature tracking. Presence of late gadolinium enhancement (LGE) was also determined. CMR parameters representing LV hypertrophy pattern or LV function were analyzed using a logistic regression to detect the best CMR parameters to predict HCM in athletes. To differentiate between HA and athletes with HCM optimal cut-off values for CMR parameters were calculated using receiver operating curve analysis. Comparing the three groups significant differences were found regarding conventional and derived CMR parameters and strain values. None of the HA showed LGE, 75% of athletic HCM and 82% of sedentary HCM patients showed LGE. The univariate regression model showed that LVEF, EDWT, EDWT/LVMi, LVM/LVEDV, GCS, GRS, SD of peak LS and CS are determinants of the diagnosis of HCM among athletes. Multivariate regression revealed that EDWT/LVMi and GCS are independent disease predictors in athletes (p&amp;lt;0.05). Cut-off value for GCS ≤−32.5 and for EDWT/LVEDVi &amp;gt;0.126 discriminate athletic HCM from HA with a sensitivity of 81.3 and 87.5% (AUC 0.93), and a specificity of 96.7 and 83.3% (AUC 0.95), respectively (Figure 1). CMR characteristics of sedentary and athletic HCM may differ, therefore establishing diagnostic parameters based on comparison between athletic HCM and HA is essential. CMR based strain and derived parameters may help to differentiate between physiological and pathological left ventricular hypertrophy in athletes. Figure 1 Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): National Research, Development and Innovation Office of Hungary (NKFIA) and National Research, Development and Innovation Office (NFKIH) of Hungary.

Left ventricular hypertrophy in athletes: How to differentiate between hypertensive heart disease and athlete's heart.

Athlete's heart is typically accompanied by a remodelling of the cardiac chambers induced by exercise. However, although competitive athletes are commonly considered healthy, they can be affected by cardiac disorders characterised by an increase in left ventricular mass and wall thickness, such as hypertension. Unfortunately, training-induced increase in left ventricular mass, wall thickness, and atrial and ventricular dilatation observed in competitive athletes may mimic the pathological remodelling of pathological hypertrophy. As a consequence, distinguishing between athlete's heart and hypertension can sometimes be challenging. The present review aimed to focus on the differential diagnosis between hypertensive heart disease and athlete's heart, providing clinical information useful to distinguish between physiological and pathological remodelling.

Left Ventricular Hypertrophy in Athletes: Differentiating Physiology From Pathology.

The changes that occur in athlete's heart are influenced by a number of factors including age, gender, ethnicity and the type of cardiovascular training. It is therefore important that the clinician is able to integrate all of these factors when assessing athletes to be able to guide investigations appropriately and to distinguish pathology from physiology. This review discusses the potential diagnostic conundrums when trying to differentiate physiological left ventricular hypertrophy from pathological hypertrophic cardiomyopathy in athletes. The mechanism of physiological and pathological hypertrophy is discussed together with history, clinical and investigational findings that can help to identify pathology. Athletes with hypertrophic cardiomyopathy are more likely to have non-concentric left ventricular hypertrophy (LVH), an elevated relative wall thickness, lateral ECG changes and a smaller LV cavity than athletes with physiological LVH. Certain diastolic echocardiographic parameters when used as part of an algorithm (e'; E/E'; E/A) can help to distinguish physiology from pathology, and there is evidence that assessment of global longitudinal strain during exercise echocardiography may be of use in the future. Cardiac MRI is an important imaging modality that can have an additive effect over echocardiography in the diagnosis of cardiomyopathy. Late gadolinium enhancement is a recognised advantage for cardiac magnetic resonance to allow detection of fibrosis in hypertrophic cardiomyopathy. T1 mapping and extracellular volume quantification may be a tool for the future to help distinguish athlete's heart from HCM. Cardiac adaptation to exercise and training in athletes, the athlete's heart causes electrophysiological and geometric changes that may mimic mild phenotypes of a pathological cardiomyopathy. This review article summarises a systematic approach to the assessment of left ventricular hypertrophy in athletes and describes pertinent clinical and investigation findings that can help to differentiate physiology from pathology.

Left ventricular hypertrophy in athletes and hypertensive patients.

Systemic hypertension and physical exercise are both associated with cardiac adaptations. The impact is most prominent on the left side of the heart, which hypertrophies leading to left ventricular hypertrophy. This article reviews structural and functional cardiac changes seen in hypertensive and athlete's hearts.

Comparison of Electrocardiographic Criteria for Identifying Left Ventricular Hypertrophy in Athletes from Different Sports Modalities

OBJECTIVES:In athletes, isolated electrocardiogram high voltage criteria are widely used to evaluate left ventricular hypertrophy, but positive findings are thought to represent normal electrocardiogram alterations. However, which electrocardiogram criterion can best detect left ventricular hypertrophy in athletes of various sport modalities remains unknown.METHODS:Five electrocardiogram criteria used to detect left ventricular hypertrophy were tested in 180 male athletes grouped according to their sport modality: 67% low-static and high-dynamic components and 33% high-static and high-dynamic components of exercise. The following echocardiogram parameters are the gold standard for diagnosing left ventricular hypertrophy: left ventricular mass index ≥134 g.m-2, relative wall thickness ≥0.42 mm, left ventricular diastolic diameter index ≥32 mm.m-2, septum wall thickness ≥13 mm, and posterior wall thickness ≥13 mm. Results for the various criteria were compared using the kappa coefficient. Significance was established at p<0.05.RESULTS:Fifty athletes (28%) presented with left ventricular hypertrophy according to electrocardiogram findings, with the following sensitivities and specificities, respectively: 38-53% and 79-83% (Perugia), 22-40% and 89-91% (Cornell), 24-29% and 90% (Romhilt-Estes), 68-87% and 20-23% (Sokolow-Lyon), and 0% and 99% (Gubner). The Perugia and Cornell criteria had higher negative predictive values for the low-static and high-dynamic subgroup. Kappa coefficients were higher for Romhilt-Estes, Cornell and Perugia criteria than for Sokolow-Lyon and Gubner criteria.CONCLUSION:All five evaluated criteria are inadequate for detecting left ventricular hypertrophy, but the Perugia, Cornell and Romhilt-Estes criteria are useful for excluding its presence. The Perugia and Cornell criteria were more effective at excluding left ventricular hypertrophy in athletes involved in a sport modality with low-static and high-dynamic component predominance.

Athletic Cardiac Adaptation in Males Is a Consequence of Elevated Myocyte Mass.

Background—Cardiac remodeling occurs in response to regular athletic training, and the degree of remodeling is associated with fitness. Understanding the myocardial structural changes in athlete’s heart is important to develop tools that differentiate athletic from cardiomyopathic change. We hypothesized that athletic left ventricular hypertrophy is a consequence of increased myocardial cellular rather than extracellular mass as measured by cardiovascular magnetic resonance.Methods and Results—Forty-five males (30 athletes and 15 sedentary age-matched healthy controls) underwent comprehensive cardiovascular magnetic resonance studies, including native and postcontrast T1 mapping for extracellular volume calculation. In addition, the 30 athletes performed a maximal exercise test to assess aerobic capacity and anaerobic threshold. Participants were grouped by athleticism: untrained, low performance, and high performance (O2max <60 or>60 mL/kg per min, respectively). In athletes, indexed cellular mass was greater in high- than low-performance athletes 60.7±7.5 versus 48.6±6.3 g/m2; P<0.001), whereas extracellular mass was constant (16.3±2.2 versus 15.3±2.2 g/m2; P=0.20). Indexed left ventricular end-diastolic volume and mass correlated with O2max (r=0.45, P=0.01; r=0.55, P=0.002) and differed significantly by group (P=0.01; P<0.001, respectively). Extracellular volume had an inverse correlation with O2max (r=−0.53, P=0.003 and left ventricular mass index (r=-0.44, P=0.02).Conclusions—Increasing left ventricular mass in athlete’s heart occurs because of an expansion of the cellular compartment while the extracellular volume becomes relatively smaller: a difference which becomes more marked as left ventricular mass increases. Athletic remodeling, both on a macroscopic and cellular level, is associated with the degree of an individual’s fitness. Cardiovascular magnetic resonance ECV quantification may have a future role in differentiating athlete’s heart from change secondary to cardiomyopathy.

Influence of Physical Activity on Hypertension and Cardiac Structure and Function.

The global burden of hypertension is rising and accounts for substantial morbidity and mortality. Lifestyle factors such as diet and physical inactivity contribute to this burden, further highlighting the need for prevention efforts to curb this public health epidemic. Regular physical activity is associated with lower blood pressure, reduced cardiovascular risk, and cardiac remodeling. While exercise and hypertension can both be associated with the development of left ventricular hypertrophy (LVH), the cardiac remodeling from hypertension is pathologic with an associated increase in myocyte hypertrophy, fibrosis, and risk of heart failure and mortality, whereas LVH in athletes is generally non-pathologic and lacks the fibrosis seen in hypertension. In hypertensive patients, physical activity has been associated with paradoxical regression or prevention of LVH, suggesting a mechanism by which exercise can benefit hypertensive patients. Further studies are needed to better understand the mechanisms underlying the benefits of physical activity in the hypertensive heart.

Differentiating Left Ventricular Hypertrophy in Athletes from That in Patients With Hypertrophic Cardiomyopathy

Identification of hypertrophic cardiomyopathy (HC) in young athletes is challenging when left ventricular (LV) wall thickness is between 13 and 15mm. The aim of this study was to revise the ability of simple echocardiographic and clinical variables for the differential diagnosis of HC versus athlete's heart. Twenty-eight athletes free of cardiovascular disease were compared with 25 untrained patients with HC, matched for LV wall thickness (13 to 15mm), age, and gender. Clinical, electrocardiographic, and echocardiographic variables were compared. Athletes had larger LV cavities (60 ± 3 vs 45 ± 5mm, p <0.001), aortic roots (34 ± 3 vs 30 ± 3 mm, p <0.001), and left atria (42 ± 4 vs 33 ± 5mm, p <0.001) than patients with HC. LV cavity <54mm distinguished HC from athlete's heart with the highest sensitivity and specificity (both 100%, p <0.001). Left atrium >40mm excluded HC with sensitivity of 92% and specificity of 71% (p <0.001). Athletes showed higher e' velocity by tissue Doppler imaging than patients with HC (12.5 ± 1.9 vs 9.3 ± 2.3cm/second, p <0.001), with values <11.5cm/second yielding sensitivity of 81% and specificity of 61% for the diagnosis of HC (p <0.001). Absence of diffuse T-wave inversion on electrocardiography (specificity 92%) and negative family history for HC (specificity 100%) also proved useful for excluding HC. In conclusion, in athletes with LV hypertrophy in the "gray zone" with HC, LV cavity size appears the most reliable criterion to help in diagnosis, with a cut-off value of <54mm useful for differentiation from athlete's heart. Other criteria, including LV diastolic dysfunction, absence of T-wave inversion on electrocardiography, and negative family history, further aid in the differential diagnosis.

Comparative study of ECG and echocardiographic parameters indicative of cardiac hypertrophy in athletes

The identification of left ventricular hypertrophy (LVH) through electrocardiographic voltage criteria has been widely studied in patients. However, their validity in “athlete’s heart” remains quite unknown. The aim of this study was to evaluate the most common electrocardiographic indices indicative of LVH compared to the known echocardiographic ones in athletes. The study group comprised 150 male adult competitive athletes (group A) and 50 sedentary participants (group B). Thirteen accepted electrocardiographic voltage criteria indicative of LVH were calculated and correlated with the common echocardiographic indices of left ventricular mass (LVM). Nine of the 13 ECG voltage criteria were significantly increased in athletes compared to controls. Statistically, the Sokolow–Lyon index, which is the most commonly used voltage index was found to be affected by the body mass index (10.7 %, p < 0.05), the group (7.3 %, p < 0.05) and systolic blood pressure (4.5 %, p < 0.05) in total variance of 16.6 % (p < 0.05). No electrocardiographic voltage criterion was significantly correlated with any echocardiographic index, except for the Cornell index that was correlated with end-diastolic volume index (r = 0.29, p < 0.05) and the Sokolow index (V6) with LVMI (r = 0.26, p < 0.05) in group A. We suggested that ECG voltage indices should not be considered valid when assessing LVH in athletes. Thus, the echocardiographic study is preferable in studying training-induced structural cardiac changes.

Efficacy of Various “Classic” Echocardiographic and Laboratory Indices in Distinguishing the “Gray Zone” between Athlete's Heart and Hypertrophic Cardiomyopathy: A Pilot Study

Left ventricular hypertrophy (LVH) with intraventricular septum thickness (IVST) between 1.2 and 1.5cm in athletes represents a "gray zone" between physiologic adaptation and mild hypertrophic cardiomyopathy (HCM). Various echo and laboratory parameters have been reported till now in the literature to discriminate the "gray zone" entities. Aim of this study was to assess the efficacy of these "classic" parameters in differentiating physiologic LVH in athletes from mild HCM in a highly selected population. Nine highly trained athletes with IVST (1.28±0.07cm), 9 patients with mild HCM (1.38±0.11cm), and 26 athletes without LVH (1.06±0.09cm; P<0.0005) underwent echocardiographic study, cardiopulmonary treadmill exercise stress test, and brain natriuretic peptide (BNP) measurement before and after exercise. Among all parameters tested, 7 were found to significantly differ between "gray zone" groups. After bootstrapping analysis, it was found that athletes with left ventricular end-diastolic diameter <4.74cm, mitral deceleration time >200ms, isovolumic relaxation time >94ms, tricuspid E/A<1.63, septum Em<9.5cm/sec, relative wall thickness >0.445, and a BNP value at rest >9.84pg/mL had a greater possibility for having underlying cardiomyopathy. A 10-point score based on these parameters showed accuracy (area under the curve=0.958 [95%CI: 0.738-1.0; P=0.00005, standard error=0.0342]) for revealing HCM in a gray zone athletic population. Differentiation of adaptive LVH versus HCM in a gray zone population could be facilitated by recognition of certain features referring to LV dimensions, diastolic function, and BNP.

Physiological versus pathological left ventricular remodeling in athletes

Intense and chronic athletic training is associated with left ventricular remodeling, including an increase in wall thickness, cavity size and mass. The extent of morphological cardiac changes depends on a variety of factors, namely body size, gender, type of sport, ethnicity and, likely, genetic factors. A subset of male athletes engaged in intense endurance sports, such as cycling and rowing, develops a more substantial increase in left ventricular dimensions that may overlap with the phenotypic expression of cardiomyopathies. A common clinical challenge in sports cardiology is the differential diagnosis between physiological left ventricular hypertrophy (i.e., "athlete's heart") and hypertrophic cardiomyopathy, which is one of the most common causes of sudden cardiac death in young athletes. This review describes the physiological determinants, characteristics and upper limits of left ventricular hypertrophy in athletes, and analyzes the criteria that can be useful in the differential diagnosis between "athlete's heart" and hypertrophic cardiomyopathy.

Speckle tracking: distinction of physiologic from pathologic LVH?

Speckle tracking: distinction of physiologic from pathologic LVH?

Left ventricular mass assessment by CMR; how to define the optimal index

Cardiac magnetic resonance imaging (CMR) is an accurate and reliable means of evaluating cardiac morphology, and therefore very well suited for identifying and characterizing patients with various manifestations of left ventricular hypertrophy (LVH) [1, 2]. For instance, CMR can resolve the question whether training-induced LVH in athletes is a physiological rather than a pathophysiological phenomenon [3–5]. A meta-analysis, involving 59 studies and 1451 athletes (both endurance-trained and strength-trained athletes), showed that the athlete’s heart demonstrated normal systolic and diastolic cardiac function, implying that training-induced LVH in athletes is predominantly a physiological phenomenon [6–10]. However, in pathophysiological LVH, such as in patients with hypertension and hypertrophic cardiomyopathy, the presence of LVH portends a poor prognosis whereby there is a negative relation between prognosis and the stage of LVH [11–21]. On the other side of the spectrum, a significant decrease in LV mass, such as in patients following myocardial infarction, may also be associated with a poor prognosis as these patients are prone to the development of heart failure [22–39]. Within the latest 10 years, research in LVH as cardiac target organ damage has uncovered its prognostic importance. Several studies have indicated that adequate pharmacological treatment, such as beta-blocking agents, ACE-inhibition, and angiotensin II receptor blockade, is very effective in reducing LVH [40–47]. In addition, reduction of LV mass is associated with substantial and significant reduction of cardiovascular morbidity and mortality [46]. Hypertension is strongly associated with increased risk of subsequent heart failure, and meta-analysis data have suggested that reduction in blood pressure and LV mass is associated with very substantial reductions in incident heart failure [47, 48]. Consequently, LV mass should be accurately calculated as mass size may have important clinical implications [49–53]. Generally, LV mass divided by body surface area (BSA) has been used clinically to account for body size, but its validity is not fully clear. Methods to index LV mass for body size have not been investigated using CMR. In the current issue of the International Journal of Cardiovascular Imaging, Brumback et al. [54] sought for new accurate indices of LV mass. The main purpose of the study was to develop allometric indices for LV mass measured by CMR and to compare estimates of the prevalence and predictive value of LVH defined new allometric indices. Two indices were derived from linear regression models fit to CMR data from the reference sample of the Multi-Ethnic Study of Atherosclerosis (MESA) participants. The indices are called allometric as they are proportional to LV mass divided by a body size variable raised to a scalar exponent. The authors evaluated 5,004 participants from the MESA trial with CMR measurements of LV mass without signs of clinical cardiovascular disease at baseline who were followed for a median of 4.1 years. The new indices and limits for hypertrophy (95th percentile) were finally derived from 822 normal-weight, normotensive, non-diabetic subjects. There were 107 events consisting of coronary heart disease or stroke. The estimated prevalence of LVH at baseline and hazard ratio for events associated with LVH were 8% and 2.4 with the new allometric height-weight index, 11% and 2.2 with LV mass/BSA, 23–24% and 2.0–2.1 with height indices, and 20% and 1.7 with un-indexed LV mass. A statistically significant difference was detected between the hazard ratios based on the new height-weight index and un-indexed LV mass. It was concluded that the prevalence of hypertrophy is higher for indices that do not account for weight. The predictive value of hypertrophy was significantly better with the new allometric height-weight index than with un-indexed LV mass and may be better than indices without weight. The current study is clinically important since an evaluation of the most suitable indices for LV mass has not previously been performed using CMR. An indexed LV mass should be more predictive of a cardiovascular event than un-indexed LV mass. Therefore, the authors should be complimented for developing new allometric indices for CMR-derived LV mass with potential major implications in clinical practice.

Evaluation of Left Atrial Function in Physiological and Pathological Left Ventricular Myocardial Hypertrophy by Real‐time Tri‐plane Strain Rate Imaging

We investigated the difference between left ventricular (LV) hypertrophy caused by primary hypertension and physiological LV hypertrophy in athletes as seen in left atrial (LA) function by real-time tri-plane strain rate imaging. A real-time tri-plane imaging technique using the same phase of the same cardiac circle was used to synchronously demonstrate the section of apical 4-chamber, 2-chamber, and apical left ventricle long axis. We measured standard Doppler echocardiographic quantitative analysis and the strain rate peak values of each LA wall in the systolic phase, in the early stage of diastole, and in the advanced stage of diastole and made a comparison of these values. The alteration of configuration and function of the left atrium in hypertensive patients is an early sign of the myocardial damage caused by hypertension. Strain rate imaging could sensitively reflect LA function changes in the early stages of hypertension. While physiological, myocardial hypertrophy is a benign reaction, LA function is significantly different from that of hypertension. Real-time tri-plane strain rate imaging techniques could simultaneously analyze 3 sections, which shortens scanning time and depletes the influence of variations of different cardiac cycles on quantitative analysis of local myocardial segments of the left atrium. This would improve the comparability of myocardial movement of different segments so that we could more comprehensively and accurately evaluate the systolic and diastolic function of the left atrium in primary hypertension and physiological LV hypertrophy in athletes.

Systolic and early diastolic left ventricular velocities assessed by tissue Doppler imaging in 100 top-level handball players

Echocardiographic tissue Doppler imaging (TDI) has been proposed for the differentiation of physiologic left ventricular hypertrophy and pathologic left ventricular hypertrophy in athletes. In addition, cutoff values for systolic (S'<9 cm/s) and early diastolic (E'<9 cm/s) myocardial velocities had been defined. The aim of our study was the analysis of the morphologic cardiac changes by standard echocardiography, and the myocardial velocities S' and E' by TDI in top-level handball players with respect to the predefined cutoff values. Pulsed-wave TDI of the systolic and early diastolic velocities was performed at the lateral and septal mitral annulus (MA) in the four-chamber view in 100 athletes (100 Caucasian men; professional handball players of the first German handball league and the German national team; mean age 25.8+/-4.8 years). Global and regional left ventricular systolic function was normal in all athletes. They showed an eccentric hypertrophy of the left ventricle (LV), which was characterized by an increased mass of the LV (287.3+/-58.4 g), and an increased end diastolic diameter of the LV (LVEDD: 58+/-5.9 mm), but no echomorphologic signs of pathologic hypertrophy or hypertrophic cardiomyopathy. TDI showed a systolic velocity S' of the MA of 9.3+/-1.5 cm/s at the septal and 10.5+/-2.1 at the lateral MA. Ten of the 100 athletes showed a S'<9 cm/s at both sides of the MA. TDI showed an early diastolic velocity E' of the MA of 13.2+/-2.8 cm/s at the septal and of 16.6+/-3.4 cm/s at the lateral MA. None of the 100 athletes showed reduced systolic or early diastolic velocities below the proposed cutoff values (S' and E'<9 cm/s) at any sides of the MA. Our study provides further insights into systolic and diastolic function as assessed by TDI in top-level handball players. Owing to the large cohort of individuals, our findings might be helpful as reference values for the echocardiographic assessment of handball players, who are performing a moderate static and high dynamic sport.

Prevalence Of LVH In Athletes Classified By Race And Gender

Evidence-based data support the role of the resting 12-lead electrocardiogram (ECG) in the pre-participation screening of young athletes, and is endorsed by the European Society of Cardiology (ESC) & International Olympic Committee (IOC) guidelines. Hypertrophic cardiomyopathy (HCM), is commonly associated with sudden cardiac arrest in young athletes. Unfortunately, it is usually not detected by history or physical examination. However, the ECG in HCM will often manifest left ventricular hypertrophy (LVH). Complicating this, physiological hypertrophy ("athletes heart“) frequently manifests LVH on the ECG, as well. PURPOSE: To document prevalence of LVH by 12-lead ECG in collegiate athletes and look for differences based on race and gender. METHODS: We studied ECGs from a group of 365 US collegiate athletes presenting for pre-participation screening. All ECGs were evaluated and classified as either normal or abnormal according to the criteria established in the ESC guidelines. An ECG was classified as having LVH if it met one of the following three criteria. 1) S-wave in V1 or V2 ≥ 3 mV 2) R-wave in lead V5 or V6 ≥ 3 mV 3) R-wave or S-wave in lead I, II, III, aVR, aVL, or aVF ≥ 2 mV. RESULTS: Among 365 subjects studied, 239 (65%) were male and 126 (35%) were female. Sixty nine percent (n=252) were Caucasian, 22% (n=79) were African-American and 5% (17) were Asian. Twenty-seven percent (n=99) of athletes demonstrated LVH on ECG; 74 (31%) were male and 25 (20%) were female (95% Confidence Interval, 2 to 20; p<0.02). LVH was present in 30% (n=77) of Caucasians, 19% (n=15) of African-Americans, and 23% (n=4) of Asian athletes (95% CI, 1 to 21; p<0.04). CONCLUSIONS: Among athletes studied with 12-lead resting ECG, approximately 27% demonstrated LVH. LVH Prevalence was highest in Caucasians (30%), followed by African-American (19%) (95% CI, 1 to 21; p<0.04). Male athletes had higher prevalence of LVH compared to female athletes (31% v/s 20%; 95% CI, 2 to 20; p<0.02). Our study suggests that prevalence of LVH may be affected by race and gender.

Left ventricular hypertrophy in athletes

Participation in regular intensive exercise is associated with a modest increase in left ventricular wall thickness (LVWT) and cavity size. The magnitude of these physiological changes is predominantly determined by a variety of demographic factors which include age, gender, size, ethnicity, and sporting discipline. A small minority of male athletes participating in sporting disciplines involving intensive isotonic and isometric exercise may exhibit substantial increases in cardiac size that overlap with the phenotypic manifestation of the cardiomyopathies. The most challenging clinical dilemma incorporates the differentiation between physiological left ventricular hypertrophy (LVH) (athlete's heart) and hypertrophic cardiomyopathy (HCM), which is recognized as the commonest cause of non-traumatic exercise related sudden cardiac death in young (<35 years old) athletes. This review aims to highlight the distribution and physiological upper limits of LVWT in athletes, determinants of LVH in athletes, and echocardiographic methods of differentiating athlete's heart from HCM.

Hypertension control is needed in elderly marathon runners!

The performance of sporting activities like cycling and running is a life style factor that improves health and increases the duration of healthy life [1, 2]. Heavy exercise, such as rowing, cycling, and marathon running at competitive levels, is considered to be healthy, although evidence of the opposite is published from time to time [3, 4]. It is known for quite some time that the hearts of extensive sport athletes develop left ventricular hypertrophy (LVH), known under the name of the ‘‘athlete’s heart’’. This type of LVH is considered physiological [5–10]. Conditions like hypertensive heart disease lead to pathological LVH [11–15], as it is often associated with perivascular and interstitial fibrosis of left ventricular myocardium [16], diastolic heart failure [17, 18], arrhythmias [19, 20] and mortality [21]. Previous studies from our institution have already addressed the issue of physiological versus pathological LVH [5, 22, 23]. First of all we studied the accuracy of M-mode echocardiography and two different twodimensional echocardiographic approaches in the assessment of left ventricular mass and volumes in endurance-trained and strength-trained athletes, using cardiovascular magnetic resonance (CMR) imaging as reference standard [23]. It was shown that in general practice the two-dimensional echocardiographic approach was the most accurate estimator of left ventricular mass and volumes in both controls and athletes. For research purposes, however, CMR remains the most accurate and reliable method to assess cardiac anatomy and function [24–27]. In a next study we addressed the question of whether training-induced left ventricular hypertrophy in athletes is a physiological rather than a pathophysiological phenomenon [28]. To that purpose we studied 21 elite cyclists and 12 healthy control subjects. Left ventricular mass, volume, and function were determined by CMR and myocardial high-energy phosphates were examined by 31P magnetic resonance spectroscopy. It was shown that LVH in cyclists was not associated with significant abnormalities of cardiac function or metabolism as assessed by CMR and spectroscopy. These observations suggested that training-induced left ventricular hypertrophy in cyclists is predominantly a physiological phenomenon. Finally in a meta-analysis paper, involving 59 studies and 1,451 athletes, i.e., endurance-trained athletes (long-distance runners), strength-trained athletes (weight lifters, power lifters, bodybuilders, wrestlers, and throwers), and athletes involved in combined forms of dynamic and static training (cyclists and rowers), we confirmed the hypothesis of divergent cardiac adaptations in dynamic and static sports [5]. Overall, the athlete’s heart demonstrated normal systolic and diastolic cardiac functions. However, our meta-analysis concerned relatively young athletes between 18 and 40 years. A. van der Laarse E. E. van der Wall (&) Department of Cardiology, Leiden University Medical Center, P.O. Box 9600, Leiden, The Netherlands e-mail: e.e.van_der_wall@lumc.nl

Athlete's heart or hypertrophic cardiomyopathy: Usefulness of N-Terminal pro-Brain Natriuretic Peptide

Background Distinguishing physiological hypertrophy from hypertrophic cardiomyopathy in athletes remains difficult, but vital in view of the risk of sudden death under effort. NT-proBNP was previously reported to be usually normal in healthy athletes, but often elevated in case of hypertrophic cardiomyopathy. Objectives o assess the interest of NT-proBNP in differential diagnosis of left ventricular hypertrophy in athletes. Methods NT-proBNP levels were measured at rest and after effort in trained athletes referred for suspectedly abnormal (≥ 13 mm) left ventricular hypertrophy. Results 17 patients were included, 10 of whom were diagnosed with hypertrophic cardiomyopathy (group I) while the other 7 presented typical signs of athlete’s heart (group II). NT-proBNP levels did not significantly differ between groups, whether at rest or after effort. NT-proBNP levels were, however, significantly elevated in 3 subjects in group I, while being consistently normal in group II. Conclusions In active athletes presenting with ambiguous left ventricular hypertrophy, abnormal NT-proBNP levels indicate hypertrophic cardiomyopathy, whereas normal values are inconclusive.