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A prática regular de esportes pode induzir adaptações no coração, sendo essa condição comumente chamada de "coração de atleta". As alterações observadas incluem dilatação das câmaras cardíacas, aumento da espessura miocárdica, melhora do enchimento ventricular, aumento da trabeculação do ventrículo esquerdo (VE), dilatação da veia cava inferior, entre outras. Essas alterações também podem ser observadas em algumas doenças cardíacas, como cardiomiopatia (CMP) dilatada, hipertrófica e outras. Dessa forma, os exames de imagem cardíaca são fundamentais na identificação dessas alterações e na diferenciação entre o "coração de atleta" e uma possível cardiopatia.(AU)

Exercise-induced adaptation may occur in amateur and professional athletes. This condition is commonly named "athlete's heart". The alterations observed include dilation of the heart chambers, increased myocardial thickness, improved ventricular filling, increased left ventricular trabeculation, dilation of the inferior vena cava, among others. These changes can also be observed in some heart diseases, such as dilated, hypertrophic and other cardiomyopathies (CMP). Thus, cardiac imaging tests are fundamental in identifying these alterations and in differentiating between "athlete's heart" and possible heart disease. (AU)

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A ultrassonografia é um dos principais métodos de diagnóstico gestacional, no qual se realiza: biometria, monitoramento de batimentos e organogênese, detecção de anormalidades e avaliação da circulação sanguínea materno-fetal. Nesse quesito, o diagnóstico ultrassonográfico intrauterino de anormalidades fetais vem adquirindo espaço com o desenvolvimento de equipamentos mais avançados, tendo potencial para se tornar uma ferramenta de triagem para tal. Baseado na escassez observada nesse aspecto, visa-se relatar o diagnóstico ultrassonográfico intrauterino de uma alteração fetal em uma felina gestante. Foi atendida uma felina da raça persa, 3 anos, com histórico de monta natural há 40 dias. Na ultrassonografia visibilizou-se quatro fetos vivos com aproximadamente 38 dias. Uma segunda avaliação ultrassonográfica ocorreu após 12 dias, notando-se um feto com cardiomegalia, oscilação da frequência cardíaca e sofrimento fetal, enquanto os demais fetos apresentavam-se dentro da normalidade. O terceiro exame foi feito após quatro dias, visibilizando ausência de batimento cardíaco e presença de líquido em espaço pleural no feto em questão, confirmando o óbito. O parto natural ocorreu após uma semana, com nascimento de três filhotes vivos e um natimorto. Ao exame necroscópico do natimorto, confirmou-se cardiomegalia generalizada. Conclui-se que a ultrassonografia é um método padrão-ouro para diagnóstico de anormalidades fetais, permitindo planejar o parto e interceder de maneira precoce conforme a situação. Assim, esse trabalho enriquece a literatura com maiores informações relacionadas a malformações fetais observadas antes do parto, contribuindo assim com as condutas obstétricas em pequenos animais.(AU)

Ultrasonography is one of the main methods of gestational diagnosis, in which it performs: biometry, monitoring of beats and organogenesis, detection of abnormalities and evaluation of maternal-fetal blood circulation. In this regard, intrauterine sonographic diagnosis of fetal abnormalities has been gaining space with the development of more advanced equipment, and has the potential to become a screening tool for this purpose. Based on the scarcity observed in this aspect, this study aimsto report the intrauterine ultrasound diagnosis of a fetal abnormality in a pregnant feline. The patient was a 3-year-old Persian female with a history of natural mounting for 40 days. At ultrasonography, four live fetuses were visualized at approximately38 days of age. Asecond ultrasonographic evaluation was performed after 12 days, and one fetus with cardiomegaly, heart rate oscillation and fetal distress was observed, while the other fetuses were within normal limits. The third scan was performed after four days, showing absence of heartbeat and presence of fluid in the pleural space in the fetus in question, confirming the death. Natural delivery occurred after one week, with the birth of three live pups and one stillborn. At necroscopic examination of the stillborn, generalized cardiomegaly was confirmed. We conclude that ultrasonography is a gold standard method for diagnosing fetal abnormalities, allowing birth planning and early intervention according to the situation. Thus, this study enriches theliterature with more information related to fetal malformations observed before delivery, thus contributing to obstetric management in small animals.(AU)

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Physical training stimulates the development of physiologic cardiac hypertrophy (CH), being a key event in this process the inhibition of the Na+/H+ exchanger. However, the role of the sodium bicarbonate cotransporter (NBC) has not been explored yet under this circumstance. C57/Bl6 mice were allowed to voluntary exercise (wheel running) for five weeks. Cardiac mass was evaluated by echocardiography and histomorphometry detecting that training promoted the development of physiological CH (heart weight/tibia length ratio, mg/mm: 6.54 ± 0.20 vs 8.81 ± 0.24; interstitial collagen content, %: 3.14 ± 0.63 vs. 1.57 ± 0.27; and cross-sectional area of cardiomyocytes, µm2: 200.6 ± 8.92 vs. 281.9 ± 24.05; sedentary (Sed) and exercised (Ex) mice, respectively). The activity of the electrogenic isoform of the cardiac NBC (NBCe1) was estimated by recording intracellular pH under high potassium concentration and by measuring action potential duration (APD). NBCe1 activity was significantly increased in isolated cardiomyocytes of trained mice. Additionally, the APD was shorter and the alkalization due to high extracellular potassium-induced depolarization was greater in this group, indicating that the NBCe1 was hyperactive. These results are online with the observed myocardial up-regulation of the NBCe1 (Western Blot, %: 100 ± 13.86 vs. 202 ± 29.98; Sed vs. Ex, n = 6 each group). In addition, we detected a reduction in H2O2 production in the myocardium of trained mice. These results support that voluntary training induces the development of physiologic CH with up-regulation of the cardiac NBCe1 in mice. Furthermore, the improvement in the antioxidant capacity contributes to the beneficial cardiovascular consequences of physical training.

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Reactive cardiac hypertrophy (CH) is an increase in heart mass in response to hemodynamic overload. Exercise-induced CH emerges as an adaptive response with improved cardiac function, in contrast to pathological CH that represents a risk factor for cardiovascular health. The Na+/H+ exchanger (NHE-1) is a membrane transporter that not only regulates intracellular pH but also intracellular Na+ concentration. In the scenario of cardiovascular diseases, myocardial NHE-1 is activated by a variety of stimuli, such as neurohumoral factors and mechanical stress, leading to intracellular Na+ overload and activation of prohypertrophic cascades. NHE-1 hyperactivity is intimately linked to heart diseases, including ischemia-reperfusion injury, maladaptive CH and heart failure. In this review, we will present evidence to support that the NHE-1 hyperactivity constitutes a "switch on/off" for the pathological phenotype during CH development. We will also discuss some classical and novel strategies to avoid NHE-1 hyperactivity, and that are therefore worthwhile to improve cardiovascular health.

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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.

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ABSTRACT 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.

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BACKGROUND: The aim of this study was to determine if cardiac hypertrophy differs between professional female and male soccer players. METHODS: Twenty-two female and 20 male professional soccer players, and their respective non-athlete controls (22 females and 19 males) were submitted to an echocardiogram. RESULTS: Females had a shorter left ventricular intracavitary diameter and wall thicknesses than males in both groups. However, these differences disappeared when cardiac dimensions were expressed relative to body mass area (P>0.05). Compared to their respective controls, female and male soccer players had a longer (P<0.05) left ventricular end-systolic diameter (female: 1.87±0.16 vs. 1.77±0.15 cm/m2 and male: 1.83±0.21 vs. 1.73±0.16 cm/m2), left ventricular end-diastolic diameter (female: 2.86±0.25 vs. 2.74±0.22 cm/m2 and male: 2.81±0.26 vs. 2.55±0.66 cm/m2), left ventricular posterior wall thickness (female: 0.44±0.06 vs. 0.39±0.04 cm/m2 and male: 0.43±0.04 vs. 0.39±0.10 cm/m2), left ventricular septal wall thickness (female: 0.47±0.06 vs. 0.41±0.04 cm/m2 and male: 0.45±0.04 vs. 0.40±0.11 cm/m2), and left ventricular mass index (female: 91.8±22.1 vs. 72.3±10.5 g/m2 and male: 121.7±20.3 vs. 99.8±13.8 g/m2 ). CONCLUSIONS: Part of the gender differences in cardiac dimensions might be attributed to differences in body dimension. Soccer training increases cardiac dimensions even with BSA correction and females seem to have similar left ventricle remodeling compared to males.

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BACKGROUND: Cardiac hypertrophy is a component of cardiac remodeling occurring in response to an increase of the activity or functional overload of the heart. OBJECTIVE: Assess hypertrophic response of the association of thyroid hormone and exercise in the rat heart. METHODS: We used 37 Wistar rats, male, adults were randomly divided into four groups: control, hormone (TH), exercise (E), thyroid hormone and exercise (H+E); the group received daily hormone levothyroxine sodium by gavage at a dose of 20 µg thyroid hormone/100g body weight, the exercise group took swimming five times a week, with additional weight corresponding to 20% of body weight for six weeks; in group H+E were applied simultaneously TH treatment groups and E. The statistics used was analysis of variance, where appropriate, by Tukey test and Pearson correlation test. RESULTS: The T4 was greater in groups TH and H+E. The total weight of the heart was greater in patients who received thyroid hormone and left ventricular weight was greater in the TH group. The transverse diameter of cardiomyocytes increased in groups TH, E and H+E. The percentage of collagen was greater in groups E and H+E Correlation analysis between variables showed distinct responses. CONCLUSION: The association of thyroid hormone with high-intensity exercise produced cardiac hypertrophy, and generated a standard hypertrophy not directly correlated to the degree of fibrosis.

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Fundamento: A hipertrofia cardíaca constitui um dos componentes do remodelamento cardíaco e ocorre em resposta a aumento da atividade ou da sobrecarga funcional do coração. Objetivo: Avaliar a resposta hipertrófica da associação do hormônio tireoidiano e do exercício físico no coração de ratos. Método: Foram utilizados 37 ratos da linhagem Wistar, machos, adultos, distribuídos aleatoriamente em quatro grupos: controle, hormônio (HT), exercício (E), hormônio tireoidiano e exercício (H + E). O grupo hormônio recebeu diariamente levotiroxina sódica por gavagem, na dose de 20 μg de hormônio tireoidiano/100 g de peso corporal; o grupo exercício realizou natação cinco vezes por semana, com peso adicional correspondente a 20% do peso corporal, durante seis semanas; no grupo H + E foram aplicados simultaneamente os tratamentos dos grupos HT e E. A estatísica utilizada foi a análise de variância complementada, quando necessário, pelo teste de Tukey e o teste de correlação de Pearson. Resultados: O T4 foi mais elevado nos grupos HT e H + E. O peso total do coração foi maior nos grupos que receberam hormônio tireoidiano, e o peso ventricular esquerdo foi maior no grupo HT. O diâmetro transversal dos cardiomiócitos aumentou nos grupos HT, E e H + E. A porcentagem de colágeno foi maior nos grupos E e H + E. A análise da correlação entre as variáveis apresentou distintas respostas. Conclusão: A associação do hormônio tireoidiano com exercício físico de elevada intensidade produziu hipertrofia cardíaca e gerou um padrão hipertrófico não correlacionado diretamente ao grau de fibrose. .

Background: Cardiac hypertrophy is a component of cardiac remodeling occurring in response to an increase of the activity or functional overload of the heart. Objective: Assess hypertrophic response of the association of thyroid hormone and exercise in the rat heart. Methods: We used 37 Wistar rats, male, adults were randomly divided into four groups: control, hormone (TH), exercise (E), thyroid hormone and exercise (H + E); the group received daily hormone levothyroxine sodium by gavage at a dose of 20 μg thyroid hormone/100g body weight, the exercise group took swimming five times a week, with additional weight corresponding to 20% of body weight for six weeks; in group H + E were applied simultaneously TH treatment groups and E. The statistics used was analysis of variance, where appropriate, by Tukey test and Pearson correlation test. Results: The T4 was greater in groups TH and H + E. The total weight of the heart was greater in patients who received thyroid hormone and left ventricular weight was greater in the TH group. The transverse diameter of cardiomyocytes increased in groups TH, E and H + E. The percentage of collagen was greater in groups E and H + E Correlation analysis between variables showed distinct responses. Conclusion: The association of thyroid hormone with high-intensity exercise produced cardiac hypertrophy, and generated a standard hypertrophy not directly correlated to the degree of fibrosis. .

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Among the molecular, biochemical and cellular processes that orchestrate the development of the different phenotypes of cardiac hypertrophy in response to physiological stimuli or pathological insults, the specific contribution of exercise training has recently become appreciated. Physiological cardiac hypertrophy involves complex cardiac remodeling that occurs as an adaptive response to static or dynamic chronic exercise, but the stimuli and molecular mechanisms underlying transduction of the hemodynamic overload into myocardial growth are poorly understood. This review summarizes the physiological stimuli that induce concentric and eccentric physiological hypertrophy, and discusses the molecular mechanisms, sarcomeric organization, and signaling pathway involved, also showing that the cardiac markers of pathological hypertrophy (atrial natriuretic factor, ß-myosin heavy chain and α-skeletal actin) are not increased. There is no fibrosis and no cardiac dysfunction in eccentric or concentric hypertrophy induced by exercise training. Therefore, the renin-angiotensin system has been implicated as one of the regulatory mechanisms for the control of cardiac function and structure. Here, we show that the angiotensin II type 1 (AT1) receptor is locally activated in pathological and physiological cardiac hypertrophy, although with exercise training it can be stimulated independently of the involvement of angiotensin II. Recently, microRNAs (miRs) have been investigated as a possible therapeutic approach since they regulate the translation of the target mRNAs involved in cardiac hypertrophy; however, miRs in relation to physiological hypertrophy have not been extensively investigated. We summarize here profiling studies that have examined miRs in pathological and physiological cardiac hypertrophy. An understanding of physiological cardiac remodeling may provide a strategy to improve ventricular function in cardiac dysfunction.

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Among the molecular, biochemical and cellular processes that orchestrate the development of the different phenotypes of cardiac hypertrophy in response to physiological stimuli or pathological insults, the specific contribution of exercise training has recently become appreciated. Physiological cardiac hypertrophy involves complex cardiac remodeling that occurs as an adaptive response to static or dynamic chronic exercise, but the stimuli and molecular mechanisms underlying transduction of the hemodynamic overload into myocardial growth are poorly understood. This review summarizes the physiological stimuli that induce concentric and eccentric physiological hypertrophy, and discusses the molecular mechanisms, sarcomeric organization, and signaling pathway involved, also showing that the cardiac markers of pathological hypertrophy (atrial natriuretic factor, β-myosin heavy chain and α-skeletal actin) are not increased. There is no fibrosis and no cardiac dysfunction in eccentric or concentric hypertrophy induced by exercise training. Therefore, the renin-angiotensin system has been implicated as one of the regulatory mechanisms for the control of cardiac function and structure. Here, we show that the angiotensin II type 1 (AT1) receptor is locally activated in pathological and physiological cardiac hypertrophy, although with exercise training it can be stimulated independently of the involvement of angiotensin II. Recently, microRNAs (miRs) have been investigated as a possible therapeutic approach since they regulate the translation of the target mRNAs involved in cardiac hypertrophy; however, miRs in relation to physiological hypertrophy have not been extensively investigated. We summarize here profiling studies that have examined miRs in pathological and physiological cardiac hypertrophy. An understanding of physiological cardiac remodeling may provide a strategy to improve ventricular function in cardiac dysfunction.

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