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AIMS: HIIT (high-intensity interval training) has the potential to reduce cardiometabolic risk factors, but the effects on cardiac remodeling and local RAS (renin-angiotensin system) in mice fed high-fat or high-fructose diets still need to be fully addressed. MAIN METHODS: Sixty male C57BL/6 mice (12weeks old) were randomly divided into three groups, control (C), High-fat (HF), or High-fructose diet (HRU) and were monitored for eight weeks before being submitted to the HIIT. Each group was randomly assigned to 2 subgroups, one subgroup was started on a 12-week HIIT protocol (T=trained group), while the other subgroup remained non-exercised (NT=not-trained group). KEY FINDINGS: HIIT reduced BM and systolic blood pressure in high-fat groups, while enhanced insulin sensitivity after high-fat or high-fructose intake. Moreover, HIIT reduced left ventricular hypertrophy in HF-T and HFRU-T. Notably, HIIT modulated key factors in the local left ventricular renin-angiotensin-system (RAS): reduced protein expression of renin, ACE (Angiotensin-converting enzyme), and (Angiotensin type 2 receptor) AT2R in HF-T and HFRU-T groups but reduced (Angiotensin type 1 receptor) AT1R protein expression only in the high-fat trained group. HIIT modulated ACE2/Ang (1-7)/Mas receptor axis. ACE2 mRNA gene expression was enhanced in HF-T and HFRU-T groups, complying with elevated Mas (Mas proto-oncogene, G protein-coupled receptor) receptor mRNA gene expression after HIIT. SIGNIFICANCE: This study shows the effectiveness of HIIT sessions in producing improvements in insulin sensitivity and mitigating LV hypertrophy, though hypertension was controlled only in the high-fat-fed submitted to HIIT protocol. Local RAS system in the heart mediates these findings and receptor MAS seems to play a pivotal role when it comes to the amelioration of cardiac structural and functional remodeling due to HIIT.

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We report the case of a rare cardiac presentation of Fabry disease. Although concentric left ventricular hypertrophy is a major cardiac finding in Fabry disease, there is no case report of dynamic obstruction at mid-left ventricular level. We describe a 59-year-old-woman suffering from a severe form of Fabry disease, mimicking an apical hypertrophic cardiomyopathy with mid-ventricular obstruction. Differentiation of Fabry disease from hypertrophic cardiomyopathy is crucial given the therapeutic and prognostic differences. Fabry disease should always be suspected in an adult, independently of the pattern of left ventricular hypertrophy.

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El diseño experimental de los estudios prospectivos sobre el tratamiento de la hipertensión arterial esencial, ha ignorado un aspecto fundamental de la fisiopatología del paciente hipertenso: Los pacientes hipertensos no son homogéneos, en lo que respecta a los mecanismos responsables del aumento de la presión arterial. La adptación cardiovascular a la hipertensión arterial es anatómica y funcionalmente heterogénea. Investigaciones clínicas recientes indican que, esta heterogeneidad, puede ser minimizada con el uso de la eco-cardiografía. El análisis de los perfiles hemodinámicos y neurohormonales de los pacientes hipertensos permite distinguir la presencia de denominadores comunes: La hipertrofia ventricular concéntrica y la hipertrofia ventricular excéntrica representan los extremos opuestos de adaptación del corazón a la hipertensión arterial. El primero se caracteriza por tener una forma geométrica elíptica, con un perfil hemodinámico de gasto cardíaco normal y resistencias vasculares periféricas elevadas. Los niveles plasmáticos de renina y de los péptidos natriuréticos están elevados.

The experimental design of clinical studies, on the pharmacological treatment of essencial hypertension, has ignored a fundamental issue: Hypertensive patiens are not a homogenous population. The adaptation of the cardiovascular system to hypertension is structurally and funtionally heterogeneous. Recent clinical investigations suggest that this heterogeneity can be minimized by echocardiography. Thus, when the hemodynamic and neurohormonal profiles of untreated hypertensive patients are considered, in the particular context of the cardiac morphologic adaptation to high blood pressure, distinct common denominator emerge. Concentric Hypertrophy is characterized by an elliptic left ventricle, normal stroke volume and high peripheral vascular resistance. Its predominant neurohormonal profile includes elevated plasma renin and natriuretic peptide levels. Conversely, most patients with eccentric hypertrophy have a spheric left ventricle, increased stroke volume and low peripheral vascular resistance. Its corresponding neurohormonal profile shows low serum renin and anhanced sympathetic nervous activity. The therapeutic response, to angiotensin II antagonists and to beta-adrenergic blockers, of these two geometric patterns is also different. Concentric hypertrophy is substantially reversed by angiotensin II blockers, where as, eccentric hypertrophy is refractory to both, angiotensin II blockerds and atenol. These facts raise a relevant question: Should ventricular geometry be considered when deciding which antihypertensive drug is to be prescribed?.

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Abuse of anabolic-androgenic steroids (AAS) for improving physical performance is associated with serious, sometimes fatal, adverse effects. The aim of the present work was to investigate the effects of AAS on the cardiac structure and the plasma lipoprotein profile isolated and in combination with exercise. Transgenic mice with a human lipaemic phenotype (expressing cholesteryl ester transfer protein on the LDL receptor knockout background) were used in this study. Sedentary and exercised mice (treadmill running, five times per week for 6 weeks) were treated with mesterolone (2 microg/g body weight) or vehicle (control-C) in the last 3 weeks. Four groups were compared: (i) exercise + mesterolone (Ex-M), (ii) exercise + vehicle (Ex-C), (iii) sedentary + mesterolone (Sed-M) and (iv) sedentary + vehicle (Sed-C). Arterial blood pressure and body mass increased in all groups along time, but Sed-M reached the highest values and Ex-C the lowest. Treatment with mesterolone increased total cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL-c) and very LDL-c (VLDL-c) plasma levels. However, exercise blunted some of these deleterious effects by increasing high-density lipoprotein cholesterol and decreasing LDL-c, VLDL-c and triglycerides. Exercise training induced beneficial effects, such as physiological cardiomyocyte hypertrophy, increase in myocardial circulation and decrease in cardiac interstitium. However, mesterolone impaired such physiological gains and in addition increased troponin T plasma levels both in sedentary and exercised mice. Thus, while mesterolone induced pro-atherogenic lipoprotein profile and pathogenic cardiac hypertrophy, exercise counteracted these effects and modified favourably both the lipoprotein profile and the cardiac remodelling induced by mesterolone.

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Objetivo: Evaluar la eficacia y la tolerancia, así como su acción sobre la regresión de la hipertrofia ventricular izquierda, de la combinación de benazepril más amlodipina (B + A) versus la monoterapia con benazepril (B). Material y métodos: Se incluyeron 33 hipertensos esenciales. Durante 6 meses de tratamiento, 18 de ellos recibieron B + A (9 varones, 55 ± 2 años) y los 15 restantes recibieron B (10 varones, 49 ± 2 años). Se realizó una presurometría (MAPA) al comienzo y a los 3 y a los 6 meses de tratamiento. En un subgrupo de 23 pacientes se calculó la masa ventricular izquierda (MVI) y el índice de MVI (IMVI) al inicio y al final del tratamiento. Resultados: A los 3 meses de tratamiento, los valores de la presión arterial (PA) fueron significativamente menores (p < 0,05) en los pacientes tratados con B + A que con B (24 horas: 123 ± 1,7 / 77 ± 1,8 versus 132 ± 1,5 / 85 ± 1,6 mm Hg; día: 127 ± 1,9 / 81 ± 1,8 versus 137 ± 1,8 / 91 ± 1,9 mm Hg; noche: 115 ± 2,0 / 68 ± 2,1 versus 122 ± 2,0 / 76 ± 1,7 mm Hg). Esto se logró con una dosis menor y hubo mejor tolerancia. En el grupo B + A, la MVI y el IMVI disminuyeron de 225,3 ± 47,4 g y 125,5 ± 19,3 g/m², a 187,2 ± 45,1 g y 104,7 ± 27,2 g/m2 (p < 0,05), mientras que en el grupo B la disminución no resultó estadísticamente significativa. Al finalizar el tratamiento, sólo en los pacientes tratados con B + A se observó una correlación positiva entre el descenso de la PAS y la MVI (r = 0,56, p < 0,025) y el IMVI (IMVI: r = 0,60; p < 0,01). Conclusión: La combinación B + A mostró una reducción de la PA más precoz. Se requirió una dosis menor y se obtuvo mejor tolerancia clínica que con B solo. En relación con la MVI y el IMVI, estos parámetros disminuyeron en forma significativa sólo en B + A.

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