Gender differences in cardiac left ventricular mass and function: Clinical and experimental observations.

BACKGROUND: The aim of this study was to evaluate gender-associated impact on left ventricular mass (LVM) and on left ventricular function (LVF) in humans and rats with aging. METHODS: Myocyte area and collagen volume fraction (CVF) were studied in rats. LVM and LVF were evaluated in animals and humans by echocardiography and LVM index (LVMI) was obtained. RESULTS: LVMI, myocyte area and CVF were similar in males and females of 1-month-old rats. LVMI in children was similar in both genders. In contrast, in 6-month-old rats (5 males and 5 females), LVMI (17.7 ± 0.7 mg/mm vs. 10.1 ± 0.2 mg/mm; p < 0.01), and myocyte area (4572.5 ± 72.6 µm² vs. 3293.85 ± 57.8 µm², p < 0.01) were higher in male animals without differences in CVF. Men (n = 25) exhibited greater LVMI than women (n = 25) (77.4 ± 3.2 g/m² vs. 63.3 ± 1.8 g/m², p < 0.01), whereas the LVF was higher in women (105.9 ± 2.9% vs. 95.3 ± 3.5%, p < 0.01). CONCLUSIONS: There is a clear gender-associated impact on LVM with aging in humans and rats. Similar CVF and LVF associated to greater myocyte size and LVM in male rats suggest a process of physiological response. However, the increase in cardiac mass without an associated improved cardiac function in men in comparison to women could likely represent a potential disadvantage in the adaptive response during growth.

Evaluación de la función sistólica del ventrículo izquierdo en jóvenes y su modificación según geometría ventricular / Evaluation of left ventricular systolic function in young and its variation according to ventricular geometry / Avaliação da função sistólica ventricular esquerda em jovens e sua variação de acordo com a geometria ventricular

Introducción. Las modificaciones en la geometría ventricular izquierda (GVI) en pacientes jóvenes y si éstas, aunque sean subclínicas, generan alteraciones en la función sistólica, no han sido evaluadas. Para este estudio se emplearon 397 (255 mujeres y 142 varones) alumnos de la Cátedra de Fisiología y Física Biológica de la Facultad de Ciencias Médicas de la Universidad Nacional de La Plata (UNLP). Métodos. En todos los casos se realizó ecocardiograma en modo M, bidimensional y con efecto Doppler. Se utilizó como punto de corte para definir hipertrofia ventricular izquierda (HVI) el valor promedio del índice de masa ventricular izquierda (IMVI) más dos desvíos estándar, surgidos del grupo estudiado sin hipertensión arterial y sin obesidad, para cada sexo. Como parámetro de función sistólica se utilizaron el acortamiento medio ventricular corregido por estrés (AMV/ESTRES) y la onda S del Doppler tisular del anillo mitral lateral (Slat). El AMV/ESTRES y Slat se analizaron según la GVI. Resultados. A medida que se progresaba hacia la HVI, se observó una disminución significativa de la onda Slat de N: 25,09; RC: 23,06; HVI: 19,08 (p<0,001); en cambio, cuando se utilizó al AMV/ESTRES, si bien existió una paulatina disminución, los valores hallados no resultaron estadísticamente significativos; N: 0,59; RC: 0,56; HVI: 0,50 (p=NS). Conclusión. Estos resultados permitirían concluir que el deterioro de la función sistólica que se produce en el progreso hacia la HVI sería detectado más precozmente por la onda Slat que por el AMV/ESTRES, reflejando esto una afectación más temprana de las fibras longitudinales cuando se las compara con las fibras transversales.

Background. Changes in left ventricular (LV) geometry in younger patients and if these, even if subclinical produce alterations in systolic function (SF), have not been evaluated. For this trial we used 397 (255 women and 142 men) students from the Department of Physiology and Biological Physics, Faculty of Medical Sciences of the Universidad Nacional de La Plata (UNLP). Methods. M-mode, bidimensional, Doppler echocardiography was performed in every case. To define left ventricular hypertrophy (LVH) the cutoff was the average value plus two standard deviations, emerged from the study group without arterial hypertension and without obesity, for each gender. As systolic function parameter were used ventricular midwall shortening corrected stress (VMWS/STRESS) and the S wave tissue Doppler mitral annulus lateral (Slat). The VMWS/STRESS and Slat were analyzed by LV geometry. Results. As they progressed towards the LVH, we observed a significant decrease of the wave Slat, N: 25.09; RC: 23.06; HVI: 19.08 (p<0.001); whereas, when VMWS/STRESS was used, although there was a gradual decline, the levels found were not statistically significant, N: 0.59; RC: 0.56; HVI: 0.50 (p=NS). Conclusion. These results allow to conclude that the deterioration of systolic function that occurs in the progress of LVH would be detected much earlier by the Slat wave than by the VMWS/STRESS, reflecting this early involvement of the longitudinal fibers when compared with the transverse fibers.

Introdução. As alterações na geometria do ventrículo esquerdo (GVE) em pacientes jovens e se estes, embora subclínicas gerem alterações na função sistólica, não foram avaliados. Para este estudo foram utilizados 397 (255 mulheres e 142 homens) estudantes do Departamento de Fisiologia e Física Biológica, Faculdade de Ciências Médicas da Universidade Nacional de La Plata (UNLP). Métodos. Em todos os casos foi feito o ecocardiograma modo M, bidimensional e efeito Doppler. Foi utilizado como ponto de corte para definir a hipertrofia ventricular esquerda (HVE) o valor médio mais dois desvios-padrão, resultantes do grupo de estudo sem hipertensão arterial e sem obesidade, para cada sexo. Como parà¢metro de função sistólica ventricular foram utilizados o encurtamento médio ventricular corrigido por stress (EMV/STRESS) e a onda S do Doppler tecidual do anel mitral lateral (Slat). O EMV/STRESS e Slat foram analisados pela GVE. Resultados. à€ medida que avanà§ou a HVE, observou-se uma diminuição significativa da onda Slat N: 25,09; RC: 23,06; LVH: 19,08 (p<0,001), em vez, quando foi usado ao EMV/STRESS, embora tenha havido um declínio gradual, os níveis encontrados não foram estatisticamente significativos, N=0,59; RC: 0,56; 0,50 HVE (p=NS). Conclusão. Estes resultados permitem concluir que a deterioração da função sistólica, que ocorre no progresso da HVE, seriam detectados mais precocemente pela onda Slat que pela EMV/STRESS, refletindo este envolvimento precoce das fibras longitudinais, quando comparado com as fibras transversais.

[Paradigms and paradoxes of left ventricular hypertrophy: from the research laboratory to the clinical consultation]. / Paradigmas y paradojas de la hipertrofia ventricular izquierda: desde el laboratorio de investigación a la consulta clínica.

Cardiac hypertrophy can occur as an adaptative response to increased cardiac workload. Different types of cardiac hypertrophy arise from a combination of genetic, physiologic, and environmental factors. When hypertophic growth of the heart leads to left ventricular dysfunction and heart failure, the response is considered as maladaptive or pathological hypertrophy. After analyzed left ventricular functional and structural changes in rats induced by arterial hypertension, banding of aortic root, isoproterenol administration, or myocardial infarction, as well as in patients with arterial hypertension, aortic stenosis, or hypertrophic miocardiopathy, we found a maladaptive response considered as pathological hypertrophy. However, the adaptation of the left ventricle, found in response to physical activity or to pregnancy in humans, seems to help the heart adapt to the increase in workload acting as physiological hypertrophy. These considerations allow us to speculate for the use of future interventions to stimulate the development of physiological hypertrophy in several pathological situations or to change a pathological into a physiological response.

Paradigmas y paradojas de la hipertrofia ventricular izquierda: desde el laboratorio de investigación a la consulta clínica / Paradigms and paradoxes of left ventricular hypertrophy: from the research laboratory to the clinical consultation

Cardiac hypertrophy can occur as an adaptative response to increased cardiac workload. Different types of cardiac hypertrophy arise from a combination of genetic, physiologic, and environmental factors. When hypertophic growth of the heart leads to left ventricular dysfunction and heart failure, the response is considered as maladaptive or pathological hypertrophy. After analyzed left ventricular functional and structural changes in rats induced by arterial hypertension, banding of aortic root, isoproterenol administration, or myocardial infarction, as well as in patients with arterial hypertension, aortic stenosis, or hypertrophic miocardiopathy, we found a maladaptive response considered as pathological hypertrophy. However, the adaptation of the left ventricle, found in response to physical activity or to pregnancy in humans, seems to help the heart adapt to the increase in workload acting as physiological hypertrophy. These considerations allow us to speculate for the use of future interventions to stimulate the development of physiological hypertrophy in several pathological situations or to change a pathological into a physiological response.