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.

[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.

Echocardiographic assessment of left ventricular midwall mechanics in spontaneously hypertensive rats.

AIMS: The present study was attempted to determine whether LV midwall mechanics yielded different conclusions about LV systolic function than the assessment of endocardial LV mechanics by echocardiography in spontaneously hypertensive rats (SHR). METHODS AND RESULTS: Thirty-six (18 Wistar normotensive (W), 18 [SHR]) anesthetized rats were studied with two-dimensional directed M-mode echocardiogram to analyze LV structure (LV diameter, left ventricular wall thickness and LV mass [LVM]) and LV function (endocardial shortening [ES] and midwall shortening [MS]). Measurements were made from three consecutive cardiac cycles on the M-mode tracings. There was no significant difference in LV dimension. LVM was higher in SHR (SHR: 595 +/- 111 mg, W: 413 +/- 83 mg--p < 0.01). ES was higher in SHR (SHR: 64.1 +/- 6%, w: 58.2 +/- 4%--p < 0.01), whereas no significant difference was found in MS (SHR: 24 +/- 4%, W: 27.6 +/- 4%--ns). Twelve of 18 (66%) SHR showed endocardial shortening higher than normally predicted, compared with 3/18 (16%) with observed enhanced MS (p < 0.01). CONCLUSION: These results suggest that the analysis of midwall mechanics by echo allows us to better understand the LV performance in SHR and that the exaggerated endocardial motion could not represent a really supernormal systolic performance.