Abstract

PISKORZ, Daniel et al. Central obesity and left ventricular hypertrophy regression. Insuf. card. [online]. 2007, vol.2, n.4, pp.159-162. ISSN 1852-3862.

Blood pressure per se may be the main determinant of left ventricle hypertrophy development in hypertensive subjects. On the other side, body mass index and waist circumference are related to left ventricle mass index (LVMI) positively, continuously and linearly even in non hypertensive patients. An insufficient treatment may be the main reason of not achieving regression of target organ damage. The objective of this trial is to establish the impact of central obesity on LVMI regression. Material and methods: 102 consecutive hypertensive patients (p) wich attended for the first time to a specialized consultory room were included. LVMI was measured with the Devereux method at the begining and after at least one year of treatment. The patients were divided into two groups: GA: waist circumference (WC) <88 cm in women and <102 cm in men and GB: WC > of those values. The statistic analysis was done with the Students t test for differences in proportions and means and a p value <0.05 was considered statistically significative. Results: 36 p (35.3%) were from GA and 66 p (64.7%) from GB, and the mean follow up was 2148 ± 1172 days. The WC was 88.5 ± 9.5 cm in GA and 105.4 ± 10.7 in GB; p<0.0005. There were any mean age differences (GA 52.8 ± 16 years and GB 57.7 ± 11 years) and any male prevalence differences (GA 21 p - 58.3% vs GB 31 p - 50%). The initial LVMI was 114.8 ± 30.2 g/m² in GA and 114.1 ± 31.8 g/m² in GB; the initial blood pressure was 157.1 ± 29 / 91.7 ± 11.5 mm Hg in GA and 163.6 ± 26 / 94.8 ± 12.9 mm Hg in GB; p=NS. At the end of the follow up the LVMI differences were - 18.5 ± 23.8 g/m² in GA (p<0.05) and - 4.3 ± 33.4 g/m² in GB (p=NS); and the differences in blood pressure were - 20.5 ± 28.4 / - 14.4 ± 13.1 mm Hg in GA (p<0.005) vs - 21.3 ± 31.7 / - 15.8 ± 17.3 in GB (p<0.005). During the follow up the blood pressure was under 130 - 85 mm Hg in 11 p (30.6%) from GA and 14 p (21.2%) from GB; p=NS. The amount of drugs used in GA was 1.3 ± 0.8 and 1.4 ± 0.9 in GB; p=NS. Conclusions: Although a similar lowering of blood pressure was achieved in both groups and there were any differences in the amount of drugs prescribed the LVMI regression was statistically significative in hypertensive patients with normal waist circumference and it was not in patients with WC increased. To sum up, visceral obesity may be an additional obstacle to achieve target organ damage regression in the treatment of arterial hypertension.

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