[A longitudinal study of the relationship between the pulse wave velocity in the aorta-iliaca vessel and the blood pressure (author's transl)]

Abstract

Temporary hypertensive increases in blood pressure, or variations in blood pressure when there was an already existing hypertension, in which the blood pressure either moved within the limits of hypertensive blood pressure values or temporarily returned to normal, occurred in 129 men ages 23-85, in whom repeated measurements of the blood pressure and pulse wave rate (PWG) were carried out in the aorta and iliac artery in the course of a longitudinal study over years. Both categories--temporary and chronic hypertensives--showed significant differences in the height of the PWG increase per 10 mm Hg (delta-c-p). The delta-c-p value for the chronic hypertensives (n equals 43) was 0.73 plus or minus 0.35 m/sec, that of the temporary hypertensives 0.56 plus or minus 0.24 m/sec (p smaller than or equal to 0.01). The mean value for both groups was 0.62 plus or minus 0.29 m/sec. Delta-c-p increased with age (0.54 m/sec yields 45th year; 0.60 m/sec from 46-55 years; 0.61 m/sec from 55-65 years; 0.67 m/sec at 66 and over). The increase of delta-c-p with age is caused by the increase in chronic hypertension. Delta-c-p was constant over a mean pressure range of 90-190 mm Hg in temporary and chronic hypertensives, irrespective of the amount of the (individual) mean difference in pressure, but it was distinctly greater in chronic than in temporary hypertensives. On lowering pressure, the delta-c-p was also greater in chronic than in temporary hypertensives. When normal pressures were attained, temporary hypertensives showed no differences from the PWG of normotensive of the same age. The differences between temporary and chronic hypertensives are explained by the different relations in the structure of the wall of the aorta, but especially because the function of the muscular layer was better maintained in temporary hypertensives. The raising of the PWG in temporary hypertensives is probably caused by the increased tension in the wall alone. Whether, in addition to the increased incorporation of collagen and a rarification of the smooth muscle, the thickness to radius ratio also increases above that usual for the age group in chronic hypertension is still not clear, but it is not essential for the explanation of the greater increase in the delta-c-p. The longitudinal delta-c-p values obtained in individual subjects confirms the transverse delta-c-p findings, with regard to size and age group, which were obtained by comparisation of cross sections of groups of normotive and hypertensive subjects.