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.
The changes in the aortal pulse-wave velocity (PWV) occurring in connection with and dependent on spontaneous fluctuations of blood pressure has been recorded at intervals over the years in 183 normotensive men, who were aged from 17-74 at the beginning of the long term study. An essential condition was that the diastolic blood pressure should not exceed 95 mm Hg and the systolic 145 mm Hg. In order to eliminate the effect of age on the PWV between 2 measurements, and so to obtain a "pure" PWV-mean pressure relationship (c-p relationships), 7 cm/sec per year was subtracted from the c-value of the second measurement before the age of 55 and 9 cm/sec per year after that age. The differences quotient delta cp as a standard for the change of c with the mean pressure p was obtained from the difference between two c values (c1-c2) taken at different times, converted to a pressure change of 10 mm Hg, and divided by the difference of the mean pressure levels belonging to them (p1-p2). In applying the appropriate age correction to c2, the time factor had no statistically recognisable effect on delta cp. In 78% of the cases in our long term study, c rose and fell with p, in 22%, the changes of c were at variance with the changes of p. Taking into consideration all the test subjects, delta cp averaged 0.40 m/sec. Before the age of 55, delta cp is smaller (0.30 m/sec) than above that age (0.55 m/sec). The age difference of delta cp is significant ( = 0.05). When the concordant c-p relationships alone were calculated, delta cp was 0.70 m/sec and scarcely differed from the delta cp values of hypertensives published earlier (0.60 m/sec: also concordant c-p relationships only). The generally lower delta cp values from group cross sections (in contrast to the longitudinal investigations) are explained by an unrecognisable admixture of discordant c-p relationships. In a range of pressure from 90-170 mm Hg, delta cp was shown to be independent of the level of the initial pressure. Also the magnitude of the (spontaneous) mean pressure variation (5-70 mm Hg, normotensives - hypertensives) seems to have no effect on the statistical mean value of delta cp. delta cp is, however, dependent on the direction of the pressure change in normotensives (just as with hypertensives), even when age is taken into account. If the pressure is reduced, c is higher and delta cp (p = 0.05) is greater than when the blood pressure is increased. The c-p relationship traverses a kind of loop (counterclockwise). In the discussion, an attempt is made to point out the effect of the vascular musculature on delta cp, which threads conspicuously through the comparison of the physiological delta cp values with the delta cp values in arteriosclerosis (hypertension; diabetes) and in endurance training. From this it can be deduced that normal values for c and delta cp in arteriosclerosis indicate that the musculature is still capable of maintaining a normal elastic function even with considerable regressive changes in the vessel wall.
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