Brachial and digital artery pulse pressures in hypertensive and normotensive subjects

To determine whether or not the pulsatile component of blood pressure (BP) measured centrally and peripherally allows a separation between hypertensive and normal subjects, as well as within hypertensive and normal subjects, as well as within hypertensive patients. We tested the hypothesis that the difference in central and peripheral pulse pressures is increased in hypertensive, compared to normotensive persons, and that this component is influenced by genetic variance. We studied 46 hypertensive patients and 56 age-matched normal subjects, as well as 10 hypertensive families with 74 members of the same age range.

Pulse pressure was measured at the brachial artery and the digital artery in the standing and supine position. The difference in the pulse pressures between these sites was calculated. Further, digital volume-pulse amplitude and stroke volume measurements were determined with impedance plethysmography.

The differences between central and peripheral pulse pressures were similar in hypertensive patients compared to normal subjects, regardless of posture. However, in the standing position the frequency distribution of this variable in hypertensive patients was bimodal and split into two significantly different distributions (P < 0.05) with peaks at -24 mm Hg and -1 mm Hg, compared to a single peak at -11 mm Hg in normal subjects. Furthermore, these two subgroups of hypertensive patients differed in their brachial systolic BP (127 +/- 10 vs 134 +/- 12 mm Hg; P < 0.05), their brachial pulse pressures (32 +/- 8 vs 42 +/- 8 mm Hg; P < 0.05), and in their peripheral compliance (1.59 +/- 0.92 vs 2.21 +/- 1.00 microliter/mm Hg per 100 ml tissue; P < 0.05). The frequency distribution of pulse pressure differences was also bimodal in members of hypertensive families, even though most (46 out of 74) were normotensive.

The difference between the digital and brachial pulsatile component may be a useful intermediary phenotype in essential hypertension. Furthermore, the nonuniform decreases in arterial compliance exhibited by our patients may be of pathogenic significance.