HAEMODYNAMIC CORRELATES OF CENTRAL ARTERIAL PRESSURE
WAVE AUGMENTATION. C.S.
Hayward*, N. Shaukat, A. Ghanbari and R.P. Kelly. Cardiology
Dept, St Vincent's Hospital, Sydney, NSW. Late
systolic augmentation of the central arterial pressure waveform, which is
associated with increased LV mass, has been variously attributed to increased
arterial stiffness, alterations in cardiac ejection and altered reflection of
the ejected pressure wave by the periphery. The contribution of cardiac and
vascular haemodynamic factors to this augmentation index (the ratio of the
augmented pressure to the pulse pressure, AIx) has not been previously defined
in a population cohort. In a community based sample of 702 subjects, aged 18-81
years, we recorded the carotid waveform by applanation tonometry, aorto-femoral
pulse wave velocity (PWV), and cardiac structure and function by thoracic
echocardiography. As previously described, we found that age (+4.9±0.4
/10years, coefficient±SEE), gender (+11.8±1.5 for female), mean BP (+3.2±0.4
/10mmHg), height (-2.2±0.7 /10cm) and heart rate (-5.4±0.5 /10bpm) contributed significantly and independently to
central AIx (r2=0.52, p<0.0001 by multivariate regression). Both
PWV and AIx increased significantly with age (r=0.62 and 0.56 respectively,
p<0.0001 for both), and were correlated in univariate analysis (r=0.32,
p<0.0001). However, in multivariate analysis, AIx was not related to PWV
after age entered the equation. Similarly, fractional shortening (FS%) and peak
aortic flow velocity were weakly correlated with AIx (r=0.08, p<0.05 for
both) but did not contribute independently to carotid AIx after inclusion of
age or BP in multivariate analysis. Indeed ageing was associated with a slight
increase in FS% (r=0.12, p=0.002) which may be expected to decrease AIx. These
results suggest that cardiac ejection is not a major determinant of AIx. Ageing
is an important determinant of AIx independent of changes in vascular stiffness
measured by PWV. Body height and gender also contribute independently to late
systolic augmentation, possibly through effects on wave reflection.
