Regional and systemic haemodynamic response to aortography in hypertensives

To study the effects of aortography and of aortic counterflow bolus injection per se on regional and systemic haemodynamics in hypertensives in comparison to normotensive matched controls.

Mean blood velocity (MBV) and pulsatility index (PI)--as an index of regional vascular resistance--by the Doppler technique, at the femoral, common carotid and brachial arteries, finger arterial pressure and electrocardiographic R-R' interval were monitored beat-by-beat, before, during and for 3 min following counterflow bolus injections into the abdominal aorta of 40 ml/2.6 s of iopamidol (I), iso-osmolar mannitol (M) and 0.9 N saline (S), in 11 hypertensive and nine normotensive patients.

After bolus injection of iopamidol, MBV increased to a peak at 35+/-5 s, both in normotensive (deltaMBV versus baseline +16.7+/-9.9 cm/s; P < 0.01) and in hypertensive subjects (deltaMBV versus baseline: +13.9+/-6.6 cm/s; P < 0.01). At the same time, the PI decreased both in normotensive (deltaPI versus baseline: -4.05+/-2.49; P < 0.01) and in hypertensive subjects (deltaPI versus baseline: -3.02+/-2.25; P < 0.01). After M boluses, the haemodynamic changes were of the same direction and magnitude as I for both groups, while after S the magnitude was approximately 50% lower. No significant differences were observed between normotensive and hypertensive subjects. In other vascular circulations, a 15% increase of the early diastolic backflow in the brachial artery, in phase with the femoral artery haemodynamic changes, was the only evidence of the procedure. Mean arterial pressure decreased and heart rate increased in phase with flow changes of the femoral artery.

(1) The regional flow and systemic pressure changes observed during aortography seem, at least partially, to be due to the hydrodynamic perturbation induced by bolus injection per se. (2) The physical and chemical properties of the contrast media and therefore the probable different shear-stress modifications induced by the fluid injected could explain why the haemodynamic changes were greater after I compared to S and were more similar to M. (3) Hypertensive subjects did not show a different vasoreactive response in comparison to normotensive subjects during aortography.