Evaluation of segmental elastic properties of the aorta in normotensive and medically treated hypertensive patients by intravascular ultrasound.

DESIGN AND METHODS

Local elastic properties of the descending aorta at different levels were evaluated by means of intravascular ultrasound images and pressure measurements. For this purpose, 30 normotensive patients and 30 age-matched medically treated patients with essential hypertension, all undergoing diagnostic cardiac catheterization, were studied.

RESULTS

Hypertension was well controlled in the essential hypertensives (137.1 +/- 6.79/74.5 +/- 2.65 mmHg). Systolic but not diastolic blood pressure in the hypertensive patients was significantly different from that of the normotensives (118.8 +/- 4.38/69.7 +/- 1.65 mmHg). The continuous loss of volume compliance with increasing distance from the heart was significantly higher in the hypertensives than in the normotensive patients [normotensives (1.45 +/- 0.19) x 10(-10) m5/N at the thoracic aorta, (0.08 +/- 0.05) x 10(-10) m5/N at the external iliac artery; hypertensives (0.81 +/- 0.09) x 10(-10) and (0.05 +/- 0.01) x 10(-10) m5/N at the corresponding sites]. Similarly, the hypertensives had an elevated elastic modulus proximal to the aortic bifurcation compared with the normotensives (244.47 +/- 44.06 versus 108.10 +/- 17.76 m/s, respectively). The decrease in buffering function of the vessel at this site is presumably caused by a turbulent flow pattern. Compared with the normotensives, the treated hypertensives had a significantly higher elastic modulus at each site where this was measured, whereas volume compliance and sectional compliance were lower.

CONCLUSION

The differences in elastic modulus and compliance between hypertensive and normotensive patients seem disproportionate to the difference in systolic blood pressure (within the normal range in both the treated hypertensives and the normotensives). Therefore, normalization of high blood pressure by long-term antihypertensive treatment may not fully reverse changes, caused by arterial hypertension, in the viscoelastic properties of the arterial wall.