Although cardiac hypertrophy is a frequent complication of end-stage renal disease
(ESRD), relatively little is known about large arterial geometry and function in vivo
in these patients, and the relationship between arterial changes and cardiac hypertrophy
is unknown. Common carotid artery (CCA) intima-media thickness and internal diameter
and left ventricular geometry and function were determined by ultrasound imaging in
70 uncomplicated ESRD patients and in 50 age-, sex-, and blood pressure-matched controls.
Arterial distensibility and compliance were determined from simultaneously recorded
CCA diameter and stroke changes in diameter and CCA pressure waveforms, obtained by
applanation tonometry, and also by the measurement of carotid-femoral pulse wave velocity.
Compared with control subjects, ESRD patients had greater left ventricular diameter
(P < 0.01), wall thicknesses and mass (P < 0.001), increased CCA diameter (6.25 +/-
0.87 vs. 5.55 +/- 0.65 mm; P < 0.001), larger CCA intima-media thickness (777 +/-
115 vs. 678 +/- 105 microns; P < 0.001) and intima-media cross-sectional area (17.5
+/- 4.5 vs. 13.4 +/- 3.3 mm2; P < 0.001). In uremic patients, arterial hypertrophy
was associated with decreased CCA distensibility (17.8 +/- 8.8 vs. 24.0 +/- 12.7 kPa-1.10(-3);
P < 0.001) and compliance (5.15 +/- 2 vs. 6.0 +/- 2.5 m2.kPa-1.10(-7); P < 0.05),
accelerated carotid-femoral pulse wave velocity (1055 +/- 290 vs. 957 +/- 180 cm/seconds;
P < 0.001), early return and increased effect of arterial wave reflections (20.5 +/-
15.4 vs. 9.2 +/- 18.4%; P < 0.001). The latter phenomenons were responsible for increased
pulsatile pressure load in CCA (58.3 +/- 21 vs. 48 +/- 17 mm Hg; P < 0.01) and were
associated with a decreased subendocardial viability index (157 +/- 31 vs. 173 +/-
30%; P < 0.001). The CCA diameter was correlated with the left ventricular diameter
(P < 0.01), and a significant correlations existed between CCA wall thickness or CCA
intima-media cross-sectional area and left ventricular wall thicknesses and/or left
ventricular mass (P < 0.01). In multivariate analysis, these relationships were independent
regarding age, sex, blood pressure and body surface area. The present study documents
parallel cardiac and vascular adaptation in ESRD, and demonstrates the potential contribution
of structural and functional large artery alterations to the pathogenesis of left
ventricular hypertrophy and functional alterations.