Cardio-ankle vascular index and subclinical heart disease.

The relationship between arterial stiffness, measured as pulse wave velocity (PWV), and the left ventricle is confounded by the effects of blood pressure. We evaluated the relationship between carotid-femoral PWV and cardio-ankle vascular index (CAVI), a less pressure-dependent measurement of the stiffness constant (β) of the aorta and the iliac, femoral and tibial arteries, and obtained prognostically relevant measurements of left ventricular structure and systolic function. CAVI, carotid-femoral PWV and echocardiographic left ventricular mass and systolic function were determined in 133 subjects with either hypertension or high-normal blood pressure (33% treated; 56 ± 16 years, blood pressure 145/89 ± 21/12 mm Hg). Carotid-femoral PWV exhibited a direct relationship with systolic and diastolic blood pressure (r = 0.33/0.26, P < 0.001/0.014), whereas CAVI demonstrated no such relationship (r = 0.12/-0.05, both P > 0.1). Both CAVI and PWV correlated significantly with left ventricular mass index (r = 0.31, P<0.001; r = 0.21, P = 0.014). Subjects with inappropriately high left ventricular masses for a given cardiac workload (n = 44) had higher CAVI values (9.1 ± 2.0 vs. 7.9 ± 1.6, P < 0.001), but not higher PWV values (8.5 ± 2.5 vs. 8.7 ± 2.4, P>0.1). In a multivariate regression model, CAVI was independently associated with inappropriate left ventricular mass (β = 0.40, P < 0.001), along with body mass index. CAVI also demonstrated a negative relationship with left ventricular midwall fractional shortening (r = -0.41, P = 0.001) that was independent of age, sex, blood pressure and left ventricular mass in a multivariate analysis. In conclusion, a high CAVI is associated with inappropriately high left ventricular mass and low midwall systolic function. As a marker of arterial diastolic-to-systolic stiffening, CAVI may have a relationship with left ventricular structure and function that is independent of blood pressure levels.