Carotid arterial stiffness is increased and related to left ventricular function in patients with hypertrophic cardiomyopathy.

Abstract

To assess the carotid mechanical properties in patients with hypertrophic cardiomyopathy and the relation between arterial stiffness and left ventricular function in this setting. We have prospectively enrolled 71 patients (52 ± 16 years, 34 men) with hypertrophic cardiomyopathy, divided into two groups depending on the presence (46 patients) or absence (25 patients) of cardiovascular risk factors associated with increased arterial stiffness. Twenty-five normal subjects similar by age and gender with hypertrophic cardiomyopathy patients without risk factors formed the control group. A comprehensive echocardiography was performed in all subjects. Carotid arterial stiffness index (β index), pressure-strain elastic modulus, arterial compliance, and pulse wave velocity were also obtained using an echo-tracking system. β index, pulse wave velocity, and pressure-strain elastic modulus were significantly higher in hypertrophic cardiomyopathy patients without risk factors compared to controls. After linear regression analysis, the increase in carotid β index was independently correlated with the presence of hypertrophic cardiomyopathy [beta = 0.49, 95% confidence interval (CI) = 1.04-3.02; P < 0.001]. In the entire hypertrophic cardiomyopathy population arterial stiffness parameters correlated with age, gender, hypertension degree, presence of hypercholesterolaemia, and the E/e' ratio. In multivariable analysis, β index (beta = 0.36, 95% CI = 0.32-1.25; P = 0.001), global left ventricular longitudinal strain, and the presence of left ventricular outflow tract obstruction were independently correlated with the E/e' ratio. In patients with hypertrophic cardiomyopathy arterial stiffness is increased independently of age or presence of cardiovascular risk factors. Carotid artery stiffness is independently related to left ventricular filling pressure, increased arterial stiffness representing a possible marker of a more severe phenotype.