Abstract 2691: Independent Relation Of Aortic Stiffness With Subclinical Left Ventricular Myocardial Dysfunction In Patients With Cardiovascular Risk Factors
Introduction: increasing evidence suggests a major role of arterial stiffness in determining transition towards heart failure in patients with cardiovascular (CV) risk factors. An increased LV mass resulting from augmented LV impedance associated with aortic stiffness may partly account for this finding.
Aim of the study: to investigate the possible association of aortic stiffness with LV geometry, mass (LVM) and load-independent indices of myocardial function in patients with CV risk factors.
Materials and methods: 129 subjects were studied, 47 healthy controls (27 males, mean age 45.6 Â± 11 years) and 82 patients with at least one major CV risk factor, and without clinical CV disease or evidence of inducible myocardial ischemia (49 males, mean age 45.5 Â± 17 years). LV mass, geometry, systolic pump function, diastolic filling and intrinsic myocardial performance were assessed by a comprehensive echocardiographic study (Aloka SSD-5500, Japan) including 2-D targeted M-mode and apical 4-chamber view of the LV, transmitral Doppler, and Tissue Doppler Imaging (TDI). LV myocardial longitudinal velocities were studied at medial mitral annulus and interventricular septum (IVS) level. Carotid-femoral pulse wave velocity (PWV), an index of aortic stiffness, was measured by the foot-to-foot method (Complior, Artech, Paris).
Results: in the overall population, PWV correlated (p<0.01) directly with LVM (r=0.410) and inversely with transmitral E/A ratio (r=- 0.528), Em/Am ratio at mitral annulus (r=-0.603) and interventricular septal level (r=-0.497). No significant relations were found with indices of LV systolic function (both chamber and myocardial). In a stepwise regression analysis model (age, CF-PWV, diastolic blood pressure, LVM) only age and CF-PWV entered as independent determinants of TDI Em/Am (squared r value: 0.55, p<0.01).
Conclusion: in a population including normal subjects and patients with risk factors and free of CV disease, an increased aortic stiffness is associated with subclinical impairment of LV myocardial diastolic function independently of LV mass and blood pressure.