Central pulse pressure, carotid artery remodeling and coronary artery calcifications

The aim of the study was to evaluate the role of central pulse pressure (PP) in carotid wall thickening and coronary artery calcification (CAC).

In an asymptomatic general population ( N  = 396, 163 men, 47-89 years), central PP was measured by applanation tonometry, CAC by computed tomography, and common carotid artery intima-media thickness (cIMT), pulse wave velocity (cPWV) and the power of the signal reflected from carotid media (cMP) by radiofrequency-based carotid ultrasound. High cIMT was defined as cIMT equal to or greater than the 75th percentile for given sex and age, and CAC presence as a CAC score greater than 0.

In the entire population, luminal diameter and cMP increased with increasing central PP ( r  = 0.32 and 0.25; P  < 0.0001). One hundred and ninety-seven individuals had high cIMT; individuals with high cIMT had higher central PP, luminal diameter, cMP and cPWV ( P  = or <0.0001), but comparable wall tensile stress ( P  = 0.23). In a logistic regression model, high cIMT was independently associated with luminal diameter and central PP. One hundred and fifty-two individuals had CAC score greater than 0; in a logistic regression model, CAC score greater than 0 was independently associated with sex, age, central PP, LDL-cholesterol, triglycerides and T2DM.

Our findings indicate that high central PP contributes both to an increase in cIMT and the development of CAC. However, while central PP was the only risk factor linked to high cIMT, multiple atherosclerotic risk factors were associated with CAC. Therefore, both high cIMT and CAC reflect the adverse impact of high pulsatile load on the vascular system, yet only CAC can be considered a marker of atherosclerosis.