BACKGROUND: Thoracic aortic aneurysm (TAA) is a disease of increasing prevalence and associated with high morbidity and mortality. As such, novel, clinically useful stcArategies for risk assessment and medical management of TAA are critically needed. To address this need, we sought to determine the predictive role of aortic stiffness and pulsatile arterial load (which reflect the aorta’s health and function) on future TAA expansion.
METHODS AND RESULTS: One hundred and six consecutive, unoperated subjects with TAA were recruited. By combining arterial tonometry with echocardiography using validated methods, we estimated measures of aortic stiffness, central blood pressure (BP), steady and pulsatile arterial load at baseline. Measures of aortic stiffness, central BP and pulsatile arterial load correlate directly with aortic health and function, while measures of steady arterial load reflect resistive load from peripheral arteries instead. Aneurysm size was measured at baseline and follow-up with imaging and indexed to height. TAA growth was calculated in (mm/m)/year. Stepwise multivariable linear regression assessed associations of baseline arterial stiffness and load measures, in separate models, with aneurysm growth. Variables considered in the models were: age, sex, BSA, mean arterial pressure, baseline aneurysm size, aneurysm etiology and location, follow-up time, concordant/discordant nature of the imaging modalities and history of hypertension, diabetes and smoking. Interaction terms for age, sex, and aneurysm etiology with each hemodynamic measure were tested in the models. Seventy five percent of subjects were men. Mean±SD age, baseline aneurysm size and follow-up time were 62.8±11.4 years, 46.5±3.9 mm and 2.3±0.9 years, respectively. Aneurysm growth rate was 0.34±0.36 mm/year in men and 0.73±0.84 mm/year in women (P=0.040). Results of the linear regression models are summarized in the Table. Measures of aortic stiffness, central BP and pulsatile arterial load independently predicted future aneurysm expansion. Conversely, brachial BP and steady arterial load did not. None of the interaction terms were significant, suggesting that results are equally applicable to all ages, both sexes, and all TAA etiologies. Potential applications of our findings are summarized in the Figure.
CONCLUSION: Measures of aortic function, including aortic stiffness and pulsatile hemodynamics, independently predict future TAA growth and provide novel insights into disease activity. Moreover, some of the hemodynamic measures were superior to baseline aneurysm size (which is the standard for clinical assessment) in the prediction of future aneurysm expansion. Our findings demonstrate a potential role for non-invasive hemodynamic assessment as a means to better predict TAA disease activity and refine risk stratification in patients with TAA.