Thoracic aortic aneurysm (TAA) is a deadly disease. TAA size is the only parameter used in clinical decisions; however it is a suboptimal predictor of disease activity and acute aortic syndromes. Thus, there is a critical need to identify non-size markers of TAA-related risk. In this context, evaluating the pressure-buffering function of the aorta and the resulting measures of pulsatile arterial load provides a window into aortic health. Thus, we hypothesized that measures of pulsatile arterial load would be associated with faster TAA growth. One hundred and thirty subjects with TAA with imaging follow-up >6 months were recruited. Maximal aneurysm sizes at the oldest and latest imaging studies were used to calculate aneurysm growth rate in mm/year. Arterial hemodynamics were non-invasively determined with validated methods that integrate arterial tonometry with echocardiography. This evaluation yielded measures of central blood pressure as well as steady and pulsatile arterial load. Multivariable linear regression analyses adjusted for potential confounders (see Table) assessed the associations of arterial hemodynamic parameters with TAA growth. Seventy three percent of participants were men. Mean±standard deviation (SD) age, baseline aneurysm size and follow-up time were 62.5±11.5 years, 45.3±4.0 mm and 3.3±3.0 years, respectively. Twenty six percent of participants were on beta-blockers and 6% were on angiotensin receptor blockers. Mean TAA growth rate was 0.59±0.76 mm/year. Multivariable regression results are summarized in the Table. Brachial blood pressure measures and steady arterial load (systemic vascular resistance) were not associated with TAA growth. However, central blood pressure measures (central systolic and pulse pressures) and several measures of pulsatile arterial load (proximal aortic compliance and amplitude of forward and reflected pressure waves) were independently associated with faster aneurysm growth. We found that brachial blood pressure measures, the only hemodynamic parameters available to clinicians in the office, are not associated with TAA growth. In contrast, central blood pressure and pulsatile arterial load, reflecting the health of the aorta, are associated with faster aneurysm growth. As accelerated aneurysm growth is a marker of disease activity and a risk factor for acute aortic syndromes, our novel findings highlight worse aortic pressure-buffering function, leading to greater pulsatile arterial load and central blood pressure, as potentially clinically useful markers of TAA instability. This may motivate studies evaluating the role of central/ pulsatile hemodynamics as risk monitoring and therapeutic targets for TAA.