Abstract
Background: Pulse pressure (PP), a marker of arterial stiffness, is a cardiovascular risk predictor. Prospective studies have not evaluated other markers of arterial stiffness as predictors of major adverse cardiovascular events (MACE) in patients with established coronary artery disease (CAD). We aimed to determine whether the aortic augmentation pressure (AP, derived from the aortic pressure waveform) predicts MACE and death independently of the PP. Methods: We prospectively followed 297 males undergoing coronary angiography at the Miami VA Medical Center for 1186±424 days. We analyzed ascending aortic pressure tracings obtained during catheterization. Augmented pressure (AP) was defined as the difference between the second and the first systolic peak. Augmentation index (AIx) was defined as AP as a percentage of PP. We evaluated whether AP (adjusted for PP) and AIx can predict the risk of MACE (unstable angina, acute myocardial infarction, coronary revascularization, stroke or death), and all-cause mortality. We used Cox regression; AIx and AP were adjusted for mean aortic pressure, ejection fraction and heart rate in all models. Results: During the follow-up, 43.1% of patients had MACE and 19.5% died. Both the AP (adjusted for PP) and AIx significantly predicted the risk of MACE. The Hazard ratio (HR) per 10 mmHg increase in AP was 1.20 (95%CI=1.08-1.34; p<h0.001); the HR for each 10% in AIx was 1.28 (95%CI=1.11-1.48; p=0.004). After adjusting for other univariate predictors, the PP-adjusted AP remained a significant predictor of MACE (adjusted HR=1.19; 95%CI=1.07–1.33; p= 0.001), as did the AIx (adjusted HR=1.27; 95%CI=1.10–1.48; p=0.001). AP was a significant predictor of death (HR per 10 mmHg increase=1.18; 95%CI=1.02-1.39; p=0.03). Higher AIx was associated with a trend towards increased all-cause mortality (HR=1.22; 95%CI=0.98–1.52; p=0.056). Conclusions: Central AP predicts MACE and death in patients with established CAD independently of pulse pressure and other risk markers. Further studies are needed to determine the prognostic value of central pressure augmentation in other populations, further understand the mechanisms affecting it, and define its role as a therapeutic target.
