Adverse outcome in aortic sclerosis is associated with coronary artery disease and inflammation Original Research Article

Objectives The present study was designed to evaluate the relationship between the presence of aortic sclerosis, serologic markers of inflammation, and adverse cardiovascular outcomes. Background Aortic sclerosis is associated with adverse cardiovascular outcomes. However, the mechanism by which such nonobstructive valve lesions impart excess cardiovascular risk has not been delineated. Methods In 425 patients (mean age 68 ± 15 years, 54% men) presenting to the emergency room with chest pain, we studied the relationship among aortic sclerosis, the presence and acuity of coronary artery disease, serologic markers of inflammation, and cardiovascular outcomes. Patients underwent echocardiography and serologic testing including C-reactive protein (CRP). Aortic valves were graded for the degree of sclerosis, and cardiovascular outcomes including cardiac death and nonfatal myocardial infarction (MI) were analyzed over one year. Results Aortic sclerosis was identified in 203 patients (49%) , whereas 212 (51%) had normal aortic valves. On univariate analysis at one year, patients with aortic sclerosis had a higher incidence of cardiovascular events (16.8% vs. 7.1%, p = 0.002) and worse event-free survival (normal valves = 93%, mild aortic sclerosis = 85%, and moderate to severe aortic sclerosis = 77%, p = 0.002). However, by multivariable analysis aortic sclerosis was not independently associated with adverse cardiovascular outcomes; the only independent predictors of cardiac death or MI at one year were coronary artery disease (hazard ratio [HR] 3.23, p = 0.003), MI at index admission (HR 2.77, p = 0.008), ascending tertiles of CRP (HR 2.2, p = 0.001), congestive heart failure (HR 2.15, p = 0.02) and age (HR 1.03, p = 0.04). Conclusions The increased incidence of adverse cardiovascular events in patients with aortic sclerosis is associated with coronary artery disease and inflammation, not a result of the effects of valvular heart disease per se.