1 unknown2 Cardiology, Herlev and Gentofte Hospital, The Capital Region of Denmark
a prospective cohort study
OBJECTIVE: Aortic stenosis (AS) shares risk factors with atherosclerotic vascular disease. Carotid intima-media thickness (IMT) and plaque may reflect the cumulative damage from exposure to different atherosclerotic risk factors. We examined the relationship of carotid IMT and plaque with incident AS in a prospective population-based study. APPROACH AND RESULTS: A random sample of participants (age, 45-68 years) in the population-based Malmö Diet and Cancer Study underwent B-mode ultrasound with measurements of IMT and the presence of plaque in the common carotid artery (n=5079). Potential risk factors for incident AS were studied in age- and sex-adjusted and expanded multivariable-adjusted Cox regression models. A total of 69 (1.4%) participants developed AS during up to 20 years of follow-up. Significant risk factors for AS in age- and sex-adjusted analyses were (P<0.05) body mass index, low-density lipoprotein cholesterol, hypertension, diabetes mellitus, smoking, C-reactive protein, plaque, and IMT. In contrast, high-density lipoprotein cholesterol, triglycerides, height, and leukocyte count were not significantly associated with AS (P>0.05). After adjustments, IMT, plaque, age, smoking, C-reactive protein, low-density lipoprotein cholesterol, and diabetes mellitus remained significantly associated with incident AS. IMT was no longer significantly associated with AS after adjustments for plaque and systolic blood pressure, but plaque remained significantly associated with incident AS. CONCLUSIONS: Traditional cardiovascular risk factors were individually associated with incident AS, and in multivariable models low-density lipoprotein cholesterol, smoking, age, presence of plaque, C-reactive protein, and diabetes mellitus remained significant predictors of incident AS. AS represents a vascular disorder related to carotid plaque, with potential implications for the pathophysiology and prevention of this disease.
Arteriosclerosis, Thrombosis, and Vascular Biology, 2014, Vol 34, Issue 10, p. 2343-8