Key result
Aortic regurgitation was not independently associated with maximum intima-media thickness (coefficient -0.034, P=0.3289 for grade ≥2) or brachial-ankle pulse wave velocity.
Why the study?
Does aortic regurgitation (and associated increased pulse pressure) increase atherosclerosis markers (intima-media thickness and pulse wave velocity) in a general patient cohort?
Cross-Sectional (n=1,149)
Does aortic regurgitation (and associated increased pulse pressure) increase atherosclerosis markers (intima-media thickness and pulse wave velocity) in a general patient cohort?
Effect estimate: Standard partial regression coefficient -0.034
p-value: p=0.3289
Aortic regurgitation, despite increasing pulse pressure, is not independently associated with increased atherosclerosis markers, challenging the hypothesis that pulse pressure is a direct cause of atherosclerosis.
Aortic regurgitation shows no independent link to atherosclerosis markers; hypothesis-generating on pulse pressure causality, needing prospective confirmation.
If pulse pressure, one of the mechanical stresses, is a risk factor for atherosclerotic cardiovascular disease, then atherosclerosis should be progressive in aortic regurgitation which is a representative disease with increased pulse pressure. This cross-sectional study included 1,149 patients. We examined the influence of aortic regurgitation on maximum intima-media thickness or brachial-ankle pulse wave velocity. The degree of aortic regurgitation was classified into 4 grades by color Doppler examination. There were 177 patients with aortic regurgitation. Pulse pressure was significantly higher in patients with aortic regurgitation than in those without it. On multiple regression analysis, aortic regurgitation was not found to be a significant independent variable for maximum intima-media thickness [standard partial regression coefficient: aortic regurgitation = grade 1, 0.011, P = 0.7635; aortic regurgitation ≥ grade 2, -0.034, P = 0.3289] and brachial-ankle pulse wave velocity [standard partial regression coefficient: aortic regurgitation = grade1, -0.043, P = 0.1197; aortic regurgitation ≥ grade2, 0.002, P = 0.9358] after adjusting for age, sex, body mass index, presence or absence of cardiovascular disease, antihypertensive treatment, diabetes, dyslipidemia, and smoking. These results found no causal association between aortic regurgitation and atherosclerosis, and were a contradiction to the opinion that pulse pressure was a risk factor of atherosclerosis.
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Shimada et al. (2018) conducted a cross-sectional in Aortic regurgitation and atherosclerosis (n=1,149). Aortic regurgitation vs. Absence of aortic regurgitation was evaluated on Maximum intima-media thickness (Standard partial regression coefficient -0.034, p=0.3289). Aortic regurgitation was not independently associated with maximum intima-media thickness (coefficient -0.034, P=0.3289 for grade ≥2) or brachial-ankle pulse wave velocity.
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