Radial artery lumen diameter and intima thickness in patients with abdominal aortic aneurysm

Abstract

ObjectiveAbdominal aortic aneurysm (AAA) is associated with dilatation of central elastic arteries, while it is uncertain whether peripheral muscular arteries are affected. The aim of this study was to investigate radial artery diastolic lumen diameter (LD), wall thickness, and circumferential wall stress (CWS) in patients with AAA. MethodsWe included 130 men with AAA (mean age, 70.4 ± 3.5 years) and 61 men without AAA (mean age, 70.5 ± 3.2 years) in the study. High-frequency ultrasound examination (50 MHz) was used to measure radial artery diameter, wall thickness, and CWS was calculated. ResultsMen with AAA exhibited smaller radial artery LD (2.34 ± 0.42 mm vs 2.50 ± 0.38 mm; P < .01), thicker intima (0.094 ± 0.024 mm vs 0.081 ± 0.018 mm; P < .001), similar intima-media (0.28 ± 0.05 vs 0.26 ± 0.05 mm; P = NS), and lower CWS (42.9 ± 10.2 kPa vs 48.6 ± 11.4 kPa; P < .001), compared with controls. Subgroup analyses including all patients showed smaller LD and thicker intima in patients on statin therapy versus no statin therapy and current/ex-smoking versus never smoking. Individuals with hypertension versus no hypertension also presented with thicker intima, but with no difference in LD. ConclusionsAAAs demonstrated a smaller LD and thicker intima in the radial artery, in contrast with the theory of a general dilating diathesis of the arteries. Apart from AAA, other factors such as atherosclerosis, smoking habits, and hypertension might also be determinants of radial artery caliber and thickness. Clinical RelevanceThe clinical relevance of this study is the added insight into the pathophysiology of abdominal aortic aneurysm (AAA). Today, the management of AAA is focused on reduction of general cardiovascular risk factors and treatment is based on surgical approaches when the AAA is already manifest. By shedding light on unknown pathophysiological aspects of AAA, it will eventually be possible to develop targeted pharmacological treatments to prevent the formation of AAA, to halt disease progression, and to find early cardiovascular markers of AAA.