Manejo del aneurisma de aorta abdominal sintomático no roto: últimos adelanto / Management of symptomatic unruptured abdominal aortic aneurysms: state of the art

RESUMEN El aneurisma de aorta abdominal (AAA) sintomático no roto es una patología que involucra a aquellos pacientes con AAA intacto, pero que presentan dolor abdominal y/o lumbar atribuido al aneurisma. Esta forma de presentación clínica es po tencialmente mortal dado que su etiopatogenia comprende cambios agudos en la pared aórtica, incluyendo inflamación, lo que incrementa la probabilidad de ruptura inminente. Está claro que estos pacientes deben ser derivados a reparación del AAA. Sin embargo, el momento de la intervención es controvertido. Por lo tanto, el objetivo del presente trabajo fue revisar la información actualizada sobre el abordaje diagnóstico-terapéutico del AAA sintomático no roto.

ABSTRACT Symptomatic unruptured abdominal aortic aneurysm (AAA) refers to a group of patients with intact AAA but who present abdominal and/or lumbar pain attributed to the aneurysm. This form of clinical presentation is potentially fatal since its etiopathogenesis, involving acute changes in the aortic wall, including inflammation, increases the probability of impending rupture. It is clear that these patients should be referred to AAA repair. However, the timing of the intervention is contro versial. Therefore, the aim of the present work was to review updated information on the diagnostic-therapeutic approach of symptomatic unruptured AAA.

Are kinking and coiling of carotid artery congenital or acquired?

Dolichoarteriopathies consist of tortuosity, kinking, or coiling of the extracranial carotid arteries. Some authors consider these alterations a consequence of atherosclerotic vessel remodeling, while others ascribe them to anatomical variations of embryological origin. The objective was to establish whether carotid dolichoarteriopathies belonged to a congenital origin or to acquired conditions. Color Doppler ultrasonography of neck vessels was performed in 885 participants, whose age ranged from 1-day-old infants to 90-year-old adults. Prevalence of kinking and coiling was evaluated, and it was related to the presence of cardiovascular risk factors. Prevalence of either kinking or coil of carotid arteries showed no increase with age, as it was comparable across all ages; furthermore, frequency of these alterations showed no relationship to cardiovascular risk factors nor to the presence of atheromatous plaques. These findings suggest that carotid dolichoarteriopathies are a result of alterations in embryological development rather than vascular remodeling secondary to aging and/or atherosclerosis.

¿La hipertensión arterial es causa de dolicoarteriopatías carotídeas?: Un estudio con eco-Doppler color / Is Hypertension a Cause of Carotid Dolicoarteriopathies?: A Study with Color Doppler Echocardiography

Introducción No existe hasta el momento un criterio uniforme acerca del papel de la hipertensión arterial (HTA) como causa de las dolicoarteriopatías carotídeas (DC). Previamente hemos comunicado que las DC serían de origen embriológico por su prevalencia similar en un grupo de niños y adolescentes (voluntarios sanos) respecto de otro de adultos. Objetivos Determinar la relación de la HTA y de otros factores de riesgo cardiovascular con DC tipos 2 (loop) y 3 (kinking). Material y métodos Estudio observacional, descriptivo, prospectivo, transversal y controlado. Se incluyeron 885 pacientes de ambos sexos, con edades desde neonatos (4 h 30 min de nacidos) hasta 90 años. Se dividieron en dos grupos: G1 (control, voluntarios sanos) n = 245: recién nacidos, niños y adolescentes de hasta 15 años y G2: n = 640, pacientes de 16 a 90 años, que habían sido derivados para la realización de un eco-Doppler de vasos del cuello. Se evaluaron antecedentes de HTA, dislipidemia, diabetes, tabaquismo y la presencia de placas ateromatosas en las zonas correspondientes a dolicoarteriopatías. Resultados G1: prevalencia de kinking 27% (n = 67) y de loop 4% (n = 10). G2: kinking 22% (n = 143) y loop 3%(n = 19) (p = ns entre ambos grupos). Factores de riesgo en G2: portadores respecto de no portadores de DC: HTA (12% versus 11%), tabaquismo (9% versus 10%), dislipidemia (5% versus 4%), diabetes (1,5% versus 2%); todos, p = ns. Placas ateromatosas intrakinking en G2: 4,3%. Conclusiones Ni la HTA ni los demás factores de riesgo cardiovascular analizados, como tampoco las placas ateromatosas, serían los causantes de las dolicoarteriopatías carotídeas.

Background Rol of arterial hypertension (AHT) as a cause of carotid dolicoarteriopathies (CD) is still uncertain. We have previously informed that CD would have an embryological origin as its prevalence is similar in a group of children and adolescents (healthy volunteers) compared with a group of adults. Objectives To determine the relationship between AHT and other cardiovascular risk factors with CD type 2 (loop) and 3 (kinking). Material and methods Observational, descriptive, prospective, transversal and controlled study. Eight hundred and eighty five patients, both sexes, were included, with ages ranging from newborn (aged 4 h 30 min) to 90 years. Patients were divided into two groups: G1 (control group, healthy volunteers), n = 245: new-born, children and adolescents up to 15 years old, and G2: n = 640, patients aged 16 to 90 years referred for a carotid echo-Doppler examination. A history of hypertension, dyslipemia, diabetes mellitus, and smoking was assessed, as well as the presence of atheromatous plaques in the area corresponding to dolicoarteriopathies. Results G1: prevalence of kinking 27% (n=67) and of loop 4% (n=10). G2: kinking 22% (n=143) and loop 3% (n=19) (p=ns between both groups). Risk factors in G2: CD carriers compared with CD non-carriers: AHT (12% vs 11%), smoking (9% vs 10%), dyslipemia (5% vs 4%), diabetes mellitus (1.5% vs 2%); all p values = ns. Atheromatous plaques intrakinking in G2: 4.3%. Conclusions Neither AHT nor other cardiovascular risk factors analyzed or atheromatous plaques are responsible for carotid dolicoarteriopathies.