ABSTRACT
Carotid artery intima-media thickness (IMT) has been used as a surrogate marker of atherosclerosis and is related to cardiovascular risk. Indices of arterial stiffness are also associated with cardiovascular risk and atherosclerosis. The aim of this study was to assess the prognostic value of the combination of surrogate markers of cardiovascular disease measured non-invasively in subjects without cardiovascular disease. In this cross-sectional study, 81 young and middle aged males (39.2+/-6.3 years) without evidence of overt cardiovascular disease or diabetes mellitus were enrolled. High-resolution B-mode ultrasonography and pulse wave analysis were used to measure carotid artery IMT and augmentation index (AI), a measure of arterial stiffness. Framingham risk score (FRS) was used as an estimate of the risk for development of cardiovascular disease. Regional differences were observed in the carotid arteries' IMT regarding their relationship with FRS: combined (average from all sites) IMT and IMT in the carotid bulb (CB), but not in the common (CC) and internal carotid artery (IC), and AI showed significant increases of FRS by their tertiles. However, subjects with both AI and IMT at any site in the highest tertile (AI>15%, CC>0.65 mm, CB>0.8 mm, IC>0.65 mm) had an increased FRS compared to subjects with one or none of these parameters in the highest tertile. In conclusion, young and middle-aged men without overt cardiovascular disease with both high IMT and AI are in high cardiovascular risk, as assessed by FRS. Epidemiological studies are needed to further validate this combination.
Subject(s)
Cardiovascular Diseases/etiology , Carotid Arteries/diagnostic imaging , Tunica Intima/diagnostic imaging , Vascular Resistance/physiology , Adult , Cardiovascular Diseases/diagnostic imaging , Cardiovascular Diseases/physiopathology , Carotid Arteries/physiopathology , Cross-Sectional Studies , Humans , Male , Middle Aged , Reference Values , Risk Factors , UltrasonographyABSTRACT
A 73-year-old man had a fast atrioventricular (AV) nodal pathway accidentally ablated 4 years before, while attempting to ablate a septally located concealed accessory pathway (AP). After initiation of treatment with beta-blockers, because of systemic arterial hypertension, the patient presented to the emergency room complaining of a markedly diminished exercise tolerance. The 12 lead ECG showed an interesting AV nodal Wenckebach sequence, interrupted by P waves retrogradely conducted through the AP. The mechanisms explaining the ECG are discussed.
