scholarly journals Intima-media thickness of the common carotid arteryas an early marker of atherosclerosis in patients withabdominal obesity

Author(s):  
O. Belyaeva ◽  
V. Mandal ◽  
N. Ananyeva ◽  
O. Berkovich ◽  
E. I. Baranova ◽  
...  

Severity of atherosclerosis of common carotid arteries in patients with abdominal obesity (aged from 30 to 55 years old) was evaluated by ultrasound duplex scan. Atherosclerotic plaques of common and/or internal carotid arteries were revealed in 35% of patients. Correlations were observed between intima-media thickness of the common carotid artery, blood pressure levels, waist circumference and metabolic parameters.

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1119.3-1120
Author(s):  
L. Nacef ◽  
H. Ferjani ◽  
H. Riahi ◽  
Y. Mabrouk ◽  
E. Labbene ◽  
...  

Background:Patients with rheumatoid arthritis (RA) are at higher cardiovascular risk (CVR) than the general population due to chronic inflammation. Several factors, both modifiable and non-modifiable, can increase this risk. Intima-media thickness (IMT) was considered as a marker for atherosclerosis.Objectives:This study aimed to identify predictor factors of increasing IMT.Methods:The prospective study was carried out on patients with RA who met the 2010 American College of Rheumatology (ACR)/European League Against Rheumatism (EULAR) classification criteria. These patients were followed in the rheumatology department of the Kassab Institute. The socio-demographic data, biological and immunological parameters were collected.Framingham’s score quantified the cardiovascular risk at 10-years. Carotid Ultrasonography (US) using a high resolution B mode carotid measured intima-media thickness (IMT) as a subclinical marker of atherosclerosis. Carotid US was performed in the supine position, according to American Society of Echocardiography guidelines. IMT was measured in the left (LCC) and right (RCC) common carotid arteries, the left (LIC) and right (RIC) internal carotid arteries, and the left (LEC) and right (RIC) internal carotid arteries. An increased IMT was defined as ≥0.9 mm.We analyzed data by the SPSS statistical package. A p-value <0.05 was considered significant.Results:Of the 47 patients surveyed, 78.7% were female. The mean age was 52.5 ±11.06 [32-76]. The duration disease was 86.25 ±63 months [5-288] and was erosive in 81.6% of cases. The rheumatoid factor (RF) was positive in 57.8% of patients, and citrullinated antipeptide antibodies (ACPA) were present in 62.2%. Eight patients had a previous CV history (hypertension, diabetes or dyslipidemia) and 16.4% were active smokers. Among women, 43.6% were postmenopausal. ITM was significantly higher in men at LIC (0.037) and LEC (0.025). Older age was associated with increased ITM in LIC (p=0.046; r=0.295), LEC (p=0.05; r=0.412), RCC (p=0.034; r=0.317), and REC (p=0.009; r=0.382). The ITM for LCC, LIC, LEC, RCC, RIC, and REC was higher in postmenopausal women, with no significant difference (p=0.782, p=0.208, p=0.877, r=0.734, p=0.808, p=0.437, respectively).Among the modifiable factors, active smoking was associated with a higher ITM at the REC level (p=0.047). However, weight was not associated with an increased ITM (LCC: p=0.092; LIC: p=0.985; LEC: p=0.952; RCC: p=0.744; RIC: p=0.210; REC: p=0.510). In our study, there was no significant association between DAS28 disease activity or inflammatory marks and ITM (LCC: p=0.784; LIC: p=0.316; LEC: p=0.420; RCC: p=0.784; RIC: p=0.484; REC: p=0.754).Conclusion:In our study, the non-modifiable factors associated with increased ITM were advanced age and male gender. The modifiable factor impacting ITM was primarily active smoking. Surprisingly, disease activity and biological inflammation did not influence ITM.References:[1]S. Gunter and al. Arterial wave reflection and subclinical atherosclerosis in rheumatoid arthritis. Clinical and experimental rheumatology 2018; 36: clinical e.xperimental.[2]Aslan and al. Assessment of local carotid stiffness in seronegative and seropositive rheumatoid Arthritis. Scandinavian cardiovascular journal, 2017.[3]Martin i. Wah-suarez and al, carotid ultrasound findings in rheumatoid arthritis and control subjects: a case-control study. Int j rheum dis. 2018;1–7.Disclosure of Interests:None declared


2020 ◽  
Vol 39 (1) ◽  
pp. 79-84
Author(s):  
Oluwagbemiga O. Ayoola ◽  
Rahman A. Bolarinwa ◽  
Oluwatoyin H. Onakpoya ◽  
Stephen O. Onigbinde ◽  
Christianah M. Asaleye ◽  
...  

2005 ◽  
Vol 109 (5) ◽  
pp. 475-481 ◽  
Author(s):  
Birger Wolff ◽  
Claudia Braun ◽  
Christina Schlüter ◽  
Hans J. Grabe ◽  
Katrin Popowski ◽  
...  

The Glu298→Asp (E298D; 894G→T) polymorphism of eNOS (endothelial nitric oxide synthase) has been related with cardiovascular disease. In the present study, we investigated the association of Glu298→Asp with atherosclerotic plaques in different carotid vessel segments and with carotid IMT (intima-media thickness). The Glu298→Asp eNOS polymorphism was determined by 5′-exonuclease assay among 2448 participants of the SHIP (Study of Health in Pomerania). Mean and maximum common carotid IMT, as well as carotid atherosclerosis, were measured by high-resolution ultrasound. The Asp/Asp298 genotype was associated with an increased risk of atherosclerotic plaques at the level of the common carotid arteries [multivariate odds ratio, 1.57 and 95% CI (confidence interval), 1.05–2.34; P=0.025], but not in the carotid bifurcations or internal or external carotid arteries. Glu298→Asp genotype was not associated with carotid IMT in the whole sample. However, the Asp/Asp298 genotype was independently associated with both higher mean [adjusted increase by 0.046 mm (95% CI, 0.013–0.078); P=0.006] and maximum carotid IMT [0.137 mm (95% CI, 0.064–0.209); P<0.001] in the low-risk group of subjects without carotid atherosclerosis. In conclusion, the Asp/Asp298 genotype is associated with atherosclerosis in the common carotid arteries and, in a low-risk group, also with carotid IMT. This suggests that the association of the Glu298→Asp genotype with atherosclerosis in the carotid arteries is site-specific and is modified by overall cardiovascular risk.


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