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Updated: Jan 25, 2026

Measuring the Carotid to Femoral Pulse Wave Velocity Cf-PWV to Evaluate Arterial Stiffness
Published on: May 3, 2018
Is there a possible relationship between gastric intestinal metaplasia and systemic arterial stiffness?
Ufuk Kutluana1, Ayse Guldem Kilciler2
1Gastroenterology, Usak University Faculty of Medicine, Türkiye.
Background And Aim:
Helicobacter pylori (H. pylori) is closely associated with pre-neoplastic lesions such as atrophic gastritis (AG) and gastric intestinal metaplasia (GIM). The relationshionship between inflammation, hyperhomocysteinemia and arterial stiffness is of pathophysiological relevance for the development of cardiovascular disease. This study aimed to investigate the relationship between vitamin B12, folic acid, homocysteine (Hcy) and pulse wave velocity (PWV) levels in patients with GIM, AG and non-atrophic non-metaplastic chronic gastritis.
Patients And Methods:
ninety-seven patients with GIM, 67 patients with AG and 69 patients with chronic gastritis were included in the study. Glucose, creatinine, total cholesterol, triglyceride, low-density lipoprotein, cholesterol, high-density lipoprotein cholesterol, vitamin B12, folic acid and Hcy levels were measured by biochemical methods. PWV and other vascular parameters were measured using the Phsyio-port AS device.
Main Results:
PWV was higher in patients with GIM and AG than in controls (p < 0.05 and p < 0.05, respectively). Vitamin B12 levels were significantly lower in patients with GIM and AG than in controls (p < 0.01 and p < 0.01, respectively). Folic acid levels were significantly lower in patients with GIM than in controls (p < 0.05). Hcy levels were significantly higher in patients with GIM and AG than in controls (p < 0.001 and p < 0.05, respectively). A logistic regression analysis showed that GIM, AG and vitamin B12 deficiency were predictors for arterial stiffness.
Conclusions:
PWV values increased in patients with GIM and AG compared to non-atrophic non-metaplastic chronic gastritis, without different conventional cardiovascular risk factors.
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