Clinical research
Carotid intima-media thickness and arterial stiffness in type 1 diabetic patients with and without microangiopathy
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Submission date: 2010-07-06
Final revision date: 2010-12-13
Acceptance date: 2010-12-13
Online publication date: 2012-07-04
Publication date: 2012-06-30
Arch Med Sci 2012;8(3):484-490
Introduction: The aim of the study was to assess carotid intima-media thickness (CIMT) as a subclinical marker of atherosclerosis and arterial stiffness in type 1 diabetic patients in relation to microangiopathy.
Material and methods: We included 87 type 1 diabetic patients (44 women, 43 men), median age 34 years (interquartile range [IQR] 29-43), median disease duration 10 years (IQR: 9-14), mean ± standard deviation (SD) glycated haemoglobin (HbA1c) 8.4 ±1.4%. Fifty patients had at least one microangiopathic complication. Intima-media thickness (IMT) of the common carotid artery was measured using high resolution ultrasonography. Arterial stiffness was assessed using digital volume pulse analysis and tonometric measurement of wave reflection and central haemodynamics.
Results: Subjects with microangiopathy compared with those without had higher values of CIMT (median [IQR]: 0.53 mm [0.45-0.60 mm] vs 0.47 mm [0.34-0.52 mm], p = 0.002), higher central augmentation index (CAIx) (mean ± SD: 120.2 ±19.4% vs. 110.5 ±17.1%, p = 0.016) and higher peripheral augmentation index (PAIx) (65.7 ±18.1% vs. 57.2 ±14.9%, p = 0.023). In the logistic regression analysis, the duration of diabetes, systolic and diastolic blood pressure, postprandial glycaemia, HbA1c and triglycerides predicted the presence of diabetic microangiopathy independently of age and sex. The CIMT, CAIx and PAIx were associated with the presence of diabetic microangiopathy only in the univariate model.
Conclusions: In type 1 diabetic patients with microangiopathic complications, increased carotid IMT and arterial stiffness were observed. The study confirms the role of traditional risk factors for late diabetic complications, such as the duration of the disease and metabolic control in the development of microangiopathy.
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