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Arterial stiffness in type 2 diabetes: determinants and indication of a discriminative value

Monteiro, Clara Italiano; Simões, Rodrigo Polaquini; Goulart, Cássia Luz; Silva, Claudio Donisete da; Borghi-Silva, Audrey; Mendes, Renata Gonçalves.
Clinics ; 76: e2172, 2021. tab, graf
Artículo en Inglés | LILACS | ID: biblio-1153940

OBJECTIVES:

To identify the clinical discriminative value and determinants of arterial stiffness in individuals with type 2 diabetes mellitus (T2DM).

METHODS:

This prospective cohort study included 51 individuals (53.57±9.35 years) diagnosed with T2DM (stage glucose≥126 mg/dL; diagnostic time 87.4±69.8 months). All participants underwent an initial evaluation of personal habits, medications, and history; arterial stiffness assessment by carotid-femoral pulse wave velocity (cfPWV) using SphygmoCor; and blood laboratory analysis. A statistical analysis was performed using SPSS software, and values of p≤0.05 were considered significant.

RESULTS:

A cut-off cfPWV value of 7.9 m/s was identified for T2DM [Sensitivity (SE) 90% and Specificity (SP) 80%]. A subgroup analysis revealed higher glycated hemoglobin (Hb1Ac) (p=0.006), obesity (p=0.036), and dyslipidemia (p=0.013) than those with cfPWV ≥7.9 m/s. Multivariate analysis identified higher stage glucose (p=0.04), Hb1Ac (p=0.04), hypertension (p=0.001), and dyslipidemia (p=0.01) as determinant factors of cfPWV; positive and significant correlation between cfPWV and glucose (r=0.62; p=0.0003) and Hb1Ac (r=0.55; p=0.0031).

CONCLUSIONS:

In T2DM, an indicator of the discriminative value of arterial stiffness was cfPWV of 7.9 m/s. Clinical findings and comorbidities, such as hypertension, glucose, poor glycemic control, and dyslipidemia, were associated with and were determinants of arterial stiffness in T2DM. Reinforcement of monitoring risk factors, such as hypertension, dyslipidemia, and glycemic control, seems to be essential to the process of arterial stiffening. Confirmation of this discriminative value in larger populations is recommended.
Biblioteca responsable: BR1.1