Effects of coexisting hypertension and type II diabetes mellitus on arterial stiffness

Tedesco, Michele Adolfo; Natale, Francesco; Salvo, Giovanni Di; Caputo, Salvatore; Capasso, Michele; Calabrò, Raffaele

doi:10.1038/sj.jhh.1001690

Cited by 90 publications

(73 citation statements)

References 28 publications

(27 reference statements)

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“…Furthermore, we cannot yet determine if the adverse outcomes associated with this pressure-metabolic interaction in these patients are mediated by increased arterial stiffening, as a cross-sectional study (such as that by Tedesco et al 8 ) does not provide any data on the prospective outcomes of these patients. Nonetheless, their study highlights the need for a more global approach to the management of patients with type II diabetes and hypertension.…”

mentioning

confidence: 99%

Arterial stiffness in diabetes and hypertension

Lim

Lip

2004

J Hum Hypertens

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mentioning

confidence: 99%

Arterial stiffness in diabetes and hypertension

Lim

Lip

2004

J Hum Hypertens

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“…Indeed, patients with both hypertension and diabetes mellitus seem to have a stiffer aorta compared with patients with only one of these conditions [17]. Several specific pathophysiological mechanisms are involved in the development of arterial stiffness in type 2 diabetes mellitus, with endothelial dysfunction playing a relevant role [14].…”

Section: Introductionmentioning

confidence: 99%

Type 2 diabetes mellitus worsens arterial stiffness in hypertensive patients through endothelial dysfunction

et al. 2012

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Aims/hypothesis Endothelium-derived factors are thought to be physiological modulators of large artery stiffness. The aim of the study was to investigate whether endothelial function could be a determinant of arterial stiffness in essential hypertensive patients, in relation with the concomitant presence of type 2 diabetes mellitus. Methods The study included 341 participants (84 hypertensive patients with and 175 without type 2 diabetes mellitus, 82 matched controls). Brachial artery endotheliumdependent flow-mediated dilation (FMD) was determined by high-resolution ultrasound and computerised edge detection system. Applanation tonometry was used to measure carotid-femoral pulse wave velocity (PWV). Results Hypertensive patients with diabetes had higher PWV (10.1±2.3 m/s vs 8.6±1.4 m/s, p<0.001) and lower FMD (3.51±2.07 vs 5.16±2.96%, p<0.001) than non-diabetic hypertensive patients, who showed impaired vascular function when compared with healthy participants (7.9±1.6 m/s and 6.68 ± 3.67%). FMD was significantly and negatively correlated to PWV only in hypertensive diabetic patients (r0−0.456, p<0.001), but not in hypertensive normoglycaemic patients (r0−0.088, p00.248) or in healthy participants (r 00.008, p 00.946). Multivariate analysis demonstrated that, in the diabetic group, FMD remained an independent predictor of PWV after adjustment for confounders (r 2 00.083, p 00.003). Subgroup analysis performed in non-diabetic hypertensive patients revealed that neither obesity nor the metabolic syndrome affected the relationship between FMD and PWV. Conclusions/interpretation Endothelial dysfunction is a determinant of aortic stiffness in hypertensive diabetic patients but not in hypertensive patients without diabetes. These results suggest that type 2 diabetes mellitus on top of hypertension might worsen arterial compliance by endothelium-related mechanisms.

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“…8 The rapidly growing number of patients with coexisting diabetes and hypertension must be intensively treated to protect them from their very high risk for premature cardiovascular morbidity and mortality. 9 Recent research into the pathophysiology of type 2 DM has led to the introduction of new medications like glucagon-like peptide 1 analogues: dipeptidyl peptidase-IV inhibitors, inhibitors of the sodium-glucose co-transporter 2 and 11ß-hydroxysteroid dehydrogenate 1, insulin-releasing glucokinase activators and pancreatic-G-protein-coupled fatty-acid-receptor agonists, glucagon-receptor antagonists, metabolic inhibitors of hepatic glucose output and quick-release bromocriptine. Inhaled insulin was licensed for use in 2006 but has been withdrawn from the market because of low patronage.…”

Section: Introductionmentioning

confidence: 99%