Therapeutic modification of arterial stiffness: An update and comprehensive review

Wu, Ching-Fen

doi:10.4330/wjc.v7.i11.742

Cited by 61 publications

(49 citation statements)

References 117 publications

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“…Life style changes in particular exercise and pharmacological interventions are two potential strategies suggested for decreasing arterial stiffness31. The association between MPV, as a marker of platelet reactivity, and arterial stiffness suggests a potential for antiplatelet agents in modulating arterial stiffness.…”

Section: Discussionmentioning

confidence: 99%

Mean Platelet Volume and Arterial Stiffness – Clinical Relationship and Common Genetic Variability

Panova‐Noeva

Arnold

Hermanns

et al. 2017

Sci Rep

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Vessel wall stiffening is an important clinical parameter, but it is unknown whether platelets, key elements in the pathogenesis of arterial thrombosis, are associated with arterial stiffness. The present studies sought to determine whether mean platelet volume (MPV), a potential marker of platelet activation, is linked to vascular elasticity as assessed by the augmentation index (AIx), in 15,010 individuals from the population-based Gutenberg Health Study. Multivariable analysis showed that MPV in both males (β 0.776; 95thCI [0.250;1.16]; p = 0.0024) and females (β 0.881[0.328;1.43]; p = 0.0018) is strongly associated with AIx. Individuals with MPV and AIx above the sex-specific medians had worse survival. Association analysis between MPV-related genetic variants and arterial stiffness identified four genetic variants in males and one in females related with AIx. Cox regression analysis for mortality identified one of these joint genetic variants close to ring finger protein 145 gene (RNF145, rs10076782) linked with increased mortality (hazard ratio 2.02; 95thCI [1.35;3.02]; p = 0.00061). Thus, these population-based data demonstrate a close relation between platelet volume as a potential marker of platelet activation and arterial stiffness in both sexes. Further research is warranted to further elucidate the mechanisms underlying larger platelets‘ role in arterial stiffening including the role of shared common genetics.

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Section: Discussionmentioning

confidence: 99%

Mean Platelet Volume and Arterial Stiffness – Clinical Relationship and Common Genetic Variability

Panova‐Noeva

Arnold

Hermanns

et al. 2017

Sci Rep

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“…Age is a major determinant of arterial stiffness in large elastic arteries and stiffness increases especially after the age of 55 (20). The patients with overt hyperthyroidism in our study were younger due to Graves' disease, which peaks in the third to fourth decade of life (21).…”

Section: Discussionmentioning

confidence: 87%

Evaluation of ambulatory arterial stiffness index in hyperthyroidism

İyidir¹,

Yalcin²,

Altınova³

et al. 2017

Turk J Med Sci

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Background/aim: Hyperthyroidism causes hemodynamic changes that are associated with adverse cardiovascular outcomes. Twentyfour-hour ambulatory blood pressure monitoring recordings provide us with some essential data: BP variability and ambulatory arterial stiffness index (AASI). In this study, we aimed to investigate AASI and short-term BP variability in both overt and subclinical hyperthyroidism and their relationship with thyroid hormones. Materials and methods:We enrolled 36 patients with subclinical hyperthyroidism, 23 patients with overt hyperthyroidism, and 25 healthy euthyroid controls. ABPM recording was performed for 24 h for all patients.Results: There were no statistically significant differences among the overt hyperthyroidism, subclinical hyperthyroidism, and control groups in terms of AASI (0.43 ± 0.15, 0.38 ± 0.12, 0.42 ± 0.13, respectively; P = 0.315). Variability of diastolic BP was significantly higher in patients with overt hyperthyroidism than in patients with subclinical hyperthyroidism (14.8 ± 2.6 vs. 12.8 ± 2.5%, P = 0.023). There were significant positive correlations between AASI and fT3 (r = 0.246, P = 0.02) and fT4 (r = 0.219, P = 0.04) while TSH was not correlated with AASI (r = 0.023, P = 0.838). After adjusting for confounders, age, 24-h systolic and diastolic BP, variability of systolic and diastolic BP, and fT4 were independent predictors of AASI (r 2 = 0.460, P < 0.001). Conclusion:Although AASI did not differ between overt and subclinical hyperthyroidism, there was a positive relationship between AASI and free thyroid hormone levels. Furthermore, short-term BP variability was higher in overt hyperthyroidism than in subclinical hyperthyroidism.

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“…A plausible connection between COPD and CVD lies in the vascular response to cigarette smoke (a risk factor for the development of COPD)19 and hypoxic pulmonary vasoconstriction 34. Evidence of endothelial dysfunction and vascular re-modeling have been detected both in individuals with COPD and in “healthy” individuals who smoke 18.…”

Section: Discussionmentioning

confidence: 99%

A randomized trial of once-daily fluticasone furoate/vilanterol or vilanterol versus placebo to determine effects on arterial stiffness in COPD

Bhatt¹,

Cockcroft²,

Wang‐Jairaj

et al. 2017

COPD

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IntroductionChronic obstructive pulmonary disease (COPD) is associated with increased cardiovascular morbidity and mortality. Elevated arterial stiffness, measured by aortic pulse wave velocity (aPWV), is a cardiovascular risk surrogate and is potentially modifiable by inhaled corticosteroid/long-acting beta2-agonist combinations in patients with COPD.Materials and methodsThe effects of once-daily inhaled fluticasone furoate/vilanterol (FF/VI) 100/25 µg, VI 25 µg, versus placebo on arterial stiffness in patients with COPD and baseline aPWV ≥11.0 m/s were investigated in a 24-week, multicenter, double-blind, randomized, stratified (by COPD exacerbation history), parallel-group, placebo-controlled trial. Eligible patients were ≥40 years old, with ≥10 pack-year smoking history, forced expiratory volume in 1 s (FEV1)/forced vital capacity ≤0.70, and post-bronchodilator FEV1 ≤70% of predicted. Patients with a major cardiovascular event in the previous 6 months/current severe heart failure/uncontrolled hypertension were excluded. Primary endpoint is change from baseline in aPWV after 24 weeks of treatment. Safety analyses included adverse events (AEs).ResultsThe intent-to-treat population included 430 patients: FF/VI (n=135), VI (n=154), and placebo (n=141). Patients were predominantly male (79%) and Asian or White (each 48%), with a mean age of 68.5 years (standard deviation [SD] =7.9), percentage predicted post-bronchodilator FEV1 50.1% (SD =13.3), and aPWV 13.26 m/s (SD =2.22) at screening. At 24 weeks, mean (standard error [SE]) changes from baseline in aPWV were −1.75 m/s (SE =0.26, FF/VI), −1.95 m/s (SE =0.24, VI), and −1.97 m/s (SE =0.28, placebo). AEs occurred in 57% (FF/VI), 51% (VI), and 41% (placebo) of patients.ConclusionNo differences were observed in aPWV-adjusted mean change from baseline for FF/VI 100/25 µg, compared with placebo.

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Therapeutic modification of arterial stiffness: An update and comprehensive review

Cited by 61 publications

References 117 publications

Mean Platelet Volume and Arterial Stiffness – Clinical Relationship and Common Genetic Variability

Mean Platelet Volume and Arterial Stiffness – Clinical Relationship and Common Genetic Variability

Evaluation of ambulatory arterial stiffness index in hyperthyroidism

A randomized trial of once-daily fluticasone furoate/vilanterol or vilanterol versus placebo to determine effects on arterial stiffness in COPD

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