Therapeutic Modulation of Aortic Stiffness

Hussein, A. M.; Shaaya, Ghazwan; Arora, Rohit; Al-Khazaali, Ali; Al-Khafaji, Khalid; Helu, Hanan K.

doi:10.1097/mjt.0000000000000408

Cited by 9 publications

(3 citation statements)

References 86 publications

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“…Reduction in inflammation can decrease arterial stiffness, which was demonstrated among others in patients with rheumatoid arthritis (RA) undergoing therapy with anti-tumor necrosis factor-α (TNF-α) agents ( 21 ). Also, statins and other cholesterol-reducing agents are reported in numerous studies to have beneficial effects on wave reflection and aortic stiffness reduction in several patient groups ( 45 , 46 ).…”

Section: Mechanisms Underlying the Link Between Inflammation And Artementioning

confidence: 99%

Inflammatory Markers for Arterial Stiffness in Cardiovascular Diseases

Malainer²,

et al. 2017

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Arterial stiffness predicts an increased risk of cardiovascular events. Inflammation plays a major role in large arteries stiffening, related to atherosclerosis, arteriosclerosis, endothelial dysfunction, smooth muscle cell migration, vascular calcification, increased activity of metalloproteinases, extracellular matrix degradation, oxidative stress, elastolysis, and degradation of collagen. The present paper reviews main mechanisms explaining the crosstalk between inflammation and arterial stiffness and the most common inflammatory markers associated with increased arterial stiffness, considering the most recent clinical and experimental studies. Diverse studies revealed significant correlations between the severity of arterial stiffness and inflammatory markers, such as white blood cell count, neutrophil/lymphocyte ratio, adhesion molecules, fibrinogen, C-reactive protein, cytokines, microRNAs, and cyclooxygenase-2, in patients with a broad variety of diseases, such as metabolic syndrome, diabetes, coronary heart disease, peripheral arterial disease, malignant and rheumatic disorders, polycystic kidney disease, renal transplant, familial Mediterranean fever, and oral infections, and in women with preeclampsia or after menopause. There is strong evidence that inflammation plays an important and, at least, partly reversible role in the development of arterial stiffness, and inflammatory markers may be useful additional tools in the assessment of the cardiovascular risk in clinical practice. Combined assessment of arterial stiffness and inflammatory markers may improve non-invasive assessment of cardiovascular risk, enabling selection of high-risk patients for prophylactic treatment or more regular medical examination. Development of future destiffening therapies may target pro-inflammatory mechanisms.

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Section: Mechanisms Underlying the Link Between Inflammation And Artementioning

confidence: 99%

Inflammatory Markers for Arterial Stiffness in Cardiovascular Diseases

Malainer²,

et al. 2017

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“…However, there is no gold standard for distinguishing between adiponectin isoform levels [32]. Finally, many prescription drugs used by the patients have been reported to affect AS, such as oral hypoglycemic agents, antihypertensive drugs, and statins [33]. However, no significant associations between these drugs and AS have been found.…”

Section: Discussionmentioning

confidence: 99%

Association of Low Serum Adiponectin Levels with Aortic Arterial Stiffness in Patients with Type 2 Diabetes

Shih

Hsu

Hou

et al. 2019

JCM

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Adiponectin, an anti-inflammatory and anti-atherogenic protein, affects glucose metabolism. High serum adiponectin levels are associated with decreased diabetes mellitus (DM) risks. Aortic arterial stiffness (AS) is associated with cardiovascular disease and mortality in type 2 DM patients. We assessed the association between adiponectin levels and aortic AS in type 2 DM patients. We measured serum adiponectin levels in 140 volunteers with type 2 DM and assigned patients with carotid–femoral pulse wave velocity (cfPWV) >10 m/s to the aortic AS group (n = 54, 38.6%). These patients had higher systolic (p = 0.001) and diastolic (p = 0.010) blood pressures; body fat masses (p = 0.041); serum triglyceride (p = 0.026), phosphorus (p = 0.037), and insulin (p = 0.040) levels; and homeostasis model assessment of insulin resistance values (p = 0.029) and lower estimated glomerular filtration rates (p = 0.009) and serum adiponectin levels (p = 0.001) than controls. Multivariable logistic regression analysis adjusted for confounders showed serum adiponectin levels (OR 0.922; 95% CI, 0.876–0.970; p = 0.002) as an independent predictor of aortic AS. Multivariable forward stepwise linear regression analyses showed that serum adiponectin levels (β = −0.283, adjusted R2 change: 0.054, p < 0.001) were negatively associated with cfPWV. Thus, serum adiponectin level is an independent predictor of aortic AS in type 2 DM patients.

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“…134, 135 Pharmacological interventions, diuretics, ACE inhibitors, AT-1R and MR antagonists have shown some effect in decreasing excessive arterial and cardiac stiffening. 9, 15, 136–139 The Joint National Committee-8 (JNC8) and the European Society of Hypertension (ESH) recommend that MR antagonists may be considered as the “fourth-line” drug in the treatment of the resistant hypertension. 140 Clinical trials also suggest that MR antagonists present an effective approach in patients with heart failure.…”

Section: Risk Factors In the Pathogenesis Of Increased Arterial And Cmentioning

confidence: 99%