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Vitamin K2-a neglected player in cardiovascular health: a narrative review.
Hariri, E, Kassis, N, Iskandar, JP, Schurgers, LJ, Saad, A, Abdelfattah, O, Bansal, A, Isogai, T, Harb, SC, Kapadia, S
Open heart. 2021;(2)
Abstract
Vitamin K2 serves an important role in cardiovascular health through regulation of calcium homeostasis. Its effects on the cardiovascular system are mediated through activation of the anti-calcific protein known as matrix Gla protein. In its inactive form, this protein is associated with various markers of cardiovascular disease including increased arterial stiffness, vascular and valvular calcification, insulin resistance and heart failure indices which ultimately increase cardiovascular mortality. Supplementation of vitamin K2 has been strongly associated with improved cardiovascular outcomes through its modification of systemic calcification and arterial stiffness. Although its direct effects on delaying the progression of vascular and valvular calcification is currently the subject of multiple randomised clinical trials, prior reports suggest potential improved survival among cardiac patients with vitamin K2 supplementation. Strengthened by its affordability and Food and Drug Adminstration (FDA)-proven safety, vitamin K2 supplementation is a viable and promising option to improve cardiovascular outcomes.
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Beneficial Effect of Statin Therapy on Arterial Stiffness.
Alidadi, M, Montecucco, F, Jamialahmadi, T, Al-Rasadi, K, Johnston, TP, Sahebkar, A
BioMed research international. 2021;:5548310
Abstract
Arterial stiffness describes the increased rigidity of the arterial wall that occurs as a consequence of biological aging and several diseases. Numerous studies have demonstrated that parameters to assess arterial stiffness, especially pulse-wave velocity, are predictive of those individuals that will suffer cardiovascular morbidity and mortality. Statin therapy may be a pharmacological strategy to improve arterial elasticity. It has been shown that the positive benefits of statin therapy on cardiovascular disease is attributable not only to their lipid-lowering capacity but also to various pleiotropic effects, such as their anti-inflammatory, antiproliferative, antioxidant, and antithrombotic properties. Additionally, statins reduce endothelial dysfunction, improve vascular and myocardial remodeling, and stabilize atherosclerotic plaque. The aim of the present review was to summarize the evidence from human studies showing the effects of statins on arterial stiffness.
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Vitamin K-Dependent Matrix Gla Protein as Multifaceted Protector of Vascular and Tissue Integrity.
Wei, FF, Trenson, S, Verhamme, P, Vermeer, C, Staessen, JA
Hypertension (Dallas, Tex. : 1979). 2019;(6):1160-1169
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Abstract
Supplemental Digital Content is available in the text.
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Uric Acid, Vascular Stiffness, and Chronic Kidney Disease: Is There a Link?
Ramirez-Sandoval, JC, Sanchez-Lozada, LG, Madero, M
Blood purification. 2017;(1-3):189-195
Abstract
Controversy exists with regard to the causal role of hyperuricemia in chronic kidney disease. Vascular stiffness may be the link that explains the relation between hyperuricemia and kidney disease. Hyperuricemia is associated with a number of effects on the vascular endothelium and vascular smooth muscle cells, including an increase in oxidative stress, production of vasoconstrictors, and changes on the structural properties of the large artery wall. Observational evidence in large epidemiological cross-sectional studies suggests that there is an independent association between uric acid and arterial stiffness. The limited evidence from cohort studies or clinical trials does not support treatment of hyperuricemia to reduce vascular stiffness in order to prevent kidney disease. Nevertheless, vascular stiffness may be a valid, reproducible, and useful surrogate endpoint. At this point there seems to be sufficient evidence to warrant larger clinical trials to determine whether lowering uric acid concentrations would be useful for prevention or treatment of vascular stiffness and, subsequently, of cardiovascular and kidney diseases. Video Journal Club 'Cappuccino with Claudio Ronco' at http://www.karger.com/?doi=452726.
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Aerobic, resistance and combined exercise training on arterial stiffness in normotensive and hypertensive adults: A review.
Li, Y, Hanssen, H, Cordes, M, Rossmeissl, A, Endes, S, Schmidt-Trucksäss, A
European journal of sport science. 2015;(5):443-57
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Exercise training has different effects on arterial stiffness according to training modalities. The optimal exercise modality for improvement of arterial function in normotensive and hypertensive individuals has not been well established. In this review, we aim to evaluate the effects of aerobic, resistance and combined aerobic and resistance training on arterial stiffness in individuals with and without hypertension. We systematically searched the Pubmed and Web of Science database from 1985 until December 2013 for relevant randomised controlled trials (RCTs). The data were extracted by one investigator and checked by a second investigator. The training effects on arterial stiffness were estimated using weighted mean differences of the relative changes (%) with 95% confidence intervals (CIs). We finally reviewed the results from 17 RCTs. The available evidence indicates that aerobic exercise tends to have a beneficial effect on arterial stiffness in normotensive and hypertensive patients, but does not affect arterial stiffness in patients with isolated systolic hypertension. Resistance exercise has differing effects on arterial stiffness depending on type and intensity. Vigorous resistance training is associated with an increase in arterial stiffness. There seem to be no unfavourable effects on arterial stiffness if the training is of low intensity, in a slow eccentric manner or with lower limb in healthy individuals. Combined training has neutral or even a beneficial effect on arterial stiffness. In conclusion, our review shows that exercise training has varying effects on arterial stiffness depending on the exercise modalities.
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Arterial stiffness and cardiovascular therapy.
Janić, M, Lunder, M, Sabovič, M
BioMed research international. 2014;:621437
Abstract
The world population is aging and the number of old people is continuously increasing. Arterial structure and function change with age, progressively leading to arterial stiffening. Arterial stiffness is best characterized by measurement of pulse wave velocity (PWV), which is its surrogate marker. It has been shown that PWV could improve cardiovascular event prediction in models that included standard risk factors. Consequently, it might therefore enable better identification of populations at high-risk of cardiovascular morbidity and mortality. The present review is focused on a survey of different pharmacological therapeutic options for decreasing arterial stiffness. The influence of several groups of drugs is described: antihypertensive drugs (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, calcium channel blockers, beta-blockers, diuretics, and nitrates), statins, peroral antidiabetics, advanced glycation end-products (AGE) cross-link breakers, anti-inflammatory drugs, endothelin-A receptor antagonists, and vasopeptidase inhibitors. All of these have shown some effect in decreasing arterial stiffness. Nevertheless, further studies are needed which should address the influence of arterial stiffness diminishment on major adverse cardiovascular and cerebrovascular events (MACCE).
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Arterial stiffness and cognitive function in the elderly.
Zeki Al Hazzouri, A, Yaffe, K
Journal of Alzheimer's disease : JAD. 2014;(0 4):S503-14
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Cognitive decline and dementia are a major cause of disability and mortality among older adults. Cross-sectional evidence from observational studies suggests that greater arterial stiffness is associated with worse cognitive performance. These associations have been observed on measures of global cognition and across multiple domains of cognition. Epidemiologic evidence on the association between arterial stiffness and rate of cognitive decline has been less definitive, and very few studies have investigated the risk of developing dementia. This review summarizes the current research on arterial stiffness and cognition, issues around measurement, and the effect that potential intervention might have on the course of cognitive aging. The evidence on pharmacological and non-pharmacological (exercise, nutrition, etc.) interventions in older adults with arterial stiffness is promising. Yet there are no studies or trials that directly evaluate how interventions of arterial stiffness reduce or prevent cognitive impairment and risk of developing dementia. More research is needed to elucidate the causal link between arterial stiffness and cognitive decline and dementia, and to identify whether potential interventions to prevent or reduce arterial stiffness may benefit cognitive health of the elderly.
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Aerobic exercise and other healthy lifestyle factors that influence vascular aging.
Santos-Parker, JR, LaRocca, TJ, Seals, DR
Advances in physiology education. 2014;(4):296-307
Abstract
Cardiovascular diseases (CVDs) remain the leading cause of death in the United States and other modern societies. Advancing age is the major risk factor for CVD, primarily due to stiffening of the large elastic arteries and the development of vascular endothelial dysfunction. In contrast, regular aerobic exercise protects against the development of large elastic artery stiffness and vascular endothelial dysfunction with advancing age. Moreover, aerobic exercise interventions reduce arterial stiffness and restore vascular endothelial function in previously sedentary middle-aged/older adults. Aerobic exercise exerts its beneficial effects on arterial function by modulating structural proteins, reducing oxidative stress and inflammation, and restoring nitric oxide bioavailability. Aerobic exercise may also promote "resistance" against factors that reduce vascular function and increase CVD risk with age. Preventing excessive increases in abdominal adiposity, following healthy dietary practices, maintaining a low CVD risk factor profile, and, possibly, selective use of pharmaceuticals and nutraceuticals also play a major role in preserving vascular function with aging.
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Evaluation of blood pressure control using a new arterial stiffness parameter, cardio-ankle vascular index (CAVI).
Shirai, K, Utino, J, Saiki, A, Endo, K, Ohira, M, Nagayama, D, Tatsuno, I, Shimizu, K, Takahashi, M, Takahara, A
Current hypertension reviews. 2013;(1):66-75
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Abstract
Arterial stiffness has been known to be a surrogate marker of arteriosclerosis, and also of vascular function. Pulse wave velocity (PWV) had been the most popular index and was known to be a predictor of cardiovascular events. But, it depends on blood pressure at measuring time. To overcome this problem, cardio-ankle vascular index (CAVI) is developed. CAVI is derived from stiffness parameter β by Hayashi, and the equation of Bramwell-Hill, and is independent from blood pressure at a measuring time. Then, CAVI might reflect the proper change of arterial wall by antihypertensive agents. CAVI shows high value with aging and in many arteriosclerotic diseases and is also high in persons with main coronary risk factors. Furthermore, CAVI is decreased by an administration of α1 blocker, doxazosin for 2-4 hours, Those results suggested that CAVI reflected the arterial stiffness composed of organic components and of smooth muscle cell contracture. Angiotensin II receptor blocker, olmesartan decreased CAVI much more than that of calcium channel antagonist, amlodipine, even though the rates of decreased blood pressure were almost same. CAVI might differentiate the blood pressure-lowering agents from the point of the effects on proper arterial stiffness. This paper reviewed the principle and rationale of CAVI, and the possibilities of clinical applications, especially in the studies of hypertension.
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Effects of antihypertensive drugs on arterial stiffness.
Dudenbostel, T, Glasser, SP
Cardiology in review. 2012;(5):259-63
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In this review, we discuss the possible pathophysiological mechanisms and the role of arterial stiffness as a biomarker, a blood pressure-independent predictor of cardiovascular morbidity and mortality. The effects of different antihypertensive drug classes on noninvasively assessed markers of arterial stiffness are also discussed. Current evidence will be reviewed regarding the effect of drugs on arterial stiffness, including the peripheral and central effects of angiotensin-converting enzyme inhibitors, angiotensin receptor antagonists, dihydropyridine calcium channel blockers, beta blockers (including vasodilating beta blockers), diuretics, and mineralocorticoid antagonists.