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Potential Mechanisms of Sodium-Glucose Co-Transporter 2 Inhibitor-Related Cardiovascular Benefits.
Verma, S
The American journal of cardiology. 2019;:S36-S44
Abstract
The findings of recent clinical trials have shown that sodium-glucose co-transporter 2 (SGLT2) inhibitors produce effects beyond glucose lowering and have demonstrated beneficial cardiovascular effects that have been observed across a broad range of patients with type 2 diabetes mellitus. In particular, the cardiovascular benefit results largely from substantial and early effects of SGLT2 inhibition on cardiovascular death and hospitalization for heart failure. Recent cardiovascular outcomes trials (CVOTs) have also shown that relative risk reductions in cardiovascular outcomes were observed with SGLT2 inhibition both in patients with current and prior heart failure. Since the observed reductions of cardiovascular outcomes with SGLT2 inhibitor therapy were observed much earlier than would be expected by an anti-atherosclerotic effect, these results have led to speculation about the potential underlying pathways. Suggested mechanisms include natriuresis and osmotic diuresis; reductions in inflammation, oxidative stress, and arterial stiffness; reductions in blood pressure and body weight; and possible renoprotective effects. These effects could produce cardiovascular benefits through a range of cardiac effects, including reduction in left ventricular load, attenuation of cardiac fibrosis and inflammation, and improved myocardial energy production. Other possible mechanisms include inhibition of sodium-hydrogen exchange, increases in erythropoietin levels, and reduction in myocardial ischemia or reperfusion injury. It is likely that a range of mechanisms underlie the observed cardiovascular benefits of SGLT2 inhibitors; further elucidation of these mechanisms will be answered by ongoing research.
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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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3.
A systematic review of arterial stiffness, wave reflection and air pollution.
Zanoli, L, Lentini, P, Granata, A, Gaudio, A, Fatuzzo, P, Serafino, L, Rastelli, S, Fiore, V, D'Anca, A, Signorelli, SS, et al
Molecular medicine reports. 2017;(5):3425-3429
Abstract
Arterial stiffening is associated with increased cardiovascular risk. Whether exposure to relatively high levels of air pollution is associated with arterial stiffening is unclear. We aimed to assess the association between exposure to major air pollutants and arterial stiffening. PubMed, SCOPUS and Web of Science databases (through 31 January 2017) were searched using a combination of terms related to exposure to gaseous [nitrogen dioxide (NO2), nitrogen oxides (NOx) and sulphur dioxide (SO2)] or particulate matter pollutants (PM2.5, PM10 and PM10-2.5), arterial stiffness (pulse wave velocity) and reflected waves (augmentation index, augmentation pressure). Pertinent information were extracted from selected studies. In this systematic review were included 8 studies with available data on air pollution and arterial stiffness/reflected waves parameters (8 studies explored the effects of exposure to particulate matter pollutants, 3 studies the effects of exposure to gaseous pollutants); seven of them reported increased arterial stiffness/reflected waves after exposure to air pollution (6 of 8 studies after particulate matter pollutants; 2 of 3 studies after gaseous pollutants). Arterial stiffness and reflected waves were increased in the majority of the studies after both short- and long-term exposure to air pollutants. In conclusion, available evidence supports an association of main air pollutants with increased arterial stiffness and reflected waves. This finding may have implications for population-based strategies for the reduction of arterial stiffness, a vascular biomarker and an intermediate endpoint for cardiovascular disease.
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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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Effect of vitamin D supplementation on measures of arterial stiffness: a systematic review and meta-analysis of randomized controlled trials.
Rodríguez, AJ, Scott, D, Srikanth, V, Ebeling, P
Clinical endocrinology. 2016;(5):645-57
Abstract
BACKGROUND Low vitamin D has been associated with poor arterial compliance in observational studies. Arterial stiffness has prognostic value for cardiovascular disease risk. The aim of this systematic review was to clarify the literature surrounding the use of vitamin D to ameliorate arterial stiffness. METHODS We conducted a systematic review of the MEDLINE, Scopus and EMBASE databases for randomized controlled clinical trials investigating the effect of vitamin D supplementation on pulse wave velocity (PWV) and/or augmentation index (AI) as indicators of arterial stiffness. We meta-analysed data and calculated standardized mean difference (SMD) and 95% confidence intervals (CI) using inverse-variance models on RevMan v5.3 software. Study quality was assessed using a modified Jadad scale. RESULTS A total of 607 unique records were identified, of which 18 satisfied our inclusion and exclusion criteria. Study quality was high, ranging from 9 to 12 (of 13). Study design in terms of vitamin D dosing protocol (range: 1000-5700 IU/day), follow-up times (range: 1-12 months), sample size (range: n = 29-183) and recruitment strategies varied markedly. Thirteen studies had data for meta-analysis. Vitamin D was associated with nonsignificant reductions in PWV [SMD = -0·10; 95% CI: -0·24, 0·04; P = 0·17; n = 806 from ten studies] and AI [-0·15; -0·32, 0·02; 0·08; n = 551 from eight studies]. DISCUSSION There is inconsistent evidence to suggest that vitamin D supplementation improves indicators of arterial stiffness. This may be attributable to the heterogeneity in study design. Therefore, large and well-designed randomized studies are required to determine the casual relationships between vitamin D and arterial stiffness and cardiovascular risk.
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Effect of cholecalciferol supplementation on arterial stiffness: a systematic review and meta-analysis.
Upala, S, Sanguankeo, A, Congrete, S, Jaruvongvanich, V
Scandinavian cardiovascular journal : SCJ. 2016;(4):230-5
Abstract
BACKGROUND Vitamin D deficiency increases risk of cardiovascular diseases, arterial stiffness, and endothelial dysfunction. We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) investigating the impact of vitamin D supplementation on arterial stiffness. METHODS A comprehensive search of the databases of the Cochrane Central Register of Controlled Trials, MEDLINE, and EMBASE was performed from inception through November 2015. The inclusion criterion was RCTs that assessed the impact of cholecalciferol supplementation in adults on the surrogate markers of arterial stiffness (aortic pulse wave velocity (PWV) and augmentation index (AIx)). Outcome was the pooled mean difference (MD) of PWV and AIx between the vitamin D supplementation (intervention) group and placebo. RESULTS The initial search yielded 1164 articles. Twenty-eight articles underwent full-length review and data were extracted from seven RCTs involving totally 547 participants. Dose of cholecalciferol supplementation varied from 1000 IU/day to 120,000 IU/month of cholecalciferol. Duration of treatment ranged from 2 to 12 months. There was no significant difference in the change of PWV (pooled MD = 0.18, 95% CI: -0.17 to 0.52 or AIx (pooled MD = 2.39, 95% CI: -4.43 to 4.92) between the intervention group and placebo. CONCLUSIONS There was no improvement of markers of arterial stiffness after vitamin D supplementation.
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Effects of statin therapy on augmentation index as a measure of arterial stiffness: A systematic review and meta-analysis.
Sahebkar, A, Pećin, I, Tedeschi-Reiner, E, Derosa, G, Maffioli, P, Reiner, Ž
International journal of cardiology. 2016;:160-8
Abstract
OBJECTIVE To evaluate the effects of statin therapy on augmentation index (AIx) as a measure of arterial stiffness using a meta-analysis of clinical trials. METHODS The search included PubMed-Medline, Embase, SCOPUS, Web of Science and Google Scholar databases to identify randomized controlled trials investigating the effects of statin therapy on arterial stiffness measured as AIx. A random-effects model and generic inverse variance method were used for quantitative data synthesis. Sensitivity analysis was conducted using the leave-one-out method. Random-effects meta-regression was performed using unrestricted maximum likelihood method to evaluate the impact of potential confounders. RESULTS 18 trials examining the effects of statin therapy on arterial stiffness were included. A significant reduction in aortic AIx following statin therapy was proven (WMD: -2.40%, 95% CI: -4.59, -0.21, p=0.032; I(2): 51.20%). HR-adjusted AIx 75% values also revealed a significant improvement by statin therapy (WMD: -5.04%, 95% CI: -7.81, -2.27, p<0.001; I(2): 0%), but not when analysis was restricted to unadjusted AIx values (WMD: -2.30%, 95% CI: -4.83, 0.23, p=0.075; I(2): 53.83%). There was no significant change in carotid (WMD: -2.75%, 95% CI: -8.06, 2.56, p=0.309; I(2): 26.86%) and peripheral (WMD: 0.25%, 95% CI: -3.31, 3.82, p=0.889; I(2): 72.19%) AIx due to statin treatment. There was also no difference in the effect size calculated for different statins subgroups. The impact of statins on AIx was independent of LDL-cholesterol level (slope: 0.05; 95% CI: -0.02, 0.13; p=0.181). CONCLUSION Statin therapy causes a significant reduction in aortic AIx which is independent of LDL-cholesterol changes.
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The impact of angiotensin receptor blockers on arterial stiffness: a meta-analysis.
Peng, F, Pan, H, Wang, B, Lin, J, Niu, W
Hypertension research : official journal of the Japanese Society of Hypertension. 2015;(9):613-20
Abstract
Some studies reported a protective role of angiotensin receptor blockers (ARBs) against arterial stiffness. Therefore, we performed a meta-analysis of published clinical trials to systematically assess the impact of ARBs on arterial stiffness as measured by using pulse wave velocity (PWV). Eligible articles were identified by searching PubMed, EMBASE, Cochrane, Wanfang and CNKI databanks before 31 July 2014. The data were extracted independently and in duplicate. Forty articles including 53 clinical trials qualified, including 1650 and 1659 subjects in ARB treatment and control groups, respectively. Overall reductions in carotid-femoral PWV (cfPWV) and brachial-ankle PWV (baPWV) were statistically significant, with an average of -42.52 cm s(-1) (95% CI: -81.82 to -3.21; P=0.034) and -107.08 cm s(-1) (95% CI: -133.98 to -80.18; P<0.0005), respectively, after receiving ARBs. Subgroup analysis by ARB type revealed that telmisartan (weighted mean difference or WMD=-100.82 cm s(-1); P<0.0005) and valsartan (WMD=-104.59 cm s(-1); P<0.0005) significantly reduced baPWV, but only valsartan reduced cfPWV (WMD=-65.58; P=0.030). cfPWV was significantly reduced in comparisons of ARBs with placebo (WMD=-79.65 cm s(-1); P=0.001), and baPWV was significantly reduced with calcium channel blockers (WMD=-130.74 cm s(-1); P<0.0005). There were low probabilities of publication bias. Taken together, our findings support the important role of ARB treatment in improving arterial stiffness.
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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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Abstract
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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Exercise and dietary influences on arterial stiffness in cardiometabolic disease.
Sacre, JW, Jennings, GL, Kingwell, BA
Hypertension (Dallas, Tex. : 1979). 2014;(5):888-93