Effects of rosuvastatin on subclinical atherosclerosis and arterial stiffness in rheumatoid arthritis: a randomized controlled pilot trial

Tam, Lai‐Shan; Li, E K; Shang, Qing; Tomlinson, Brian; Lee, V W; Lee, K K; Li, M; Kuan, Woon Pang; Li, T K; Tseung, Lorraine; Yip, Gabriel Wai-Kwok; Freedman, Ben; Yu, CM

doi:10.3109/03009742.2011.586649

Cited by 43 publications

(29 citation statements)

References 57 publications

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“…202 Generally, it is thought that statins do not induce any improvement in arterial stiffness, yet some clinical trials have suggested that statins are beneficial in reducing arterial stiffness because of their pleiotropic anti-inflammatory effects. [203][204][205] SUMMARY Stiffening of the PAs (both large elastic and, likely, small resistance vessels) occurs in all forms of PH to some degree or another. In PH, it is still not clear whether arterial stiffening is a cause or a consequence, a question that will have to be addressed separately in all the different classes and forms of PH.…”

Section: Anti-inflammatory Agentsmentioning

confidence: 99%

Vascular Stiffening in Pulmonary Hypertension: Cause or Consequence? (2013 Grover Conference Series)

et al. 2014

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Recent studies have indicated that systemic arterial stiffening is a precursor to hypertension and that hypertension, in turn, can perpetuate arterial stiffening. Pulmonary artery (PA) stiffening is also well documented to occur in pulmonary hypertension (PH), and there is evidence that pulmonary vascular stiffness (PVS) may be a better predictor of outcome than pulmonary vascular resistance (PVR). We have hypothesized that the decreased flow-damping function of elastic PAs in PH likely initiates and/or perpetuates dysfunction of pulmonary microvasculature. Recent studies have shown that large-vessel stiffening increases flow pulsatility in the distal pulmonary vasculature, leading to endothelial dysfunction within a proinflammatory, vasoconstricting, and profibrogenic environment. The intricate role of stiffening-stimulated high pulsatile flow in endothelial cell dysfunction includes stepwise molecular events underlying PA hypertrophy, inflammation, endothelial-mesenchymal transition, and fibrosis. In addition to contributing to microenvironmental alterations of the distal vasculature, disordered proximal-distal PA coupling likely also plays a role in increasing ventricular afterload, ultimately causing right ventricle (RV) dysfunction and death. Current therapeutic treatments do not provide a realistic approach to destiffening arteries and, thus, to potentially abrogating the effects of high pulsatile flow on the distal pulmonary vasculature or the increased work imposed by stiffening on the RV. Scrutinizing the effect of PA stiffening on high pulsatile flow-induced cellular and molecular changes, and vice versa, might lead to important new therapeutic options that abrogate PA remodeling and PH development. With a clear understanding that PA stiffening may contribute to the progression of PH to an irreversible state by contributing to chronic microvascular damage in lungs, future studies should be aimed first at defining the underlying mechanisms leading to PA stiffening and then at improved treatment approaches based on these findings.Keywords: pulmonary hypertension, arterial stiffening, wave reflection, smooth muscle cell, endothelial cell, inflammation, right ventricle, treatment. Arterial stiffening is increasingly recognized as a risk factor of cardiovascular events as well as a guide for pharmacological treatment of cardiovascular diseases. Yet its exact role in the development and progression of cardiovascular diseases such as hypertension remains elusive. A recent study, however, presented convincing data supporting the possibility of a cause-effect relationship between arterial stiffness and systemic hypertension: higher levels of arterial stiffness and central pressures preceded and were associated with an increased risk of hypertension, but hypertension did not cause arterial stiffness. 1This work demonstrated that increased vascular stiffness could be a precursor to hypertension. A key implication from these observations is that arterial stiffness, when used as a measure of cardiovascula...

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Section: Anti-inflammatory Agentsmentioning

confidence: 99%

Vascular Stiffening in Pulmonary Hypertension: Cause or Consequence? (2013 Grover Conference Series)

et al. 2014

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“…This raised the hypothesis that the pleiotropic anti-inflammatory effects of statins may have similar benefits. Early clinical trials suggest that they may do 45,46 but absence of an antihypertensive effect of statins argues against an important improvement of arterial stiffness. 47 Benefits for statin treatment in reduction of arterial stiffness above general cardiovascular risk reduction have not been demonstrated.…”

Section: Therapeutic Interventionmentioning

confidence: 99%

Arterial stiffness

Quinn

Tomlinson

Cockcroft³

2012

JRSM Cardiovascular Disease

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Measurements of biomechanical properties of arteries have become an important surrogate outcome used in epidemiological and interventional cardiovascular research. Structural and functional differences of vessels in the arterial tree result in a dampening of pulsatility and smoothing of blood flow as it progresses to capillary level. A loss of arterial elastic properties results a range of linked pathophysiological changes within the circulation including increased pulse pressure, left ventricular hypertrophy, subendocardial ischaemia, vessel endothelial dysfunction and cardiac fibrosis. With increased arterial stiffness, the microvasculature of brain and kidneys are exposed to wider pressure fluctuations and may lead to increased risk of stroke and renal failure. Stiffening of the aorta, as measured by the gold-standard technique of aortic Pulse Wave Velocity (aPWV), is independently associated with adverse cardiovascular outcomes across many different patient groups and in the general population. Therefore, use of aPWV has been proposed for early detection of vascular damage and individual cardiovascular risk evaluation and it seems certain that measurement of arterial stiffness will become increasingly important in future clinical care. In this review we will consider some of the pathophysiological processes that result from arterial stiffening, how it is measured and factors that may drive it as well as potential avenues for therapy. In the face of an ageing population where mortality from atheromatous cardiovascular disease is falling, pathology associated with arterial stiffening will assume ever greater importance. Therefore, understanding these concepts for all clinicians involved in care of patients with cardiovascular disease will become vital.

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“…To our knowledge only two studies have examined the SEVR in patients with RA [17,18]; one small pilot study revealed that the SEVR improved following 12 months of lipid-lowering treatment when compared with a group receiving only a placebo drug [17], while in another study the SEVR was worse following 7 weeks of anti-inflammatory treatment in RA and ankylosing spondylitis patients [18]. However, the small sample sizes of both studies, as well as the inclusion of different patient groups in the latter study, make these findings difficult to interpret.…”

Section: Introductionmentioning

confidence: 99%

The role of inflammation, the autonomic nervous system and classical cardiovascular disease risk factors on subendocardial viability ratio in patients with RA: a cross-sectional and longitudinal study

Sandoo

Protogerou²,

Hodson

et al. 2012

Arthritis Res Ther

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IntroductionEvidence indicates that rheumatoid arthritis (RA) patients have increased susceptibility to myocardial ischaemia that contributes to myocardial infarction. The subendocardial viability ratio (SEVR) can be measured using pulse wave analysis and reflects myocardial oxygen supply and demand. The objective of the present study was to examine specific predictors of SEVR in RA patients, with a specific focus on inflammation and classical cardiovascular disease (CVD) risk factors.MethodsTwo patient cohorts were included in the study; a primary cohort consisting of 220 RA patients and a validation cohort of 127 RA patients. All patients underwent assessment of SEVR using pulse wave analysis. Thirty-one patients from the primary cohort who were about to start anti-inflammatory treatment were prospectively examined for SEVR at pretreatment baseline and 2 weeks, 3 months and 1 year following treatment. Systemic markers of disease activity and classical CVD risk factors were assessed in all patients.ResultsThe SEVR (mean ± standard deviation) for RA in the primary cohort was 148 ± 27 and in the validation cohort was 142 ± 25. Regression analyses revealed that all parameters of RA disease activity were associated with SEVR, along with gender, blood pressure and heart rate. These findings were the same in the validation cohort. Analysis of longitudinal data showed that C-reactive protein (P < 0.001), erythrocyte sedimentation rate (P < 0.005), Disease Activity Score in 28 joints (P < 0.001), mean blood pressure (P < 0.005) and augmentation index (P < 0.001) were significantly reduced after commencing anti-TNFα treatment. Increasing C-reactive protein was found to be associated with a reduction in SEVR (P = 0.02) and an increase in augmentation index (P = 0.001).ConclusionThe present findings reveal that the SEVR is associated with markers of disease activity as well as highly prevalent classical CVD risk factors in RA, such as high blood pressure and diabetes. Further prospective studies are required to determine whether the SEVR predicts future cardiac events in RA.

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Effects of rosuvastatin on subclinical atherosclerosis and arterial stiffness in rheumatoid arthritis: a randomized controlled pilot trial

Abstract: Our data suggest that rosuvastatin has a modest anti-inflammatory effect in RA patients with low disease activity in terms of reduction in DAS and fibrinogen level. Rosuvastastin may also improve subendocardial perfusion and lower the urate level.

Cited by 43 publications

References 57 publications

Vascular Stiffening in Pulmonary Hypertension: Cause or Consequence? (2013 Grover Conference Series)

Vascular Stiffening in Pulmonary Hypertension: Cause or Consequence? (2013 Grover Conference Series)

Arterial stiffness

The role of inflammation, the autonomic nervous system and classical cardiovascular disease risk factors on subendocardial viability ratio in patients with RA: a cross-sectional and longitudinal study

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