Cardiovascular involvement in systemic rheumatic diseases: An integrated view for the treating physicians

Lee, Kwang Seob; Kronbichler, Andreas; Eisenhut, Michael; Lee, Keum Hwa; Smıth, Lee

doi:10.1016/j.autrev.2017.12.001

Cited by 44 publications

(38 citation statements)

References 209 publications

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“…These factors together support normal circulatory function and its adaptive response to adverse environmental challenges, disturbance of which can predispose to atherosclerosis (Kim et al, 2013; Lee et al, 2013). Factors leading to atherosclerosis include consumption of high-fat and cholesterol diet (Marir et al, 2013), dyslipidemia (Sanin et al, 2017), diabetes (Lehrke and Marx, 2017), chronic inflammation (Lee et al, 2018), genetic risk (Whayne, and Saha, 2019), lack of exercise (Yang J. et al, 2017), hypertension (Hurtubise et al, 2016), social stress (Meng et al, 2019), smoking and other unhealthy life-styles or environmental factors (Niemann et al, 2017). As shown in a cohort study in Mexico, the coronary risk factors observed were dyslipidemia (100%), hypertension (86%), obesity/overweight (75%), metabolic syndrome (71%), smoking (68%), and diabetes (58%) (Rettori et al, 2014).…”

Section: Atherosclerosis and Cardioprotective Effect Of Otmentioning

confidence: 99%

Therapeutic Potential of Oxytocin in Atherosclerotic Cardiovascular Disease: Mechanisms and Signaling Pathways

Wang

Yang

et al. 2019

Front. Neurosci.

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Coronary artery disease (CAD) is a major cardiovascular disease responsible for high morbidity and mortality worldwide. The major pathophysiological basis of CAD is atherosclerosis in association with varieties of immunometabolic disorders that can suppress oxytocin (OT) receptor (OTR) signaling in the cardiovascular system (CVS). By contrast, OT not only maintains cardiovascular integrity but also has the potential to suppress and even reverse atherosclerotic alterations and CAD. These protective effects of OT are associated with its protection of the heart and blood vessels from immunometabolic injuries and the resultant inflammation and apoptosis through both peripheral and central approaches. As a result, OT can decelerate the progression of atherosclerosis and facilitate the recovery of CVS from these injuries. At the cellular level, the protective effect of OT on CVS involves a broad array of OTR signaling events. These signals mainly belong to the reperfusion injury salvage kinase pathway that is composed of phosphatidylinositol 3-kinase-Akt-endothelial nitric oxide synthase cascades and extracellular signal-regulated protein kinase 1/2. Additionally, AMP-activated protein kinase, Ca 2+ /calmodulin-dependent protein kinase signaling and many others are also implicated in OTR signaling in the CVS protection. These signaling events interact coordinately at many levels to suppress the production of inflammatory cytokines and the activation of apoptotic pathways. A particular target of these signaling events is endoplasmic reticulum (ER) stress and mitochondrial oxidative stress that interact through mitochondria-associated ER membrane. In contrast to these protective effects and machineries, rare but serious cardiovascular disturbances were also reported in labor induction and animal studies including hypotension, reflexive tachycardia, coronary spasm or thrombosis and allergy. Here, we review our current understanding of the protective effect of OT against varieties of atherosclerotic etiologies as well as the approaches and underlying mechanisms of these effects. Moreover, potential cardiovascular disturbances following OT application are also discussed to avoid unwanted effects in clinical trials of OT usages.

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Section: Atherosclerosis and Cardioprotective Effect Of Otmentioning

confidence: 99%

Therapeutic Potential of Oxytocin in Atherosclerotic Cardiovascular Disease: Mechanisms and Signaling Pathways

Wang

Yang

et al. 2019

Front. Neurosci.

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“…15 A growing body of evidence over the last years revealed an excessive burden of both CVD and impaired bone health in patients with systemic autoimmune disorders. [16][17][18] For instance, in SLE, heightened rates of both subclinical atherosclerosis, 16 osteoporosis as well as peripheral and vertebral fractures have been repeatedly reported. 19 20 Moreover, low 25-OHD levels (<20 ng/mL) were found to be prevalent in patients with SLE .…”

Section: Introductionmentioning

confidence: 99%

Atherosclerosis in SLE: a potential role for serum parathormone levels

Giannelou

Skarlis

Stamouli³

et al. 2020

Lupus Sci Med

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ObjectiveA link between bone metabolism and cardiovascular (CV) disease has been suggested mainly in the general population. In the current study we explored whether altered bone metabolism influence CV risk in patients with SLE.MethodsIn 138 consecutive patients with SLE, atherosclerosis was assessed by the presence of plaque and/or arterial wall thickening in carotid/femoral arteries by ultrasound. Bone mineral density (BMD) levels and hip/spinal cord fractures together with classical CV disease and osteoporosis risk factors including serum 25(OH) vitamin D3 and parathormone (PTH) levels were recorded in all patients. Serum osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-Β ligand were quantitated by commercial ELISA. Statistical analysis included both univariate and multivariate models.ResultsAbnormal PTH serum concentrations (>65 pg/mL)—but not 25(OH) vitamin D3 serum levels—were identified as a risk factor for both plaque formation and arterial wall thickening in patients with SLE (ORs (95% CIs): 8.2 (1.8 to 37.4) and 3.9 (1.3 to 11.8), respectively). This association remained significant following adjustment for vitamin D3 levels and classical CV risk factors. Moreover, an independent association between osteoporosis with plaque formation and arterial wall thickening was detected following adjustment for total steroid dose, premature menopause and disease duration (ORs (95% CIs): 5.3 (1.1 to 26.2) and 3.5 (1.1 to 11.4), respectively). An inverse correlation between femoral neck BMD values and intima–medial thickness scores was also observed (r: −0.42, p=0.008).ConclusionsThese findings further strengthen the concept of shared pathophysiological mechanisms between atherogenesis and altered bone metabolism in autoimmune populations, revealing heightened PTH levels as a potential marker for atherosclerosis among patients with SLE.

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“…Compared with the general population, patients with RDs suffer from a significantly reduced life expectancy that is mainly due to atherosclerotic cardiovascular disease 2,3 . This excess of cardiovascular mortality, only partially predicted by conventional risk factors, has been linked to early endothelial dysfunction and accelerated arterial stiffening 2–4 . In fact, peripheral and central endothelial dysfunction, a measure of nitric-oxide (NO) availability and vasodilatory function, has been shown to be more prevalent in RDs than in the general population 5–7 .…”

Section: Introductionmentioning

confidence: 99%

Meta-Analysis of Asymmetric Dimethylarginine Concentrations in Rheumatic Diseases

Erre

Mangoni

Castagna

et al. 2019

Sci Rep

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Raised circulating concentrations of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), have been reported in several rheumatic diseases (RDs). However, the strength of this relationship is unclear. Therefore, the aim of this systematic review and meta-analysis was to evaluate the magnitude and the robustness of the association between ADMA concentrations and RDs. We calculated standardized mean differences (SMD, with 95% confidence intervals, CI). Study heterogeneity was evaluated by meta-regressions and sensitivity analyses according to type of RDs, conventional cardiovascular risk factors, inflammatory markers, and type of ADMA assessment methodology. Thirty-seven studies with a total of 2,982 subjects (1,860 RDs patients and 1,122 healthy controls) were included in our meta-analysis. Pooled results showed that ADMA concentrations were significantly higher in patients with RDs than in healthy controls (SMD = 1.27 µmol/L, 95% CI 0.94–1.60 µmol/L; p < 0.001). However, the between-studies heterogeneity was high. Differences in ADMA concentrations between controls and RDs patients were not significantly associated with inflammatory markers, increasing age, lipid concentrations, body mass index, blood pressure, or methodology used to assess ADMA. Furthermore, subgroup analysis showed no difference across RDs. This meta-analysis showed that, in the context of significant between-study heterogeneity, circulating concentrations of ADMA are positively related to RDs.

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Cardiovascular involvement in systemic rheumatic diseases: An integrated view for the treating physicians

Cited by 44 publications

References 209 publications

Therapeutic Potential of Oxytocin in Atherosclerotic Cardiovascular Disease: Mechanisms and Signaling Pathways

Therapeutic Potential of Oxytocin in Atherosclerotic Cardiovascular Disease: Mechanisms and Signaling Pathways

Atherosclerosis in SLE: a potential role for serum parathormone levels

Meta-Analysis of Asymmetric Dimethylarginine Concentrations in Rheumatic Diseases

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