scholarly journals The role of endothelial damage and dyslipidemia in the development of cardiovascular pathology in psoriatic arthritis

2021 ◽  
Vol 97 (2) ◽  
pp. 16-22
Author(s):  
Zarema R. Khismatullina ◽  
Ksenia M. Koreshkova

An increased risk of cardiovascular events has now been identified in patients with psoriatic arthritis. The chronic immune-mediated inflammation underlying psoriatic arthritis (PA) leads to the development of dyslipidemia, atherosclerosis and its complications, in particular, a high risk of cardiovascular complications. For PA, dyslipidemias are most characteristic, manifested by an increased level of low and very low density lipoproteins, triglycerides and total cholesterol, which correlates with the activity of the disease. The literature review studied the pathogenesis of dyslipidemias and vascular wall lesions in psoriatic arthritis, analyzed the literature on cardiovascular complications and mortality among patients with PA, studied the issues of total cardiovascular risk, presented the results of numerous clinical studies that allow PA to be considered a disease associated with increased the risk of cardiovascular complications. Considering the role of proinflammatory cytokines in the pathogenesis of psoriatic arthritis, early detection of endothelial lesions represents the most promising direction in the prevention of cardiovascular diseases, which are the main cause of mortality in this group of patients.

2016 ◽  
Vol 13 (2) ◽  
pp. 17-23
Author(s):  
O D Ostroumova ◽  
A I Kochetkov ◽  
M V Lopukhina

The article discusses the factors that increase the arterial stiffness: the blood pressure, atherosclerosis, smoking, diabetes, age. Given evidence that pulse wave velocity and a number of other indicators that reflect the state of the vascular wall, are markers for increased risk of cardiovascular complications and mortality. The influence of antihypertensive drugs of different groups on the stiffness of the vascular wall, with particular attention paid to the effects of drugs from group of diuretics. We discuss possible mechanisms of the influence of indapamide retard on the elastic properties of vessels. It is emphasized that the influence on the stiffness of the arteries of different antigipertenzivny medicines, even belong to the same class, is different, due to differences in pharmacokinetic properties.


2015 ◽  
Vol 12 (2) ◽  
pp. 43-48
Author(s):  
O D Ostroumova ◽  
A I Kochetkov ◽  
I I Kopchenov ◽  
T F Guseva ◽  
O V Bondarec

The article deals with the role of the hardness of the vessel wall in the pathogenesis of arterial hypertension and its complications and cardiovascular mortality. We discussed the factors increasing the hardness of the vessel wall, such as age, blood pressure level, atherosclerosis, smoking and diabetes mellitus. We showed the indicators reflecting the status of the vascular wall and which could play a role of markers of increased risk of cardiovascular complications. We reviewed the data concerning the improvement of the parameters of the hardness of the vessel wall under the influence of antihypertensive therapy using the angiotensin II type 1 receptor blocker - candesartan. We discussed the possible mechanisms of the candesartan influence on the elastic properties of the vessels. We stressed that the effect on the hardness of the arteries on using antihypertensive drugs, even within the same class, was different, which, apparently, was associated with the difference in the pharmacokinetic properties.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Diana Prieto-Peña ◽  
Sara Remuzgo-Martínez ◽  
Fernanda Genre ◽  
Verónica Pulito-Cueto ◽  
Belén Atienza-Mateo ◽  
...  

AbstractCytokines signalling pathway genes are crucial factors of the genetic network underlying the pathogenesis of Immunoglobulin-A vasculitis (IgAV), an inflammatory vascular condition. An influence of the interleukin (IL)33- IL1 receptor like (IL1RL)1 signalling pathway on the increased risk of several immune-mediated diseases has been described. Accordingly, we assessed whether the IL33-IL1RL1 pathway represents a novel genetic risk factor for IgAV. Three tag polymorphisms within IL33 (rs3939286, rs7025417 and rs7044343) and three within IL1RL1 (rs2310173, rs13015714 and rs2058660), that also were previously associated with several inflammatory diseases, were genotyped in 380 Caucasian IgAV patients and 845 matched healthy controls. No genotypes or alleles differences were observed between IgAV patients and controls when IL33 and IL1RL1 variants were analysed independently. Likewise, no statistically significant differences were found in IL33 or IL1RL1 genotype and allele frequencies when IgAV patients were stratified according to the age at disease onset or to the presence/absence of gastrointestinal (GI) or renal manifestations. Similar results were disclosed when IL33 and IL1RL1 haplotypes were compared between IgAV patients and controls and between IgAV patients stratified according to the clinical characteristics mentioned above. Our results suggest that the IL33-IL1RL1 signalling pathway does not contribute to the genetic network underlying IgAV.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 811.1-811
Author(s):  
S. Smiyan ◽  
A. Bilukha ◽  
B. Koshak

Background:Psoriatic arthritis (PsA) is a chronic inflammatory joint disease which develops in patients with psoriasis. Mortality among patients with PsA is 1.28 times higher than population levels and in most cases it is caused by cardio-vascular diseases (CVD). Those patients have increased risk of clinical and subclinical CVD, mostly due to endothelial dysfunction (ED) and accelerated atherosclerosis. Elevated levels of circulating endothelial cells (CEC) have been described in different cardiovascular pathologies, suggesting their potential use as diagnostic biomarkers for dysfunction of endothelium.Objectives:To identify the potential role of circulating endothelial cells as a marker of cardiovascular diseases in patients with psoriatic arthritis.Methods:In total, ninety-four patients with PsA, who fulfilled the disease criteria (CASPAR) were examined using standard diagnostic methods (including C-reactive protein (CRP), lipid profile) and evaluation endothelium-dependent vasodilation in response to reactive hyperemia (EDVD). Circulating endothelial cells were determined in the peripheral venous blood samples by flow cytometry and counted according to a standardized protocol using a fluorescence microscope after acridine orange labeling. The control group, which were consisted from thirty healthy adults were also examined.Results:CEC were quantified in patients with PsA (7,15 ± 0,19 cells mL−1) and in the control group (4,05 ± 0,11 cells mL−1). Comparing two groups of patients, endothelial circulating cell level was significantly different (p = 0.0001). Finally, we analyzed the relationship between CEC count, comorbidities, cardiovascular risk factors and EDVD in patients with PsA. Increased CEC levels were associated with obesity (r=0,62), duration of disease (r=0,65), age (r=0,67), increased CRP (r=0,76), high blood pressure (r=0,87) and decreased EDVD (r=–0,91).Conclusion:CEC counts were significantly higher in patients with PsA, positively correlated with the main factors of CVD, and another specific marker of ED - EDVD. Elevated CEC levels were also associated with high concentrations of CRP, which plays a direct role in promoting vascular inflammation, vessel damage and clinical CVD events. In conclusion, increased CEC counts provide a direct proof of endothelial damage in patient with PsA and a clinically informative diagnostic tool for endothelial damage in pre-symptomatic CVD. As CEC are one of the most sensitive biomarker for ED, further efforts should concentrate on improving the sensitivity of its detection in order to increase diagnostic sensitivity.References:[1]Maura Farinacci, Thomas Krahn, Wilfried Dinh, et al. Circulating endothelial cells as biomarker for cardiovascular diseases. Res Pract Thromb Haemost, Vol. 3, Issue, 2019, P.49-58;[2]C. Horreau, C. Pouplard, E. Brenautet, et al. Cardiovascular morbidity and mortality in psoriasis and psoriatic arthritis: a systematic literature review. J Eur Acad Dermatol Venereol, Vol. 27, Issue 3, 2013, P.12-19;[3]Frank Verhoeven, Clément Prati, Céline Demougeot, Daniel Wendling. Cardiovascular risk in psoriatic arthritis, a narrative review. Joint Bone Spine, Vol. 87, Issue 5, 2020, P.413-418;Disclosure of Interests:None declared.


2012 ◽  
Vol 39 (7) ◽  
pp. 1433-1440 ◽  
Author(s):  
ANNE GRETE SEMB ◽  
TORE K. KVIEN ◽  
DAVID A. DeMICCO ◽  
RANA FAYYAD ◽  
CHUAN-CHUAN WUN ◽  
...  

Objective.To evaluate lipids and apolipoproteins as predictors of cardiovascular mortality and morbidity (CVD) in patients with spondyloarthritis (SpA).Methods.In the pooled cohort of participants in the IDEAL, TNT, and CARDS trials, 50 had ankylosing spondylitis (AS), 36 had psoriatic arthritis (PsA), and 21,641 did not have AS or PsA (non-SpA). We compared lipid levels at baseline between AS or PsA and non-SpA, and hazard ratios (HR) for CVD were calculated in a Cox proportional hazard model.Results.Atherogenic lipids were lower in samples from AS, but not in PsA, compared to non-SpA. The HR for 1 SD increase in baseline lipids for future CVD was for total cholesterol 1.39 (95% CI 0.82, 2.36) in AS, 1.01 (95% CI 0.44, 2.31) in PsA, and 1.10 (95% CI 1.07, 1.14) in non-SpA. Both high-density lipoprotein (HDL) and apolipoprotein (ApoA-1) were significantly associated with CVD in AS (HR 3.67, 95% CI 1.47, 9.06, and HR 1.89, 95% CI 1.02, 3.54, respectively), in contrast to PsA (HDL: HR 1.03, 95% CI 0.49, 2.15; ApoA-1: HR 0.79, 95% CI 0.34, 1.89) and non-SpA (HDL: HR 0.86, 95% CI 0.84, 0.89; ApoA-1: HR 0.88, 95% CI 0.85, 0.91).Conclusion.HDL and ApoA-1 were surprisingly associated with increased risk of future CVD in patients with AS, whereas these lipids were protective in non-SpA.


Author(s):  
A. V. Melentev ◽  
P. V. Serebryakov

The influence of noise and vibration on the development of arterial hypertension in workers employed in adverse working conditions was studied. It is shown that these physical factors of the working environment make a significant contribution to the formation of an increased risk of cardiovascular complications


2013 ◽  
Vol 88 (6) ◽  
pp. 1029-1035 ◽  
Author(s):  
Emerson de Andrade Lima ◽  
Mariana Modesto Dantas de Andrade Lima ◽  
Cláudia Diniz Lopes Marques ◽  
Angela Luzia Branco Pinto Duarte ◽  
Ivan da Rocha Pita ◽  
...  

Psoriasis is a polygenic, inflammatory and progressive disease, characterized by an abnormal differentiation and hyperproliferation of keratinocytes, associated with impaired immunologic activation and systemic disorders, while psoriatic arthritis is a chronic inflammatory articular disease. Pathophysiology of psoriasis comprises a dysfunction of the immune system cells with an interactive network between cells and cytokines supporting the initiation and perpetuation of disease and leading to inflammation of skin, enthesis and joints. Recent studies have shown an important role of systemic inflammation in the development of atherosclerosis. Corroborating these findings, patients with severe Psoriasis have marked incidence of psoriatic arthritis, cardiovascular diseases, hypertension, dyslipidemia, obesity and diabetes mellitus, showing an increased risk for acute myocardial infarction, which suggests that the condition is not restricted to the skin. Nuclear receptors are ligand-dependent transcription factors, whose activation affects genes that control vital processes. Among them the peroxisome proliferator-activated receptor is responsible for establishing the relationship between lipids, metabolic diseases and innate immunity. In the skin, peroxisome proliferator-activated receptors have an important effect in keratinocyte homeostasis, suggesting a role in diseases such as psoriasis. The peroxisome proliferator-activated receptors agonists represent a relevant source of research in the treatment of skin conditions, however more clinical studies are needed to define the potential response of these drugs in patients with psoriasis and psoriatic arthritis.


2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Morena Scotece ◽  
Javier Conde ◽  
Rodolfo Gómez ◽  
Verónica López ◽  
Jesús Pino ◽  
...  

Patients with rheumatic diseases have an increased risk of mortality by cardiovascular events. In fact, several rheumatic diseases such as rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, and ankylosing spondylitis are associated with a higher prevalence of cardiovascular diseases (CVDs). Although traditional cardiovascular risk factors have been involved in the pathogenesis of cardiovascular diseases in rheumatic patients, these alterations do not completely explain the enhanced cardiovascular risk in this population. Obesity and its pathologic alteration of fat mass and dysfunction, due to an altered pattern of secretion of proinflammatory adipokines, could be one of the links between cardiovascular and rheumatic diseases. Indeed, the incidence of CVDs is augmented in obese individuals with rheumatic disorders. Thus, in this paper we explore in detail the relationships among adipokines, rheumatic diseases, and cardiovascular complications by giving to the reader a holistic vision and several suggestions for future perspectives and potential clinical implications.


Life ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 395
Author(s):  
Alberto Palazzuoli ◽  
Michela Giustozzi ◽  
Gaetano Ruocco ◽  
Francesco Tramonte ◽  
Edoardo Gronda ◽  
...  

SARS-Cov-2 infection, a pandemic disease since March 2020, is associated with a high percentage of cardiovascular complications mainly of a thromboembolic (TE) nature. Although clinical patterns have been described for the assessment of patients with increased risk, many TE complications occur in patients with apparently moderate risk. Notably, a recent statement from the European Society of Cardiology (ESC) atherosclerosis and vascular biology working group pointed out the key role of vascular endothelium for the recruitment of inflammatory and thrombotic pathways responsible for both disseminated intravascular coagulation and cardiovascular complications. Therefore, a better understanding of the pathophysiological process linking infection to increased TE risk is needed in order to understand the pathways of this dangerous liaison and possibly interrupt it with appropriate treatment. In this review, we describe the histological lesions and the related blood coagulation mechanisms involved in COVID-19, we define the laboratory parameters and clinical risk factors associated with TE events, and propose a prophylactic anticoagulation treatment in relation to the risk category. Finally, we highlight the concept that a solid risk assessment based on prospective multi-center data would be the challenge for a more precise risk stratification and more appropriate treatment.


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