Chronic Inflammatory Diseases and Endothelial Dysfunction

被引:160
作者
Castellon, Xavier [1 ]
Bogdanova, Vera [1 ]
机构
[1] Privat Hosp, F-91200 Paris, France
关键词
endothelial dysfunction; atherosclerosis; inflammatory diseases; non-invasive artery age testing methods; FMD; ANGIOTENSIN-ALDOSTERONE SYSTEM; INTIMA-MEDIA THICKNESS; CORONARY-HEART-DISEASE; VON-WILLEBRAND-FACTOR; C-REACTIVE PROTEIN; RISK-FACTORS; SUBCLINICAL ATHEROSCLEROSIS; ANTIPHOSPHOLIPID SYNDROME; RESISTANCE ARTERIES; METABOLIC SYNDROME;
D O I
10.14336/AD.2015.0803
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
030301 [社会学]; 100201 [内科学];
摘要
Chronic inflammatory diseases are associated with increases in cardiovascular diseases (CVD) and subclinical atherosclerosis as well as early-stage endothelial dysfunction screening using the FMD method (Flow Mediated Dilation). This phenomenon, referred to as accelerated pathological remodeling of arterial wall, could be attributed to traditional risk factors associated with atherosclerosis. Several new non-invasive techniques have been used to study arterial wall's structural and functional alterations. These techniques (based of Radio Frequency, RF) allow for an assessment of artery age through calculations of intima-media thickness (RF-QIMT), pulse wave rate (RF-QAS) and endothelial dysfunction degree (FMD). The inflammatory and autoimmune diseases should now be considered as new cardiovascular risk factors, result of the major consequences of oxidative stress and RAS (Renin Angiotensin System) imbalance associated with the deleterious effect of known risk factors that lead to the alteration of the arterial wall. Inflammation plays a key role in all stages of the formation of vascular lesions maintained and exacerbated by the risk factors. The consequence of chronic inflammation is endothelial dysfunction that sets in and we can define it as an integrated marker of the damage to arterial walls by classic risk factors. The atherosclerosis, which develops among these patients, is the main cause for cardiovascular morbi-mortality and uncontrolled chronic biological inflammation, which quickly favors endothelial dysfunction. These inflammatory and autoimmune diseases should now be considered as new cardiovascular risk factors.
引用
收藏
页数:9
相关论文
共 61 条
[41]
Genes and atherosclerosis: at the origin of the predisposition [J].
Puddu, P ;
Cravero, E ;
Puddu, GM ;
Muscari, A .
INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, 2005, 59 (04) :462-472
[42]
Reiner Z, 2001, Lijec Vjesn, V123, P26
[43]
Hypoxia-inducible factor-1-dependent mechanisms of vascularization and vascular remodelling [J].
Rey, Sergio ;
Semenza, Gregg L. .
CARDIOVASCULAR RESEARCH, 2010, 86 (02) :236-242
[44]
Role of the renin-angiotensin system in vascular diseases -: Expanding the field [J].
Ruiz-Ortega, M ;
Lorenzo, O ;
Rupérez, M ;
Esteban, V ;
Suzuki, Y ;
Mezzano, S ;
Plaza, JJ ;
Egido, J .
HYPERTENSION, 2001, 38 (06) :1382-1387
[45]
C-reactive protein, the metabolic syndrome, and prediction of cardiovascular events in the Framingham Offspring Study [J].
Rutter, MK ;
Meigs, JB ;
Sullivan, LM ;
D'Agostino, RB ;
Wilson, PWF .
CIRCULATION, 2004, 110 (04) :380-385
[46]
From bedside to bench to bedside: role of renin-angiotensin-aldosterone system in remodeling of resistance arteries in hypertension [J].
Schiffrin, EL ;
Touyz, RM .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2004, 287 (02) :H435-H446
[47]
Comparison of risk factors for vascular disease in the carotid artery and systemic lupus aorta in women with erythematosus [J].
Selzer, F ;
Sutton-Tyrrell, K ;
Fitzgerald, SG ;
Pratt, JE ;
Tracy, RP ;
Kuller, LH ;
Manzi, S .
ARTHRITIS AND RHEUMATISM, 2004, 50 (01) :151-159
[48]
Emerging Trends in CV Flow Visualization [J].
Sengupta, Partho P. ;
Pedrizzetti, Gianni ;
Kilner, Philip J. ;
Kheradvar, Arash ;
Ebbers, Tino ;
Tonti, Giovanni ;
Fraser, Alan G. ;
Narula, Jagat .
JACC-CARDIOVASCULAR IMAGING, 2012, 5 (03) :305-316
[49]
Accelerated atherosclerosis in autoimmune rheumatic diseases [J].
Shoenfeld, Y ;
Gerli, R ;
Doria, A ;
Matsuura, E ;
Cerinic, MM ;
Ronda, N ;
Jara, LJ ;
Abu-Shakra, M ;
Meroni, PL ;
Sherer, Y .
CIRCULATION, 2005, 112 (21) :3337-3347
[50]
Singh Uma, 2006, Pathophysiology, V13, P129, DOI 10.1016/j.pathophys.2006.05.002