Soluble adhesion molecules and C-reactive protein in the progression of silent cerebral infarction in patients with type 2 diabetes mellitus

Kawamura, Takahiko; Umemura, Toshitaka; Kanai, Akio; Nagashima, Masahito; Nakamura, Nobuhisa; Uno, Tomoko; Nakayama, Mikihiro; Sano, Takahisa; Hamada, Yoji; Nakamura, Jiro; Hotta, Nigishi

doi:10.1016/j.metabol.2005.10.007

Cited by 41 publications

(36 citation statements)

References 39 publications

(60 reference statements)

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“…27 Interestingly, VCAM-1 levels were found to be elevated even in patients with silent cerebral infarction. 28 However, the role of adhesion molecules has not yet been clarified in patients with AF. Preliminary data from our group showed that systemic plasma levels of ICAM-1 and VCAM-1 are increased in patients with AF, reaching the highest levels with overt atrial thrombi.…”

Section: Af and Adhesion Moleculesmentioning

confidence: 99%

Angiotensin II Receptor Blockade Reduces Tachycardia-Induced Atrial Adhesion Molecule Expression

et al. 2008

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Background-Increased levels of inflammatory markers are predictors of thromboembolic events during atrial fibrillation (AF).Increased endocardial expression of adhesion molecules (ie, vascular cell adhesion molecule [VCAM] and intercellular adhesion molecule [ICAM]) could be an important link between initiation of inflammatory and prothrombogenic mechanisms responsible for thrombus development at the atrial endocardium (endocardial remodeling). Methods and Results-Tissue microarrays were used to screen right atrial tissue specimens obtained from 320 consecutive patients for differences in atrial expression of the prothrombogenic proteins VCAM-1, ICAM-1, thrombomodulin, plasminogen activator inhibitor-1, and von Willebrand factor. An in vitro organotypic human atrial tissue model and a pig model of rapid atrial pacing were used to determine the therapeutic impact of angiotensin II receptor blockade.Immunohistochemical analyses showed that all prothrombogenic proteins are expressed by endocardial cells. Using multivariable analysis, only the intensity of VCAM-1 expression was increased in patients with AF (Pϭ0.03). Increased atrial VCAM-1 expression was confirmed by Western blotting in patients with persistent and paroxysmal AF (persistent AF 207Ϯ42% versus sinus rhythm 100Ϯ16%, Pϭ0.028; paroxysmal AF 193Ϯ42%, Pϭ0.024 versus sinus rhythm). In vitro pacing of ex vivo human atrial tissue slices confirmed that rapid activation causes VCAM-1 upregulation (mRNA and protein levels). Pacing-induced VCAM-1 expression was abolished by olmesartan. To confirm this finding in vivo, VCAM-1 expression was determined in 14 pigs after rapid atrial pacing (600 bpm). Atrial tachycardia caused an upregulation of VCAM-1 expression, which was prevented by irbesartan, consistent with the observed increase in plasma levels of angiotensin II. Alterations in the in vivo VCAM-1 expression were more pronounced in the left atrium (Ͼ5-fold compared with sham) than in the right atrium (3.5-fold compared with sham). Conclusions-AF and rapid atrial pacing both increase endocardial VCAM-1 expression, which can be attenuated by angiotensin II receptor blockade. This provides evidence that angiotensin II plays a pathophysiological role in prothrombotic endocardial remodeling. (Circulation. 2008;117:732-742.)

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Section: Af and Adhesion Moleculesmentioning

confidence: 99%

Angiotensin II Receptor Blockade Reduces Tachycardia-Induced Atrial Adhesion Molecule Expression

et al. 2008

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“…20 Interestingly, soluble ICAM-1 and vascular cellular adhesion molecule (VCAM)-1 levels were also found to be elevated in patients with silent cerebral infarction. 21 It is of note that soluble adhesion molecule levels were found to have a high predictive value with membrane-bound intramyocardial adhesion molecules. 22 In line with these study results, it was demonstrated that systemic plasma levels of ICAM-1 and VCAM-1 levels are increased in patients with atrial fibrillation, reaching the highest levels in patients with atrial thrombi.…”

Section: Dovepressmentioning

confidence: 98%

“…13 In turn, increased inflammatory markers and increased leukocyte-platelet interactions are predictors of atrial thrombus formation and thromboembolic stroke. 20,21 Increased endothelial expression of adhesion molecules and reduced levels of nitric oxide could be an important link between the initiation of proinflammatory and prothrombogenic mechanisms responsible for atrial thrombus formation. 12,14,18 Atrial fibrillation-induced thromboemboli are very leukocyte-rich, showing the close link between coagulation and inflammation in atrial thrombus formation.…”

Section: Dovepressmentioning

confidence: 99%

Dabigatran for prophylaxis of thromboembolic events in patients with atrial fibrillation

Ehrlich¹,

Hammwöhner²,

Goette

2012

RRCC

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Atrial fibrillation is the most common clinically relevant cardiac arrhythmia. Prevalence and incidence rates are constantly rising with advancing population age. A severe complication of untreated atrial fibrillation is thrombus formation in the left atrial appendage with consecutive peripheral thromboembolism. Thus, atrial fibrillation is a major contributor to thromboembolic events, especially in the older population. Depending on the CHADS 2 risk score for thromboembolic events, oral anticoagulation therapy with vitamin K antagonists is currently the treatment of choice for the prevention of thromboembolism, including apoplectic strokes. However, due to the drawbacks of current anticoagulation therapy, new substances for oral anticoagulation therapy are currently being evaluated in various clinical studies. This article will provide an up to date overview of orally active compounds for the future treatment of atrial fibrillation using the direct thrombin inhibitor, dabigatran.

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“…49 Besides, endothelial damage markers have also been involved not only in the presence but also in the progression of SBIs over time, and in fact they might be predictive in diabetic populations. 50,51 White matter hyperintensities have also been related to higher levels of several endothelial dysfunction markers like soluble E-selectin, soluble intercellular adhesion molecule 1, soluble P-selectin, and soluble vascular cell adhesion molecule 1 in cross-sectional studies. [52][53][54][55][56] Moreover, both baseline WMH load and intercellular adhesion molecule 1 were independent predictors of WMH progression after adjustment by potential confounders in a longitudinal assessment of the community-based Austrian Stroke Prevention study.…”

Section: Endothelial Dysfunctionmentioning

confidence: 99%

Blood and CSF biomarkers in brain subcortical ischemic vascular disease: Involved pathways and clinical applicability

Vilar-Bergua

Riba‐Llena

Nafría

et al. 2015

J Cereb Blood Flow Metab

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Vascular dementia is the second most common type of dementia after Alzheimer's disease (AD). Subcortical ischemic vascular disease refers to a form of vascular cognitive impairment characterized by the presence of diffuse white matter hyperintensities (WMHs) and multiple lacunar infarcts. These neuroimaging findings are mainly caused by cerebral smallvessel disease (cSVD) and relate to aging and cognitive impairment, but they can also be silent and highly prevalent in otherwise healthy individuals. We aimed to review studies on blood and cerebrospinal fluid (CSF) markers related to the presence of WMHs and lacunar infarcts that have been conducted in the past in large population-based studies and in high-risk selected patients (such as those with vascular risk factors, vascular cognitive impairment, or AD). Relevant associations with the presence and progression of cSVD have been described in the blood for markers related to inflammatory processes, endothelial damage and coagulation/fibrinolysis processes, etc. Also, different combinations of CSF markers might help to differentiate between etiologic types of dementia. In the future, to translate these findings into clinical practice and use biomarkers to early diagnosis and monitoring vascular cognitive impairment would require the replication of candidate markers in large-scale, multicenter, and prospectively designed studies.

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Soluble adhesion molecules and C-reactive protein in the progression of silent cerebral infarction in patients with type 2 diabetes mellitus

Cited by 41 publications

References 39 publications

Angiotensin II Receptor Blockade Reduces Tachycardia-Induced Atrial Adhesion Molecule Expression

Angiotensin II Receptor Blockade Reduces Tachycardia-Induced Atrial Adhesion Molecule Expression

Dabigatran for prophylaxis of thromboembolic events in patients with atrial fibrillation

Blood and CSF biomarkers in brain subcortical ischemic vascular disease: Involved pathways and clinical applicability

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