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INTRODUCCIÓN: REVISIÓN CRITICA DEL PROBLEMA

INTRODUCCIÓN: REVISIÓN CRITICA DEL PROBLEMA

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RESULTADOS<br />

Additionally, we observed that sRAGE and fluorescent AGE levels were higher in<br />

patients with atrial fibrillation as compared with those in sinus rhythm (1562.2 vs.<br />

1051.3 pg/mL for sRAGE, P = 0.015 and 72.8 vs. 61.6 AU for fluorescent AGE, P<br />

= 0.018).<br />

Discussion<br />

Several conclusions may be derived from the current study. First, we have<br />

demonstrated that plasma levels of sRAGE, but not the AGEs evaluated in this<br />

study (fluorescent AGE and glycated albumin) are correlated with ischaemic heart<br />

disease in ambulatory HF patients, independently of age, sex, diabetes, renal<br />

function, clinical severity or other confounding variables. Moreover, sRAGE was<br />

directly associated with extent of coronary artery disease, but the same could not<br />

be said for the AGEs evaluated. We also confirmed the previously observed<br />

correlation between sRAGE and severity of HF, whereby sRAGE plasma levels<br />

are higher in patients with a higher NYHA dyspnoea class and/or higher BNP<br />

levels, although in the current study we did not find any significant correlation<br />

between these variables and AGE levels. We found a direct and statistically<br />

significant correlation between fluorescent AGE and glycated albumin, and a non<br />

significant tendency towards a positive correlation between fluorescent AGE and<br />

sRAGE. Finally, AGE–RAGE was significantly associated with plasma<br />

fructosamine levels, but not with other diabetes-related parameters such as<br />

glycated haemoglobin or fasting glycaemia. The current study also shows for the<br />

first time, a direct correlation between sRAGE and ischaemic cardiomyopathy as<br />

well as with the extent of coronary artery disease in HF patients, suggesting that<br />

the soluble AGE receptor could play a role in the pathophysiology of HF.<br />

The involvement of RAGE in the initiation and progression of vascular<br />

atherosclerotic disease has been widely demonstrated in both animal and human<br />

studies 282,284 . While cell-surface RAGE has been shown to be up-regulated and<br />

co-localized with inflammatory markers in atherosclerotic plaques 170 , sRAGE has<br />

been found to slow progression of atherosclerosis 169 AGE cross-link breakers<br />

119

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