In:
European Journal of Clinical Investigation, Wiley, Vol. 46, No. 5 ( 2016-05), p. 386-391
Kurzfassung:
Inflammatory responses are pivotal in the initiation and development of premature atherosclerotic lesions. Galectin‐3 represents a valuable biomarker for both progression and destabilization of atherosclerotic lesions. This study aims to assess the involvement of galectin‐3 in premature myocardial infarction. Design In this multicentre case–control study, we assessed circulating galectin‐3 levels in 144 patients comprising 72 consecutive survivors of acute myocardial infarction (≤ 40 years) and 72 hospital controls frequency matched for age, gender and centre. Results Patients with acute myocardial infarction showed significantly higher galectin‐3 levels as compared to controls in the acute phase of acute myocardial infarction (2552 ± 1992 vs. 1666 ± 829 pg/mL; P 〈 0·001) as well as in the stable phase 1 year after the index event (3692 ± 1774 vs. 1666 ± 829 pg/mL; P 〈 0·001). Circulating galectin‐3 was significantly and independently associated with premature myocardial infarction in the logistic regression analysis (acute phase: adj. OR per 1‐ SD change 2·03, 95% CI 1·30−3·19; P = 0·002; stable phase: adj. OR of 6·54 (95% CI 2·56−16·68; P 〈 0·001). Moreover, we observed a significant correlation between circulating galectin‐3 and leucocyte count ( r = 0·35, P 〈 0·001), non‐ HDL cholesterol ( r = 0·23, P = 0·014) and HDL cholesterol ( r = −0·29, P = 0·002). Conclusion We demonstrated that elevated levels of circulating galectin‐3 are strongly associated with premature myocardial infarction. Galectin‐3 might serve as link between dyslipidaemia as driving force of plaque formation with inflammation as initiator of plaque rupture in patients with premature acute myocardial infarction.
Materialart:
Online-Ressource
ISSN:
0014-2972
,
1365-2362
DOI:
10.1111/eci.2016.46.issue-5
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2016
ZDB Id:
2004971-7
