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Lipoprotein(a) and inflammation in patients with atrial fibrillation after electrical cardioversion

DOI: 10.1186/1477-5751-10-15

Keywords: atrial fibrillation, lipoprotein(a), cardioversion, inflammation

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Abstract:

Data of 79 patients admitted due to planned EC was analyzed. After successful procedure patients were monitored for 2 years. For analytical purposes patients were divided in two groups according to AF recurrence. There was no significant difference between Lp(a) levels in both groups. We also didn't find any positive correlation between Lp(a) and CRP levels, as well as between Lp(a) levels and left atrium diameter. For logistic and survival analysis optimal cut-off value of Lp(a) ≥ 0.32 (upper quartile) was used. In logistic regression model with AF recurrence as dependent variable Lp(a) didn't show any statistically significant association with AF recurrence. Survival analysis showed slightly higher AF recurrence rate in group with higher Lp(a) levels but not to the level of statistical significance (log rank test, p = 0.62).We weren't able to confirm the association between Lp(a) levels and AF recurrence, inflammation and left atrium diameter in patients after successful EC of persistent AF. Further studies are needed to elucidate the role of Lp(a) in this clinical setting.Atrial fibrillation (AF) is one of major causes for morbidity and hospitalization [1]. It is also important risk factor for thrombembolic complications and cerebrovascular disease[2]. Existing data strongly support its connection with ishemic heart disease, arterial hypertension, heart failure, obesity and metabolic syndrome [3-7]. In past years few studies tried to elucidate the association between AF and lipoprotein(a), particularly in connection with thrombembolic complications [8,9]. Major component of lipoprotein(a), or Lp(a) is large glycoprotein molecule named apoprotein(a), which is produced in hepatocytes. It binds with apo B100 component of LDL to form Lp(a). It was suggested that apoprotein(a) because of its homology to plasminogen interferes with fibrinolytic system and hence modulates thrombogenic activity in plasma [10]. Concomitantly in AF patients extensive inflammation takes pla

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