Endothelial damage and activation of the hemostatic system during radiofrequency catheter isolation of pulmonary veins
Language English Country Netherlands Media print
Document type Comparative Study, Evaluation Study, Journal Article
PubMed
15133367
DOI
10.1023/b:jice.0000026924.96281.be
PII: 5273081
Knihovny.cz E-resources
- MeSH
- Tachycardia, Atrioventricular Nodal Reentry blood surgery MeSH
- Biomarkers blood MeSH
- Biotransformation drug effects physiology MeSH
- Adult MeSH
- Echocardiography, Transesophageal MeSH
- Endothelium metabolism pathology MeSH
- Atrial Fibrillation blood surgery MeSH
- Fibrin Fibrinogen Degradation Products drug effects metabolism MeSH
- Fibrinolytic Agents therapeutic use MeSH
- Fibrinolysis drug effects physiology MeSH
- Hemostasis drug effects physiology MeSH
- Heparin therapeutic use MeSH
- Plasminogen Activator Inhibitor 1 blood MeSH
- Catheter Ablation * MeSH
- Middle Aged MeSH
- Humans MeSH
- Intraoperative Complications blood etiology MeSH
- Statistics as Topic MeSH
- Tissue Plasminogen Activator blood drug effects MeSH
- Pulmonary Veins diagnostic imaging physiopathology surgery MeSH
- von Willebrand Factor drug effects metabolism MeSH
- Treatment Outcome MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Evaluation Study MeSH
- Comparative Study MeSH
- Names of Substances
- Biomarkers MeSH
- fibrin fragment D MeSH Browser
- Fibrin Fibrinogen Degradation Products MeSH
- Fibrinolytic Agents MeSH
- Heparin MeSH
- Plasminogen Activator Inhibitor 1 MeSH
- Tissue Plasminogen Activator MeSH
- von Willebrand Factor MeSH
AIMS: To determine the systemic thrombogenic effect of radiofrequency catheter isolation of the pulmonary veins (PVI) in the treatment of atrial fibrillation. METHODS AND RESULTS: We studied endothelial damage marker (von Willebrand factor [vWf]), fibrinolysis markers (tissue plasminogen activator [t-PA], plasminogen activator inhibitor-1 [PAI-1]) and coagulation activation markers (D-dimer [DD]) in 30 patients (pts) undergoing PVI. Heparin was administered continuously after double transseptal puncture in all pts. Concentrations of vWf and t-PA were significantly increased after accomplishing PVI compared to the baseline values, and elevated levels persisted 24 hours later ( p < 0.01). PAI-1 levels decreased following PVI compared to the baseline levels ( p = 0.02). PAI-1 levels normalized 24 hours after the procedure. DD increased continuously during the procedure with the peak following PVI ( p < 0.01). Higher DD concentrations persisted 24 hours later ( p = 0.02). In a multivariate analysis, total procedure time correlated significantly with the peak vWf and DD concentrations, while total RF energy dose correlated only with peak vWf ( r = 0.82). Time to heparin administration correlated with DD levels prior to the first RF pulse ( r = 0.83, p < 0.01) as well as after PVI ( r = 0.75, p < 0.01). A group of patients heparinized within the first hour of the PVI procedure had normal preablation DD levels and significantly mitigated DD levels following PVI compared to the group of patients heparinized later ( p < 0.01). CONCLUSIONS: Pulmonary vein ablations cause an increased systemic procoagulant state as reflected by fibrin turnover, fibrinolysis activation and endothelial perturbation. The activation of the coagulation cascade could be decreased by early heparin administration.
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