Markers of myocardial damage, tissue healing, and inflammation after radiofrequency catheter ablation of atrial tachyarrhythmias.

Abstract

Radiofrequency ablation produces a localized endomyocardial necrosis that may result in release of biochemical markers reflecting myocardial cell damage, inflammation, and tissue reparation. The aim of this study was to determine the extent of rise and time course of markers of inflammation and tissue reparation in patients undergoing radiofrequency catheter ablation. Serial blood samples were taken from patients with AV nodal reentrant tachycardia (n = 5), Wolff-Parkinson-White syndrome (n = 3), and atrial flutter (n = 5) undergoing radiofrequency ablation. Blood was taken before ablation (day 0, baseline) and at day 1 and day 120 after ablation. The proinflammatory marker interleukin-6 (IL-6), troponin I (TNI), and myoglobin, as well as matrix metalloproteinase-9 (MMP-9), a marker for myocardial healing, were measured by enzyme-linked immunosorbent assay. Levels of IL-6, TNI, myoglobin, and MMP-9 were significantly elevated on day 1 after ablation compared to baseline levels. Seven of the 13 patients had troponin levels greater than the threshold of significant myocardial damage (>0.1 ng/mL) on day 1. Plasma levels of MMP-9 were still elevated on day 120 compared to values before ablation (P = 0.021). Markers of inflammation, wound healing, and myocardial damage are increased in patients who undergo radiofrequency ablation. Levels of MMP-9, a marker for myocardial healing and repair, are still elevated 120 days after the procedure, suggesting that radiofrequency ablation induces tissue damage leading to a long-term process of reparation.