Background-Previous work from our laboratory demonstrated that interleukin (IL)-6 plays a potentially critical role in postreperfusion myocardial injury and is the major cytokine responsible for induction of intracellular adhesion molecule (ICAM)-1 on cardiac myocytes during reperfusion. Myocyte ICAM-1 induction is necessary for neutrophil-associated myocyte injury. We have previously demonstrated the induction of IL-6 in the ischemic myocardium, and the current study addresses the cells of origin of IL-6. Methods and Results-In the present study, we combined Northern blot analysis and in situ hybridization to demonstrate IL-6 gene expression in cardiac myocytes. Isolated ventricular myocytes were stimulated with tumor necrosis factor-␣, IL-1␤, lipopolysaccharide, preischemic lymph, and postischemic lymph. Unstimulated myocytes showed no significant IL-6 mRNA expression. Myocytes stimulated with preischemic lymph showed minimal or no IL-6 mRNA expression, whereas myocytes stimulated with tumor necrosis factor-␣, IL-1␤, lipopolysaccharide, or postischemic lymph showed a strong IL-6 mRNA induction. Northern blot with ICAM-1 probe revealed ICAM-1 expression under every condition that demonstrated IL-6 induction. We then investigated the expression of IL-6 mRNA in our canine model of ischemia and reperfusion. Cardiac myocytes in the viable border zone of a myocardial infarction exhibited reperfusion-dependent expression of IL-6 mRNA within 1 hour after reperfusion. Mononuclear cells infiltrate the border zone and express IL-6 mRNA. Conclusions-Isolated cardiac myocytes produce IL-6 mRNA in response to several cytokines as well as postischemic cardiac lymph. In addition to its production by inflammatory cells, we demonstrate that IL-6 mRNA is induced in myocytes in the viable border zone of a myocardial infarct. The potential roles of IL-6 in cardiac myocytes in an infarct border are discussed. (Circulation. 1999;99:546-551.)

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Aims The study was intended to assess the prognostic value of inducibility of atrial fibrillation (AF) after radio frequency ablation. Methods and results Two hundred and thirty four patients with drug-resistant paroxysmal (n ¼ 165) or persistent AF (n ¼ 69) underwent either Lasso-guided segmental pulmonary vein isolation (n ¼ 83) or CARTO-guided left atrial circumferential ablation (n ¼ 151). After ablation, two attempts to induce AF (.1 min) by decremental coronary sinus stimulation were performed. Patients were followed for at least 6 months (median: 12.7 months). At 6 months of follow-up, 67% of patients with paroxysmal and 48% of patients with persistent AF were AF-free. Inducibility of AF was a significant predictor of AF recurrence in univariate [hazard ratio (HR) ¼ 2.32, P , 0.001] and multivariable (HR ¼ 2.19, P , 0.001) Cox regression analyses. The prognostic value of inducibility was present in both patients with paroxysmal (HR ¼ 2.38, P ¼ 0.001) and persistent AF (HR ¼ 1.91, P ¼ 0.034) and did not significantly differ between both ablation techniques. The sensitivity, specificity, positive, and negative predictive values of the AF induction test to predict the 6-month ablation outcome were 46.7, 75, 53.8, and 69.2%, respectively. Conclusion Inducibility of AF after ablation is a significant predictor of recurrent AF. However, owing to the low diagnostic accuracy of the AF induction test, non-inducibility does not qualify as reliable procedural endpoint.

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