Heart rhythm · 2007
Markers of inflammation before and after curative ablation of atrial flutter.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Marcus Gregory M, Smith Lisa M, Glidden David V, Wilson Emily, McCabe Jamie M, Whiteman Dean, Tseng Zian H, Badhwar Nitish, Lee Byron K, Lee Randall J, Scheinman Melvin M, Olgin Jeffrey E
Аннотация
BACKGROUND: Atrial arrhythmias are associated with inflammation. The cause and effect of the association are unknown.
OBJECTIVE: The purpose of this study was to test the hypothesis that atrial tachyarrhythmias contribute to inflammation.
METHODS: We performed a prospective observational study wherein C-reactive protein (CRP) and interleukin-6 (IL-6) levels from the femoral vein and coronary sinus (CS) were compared before curative ablation for atrial flutter (AFL; n = 59) and paroxysmal supraventricular tachycardia (SVT; n = 110). Follow-up levels were obtained at 1 and 6 months.
RESULTS: Peripheral levels of both biomarkers were significantly higher in the AFL group. After multivariate adjustment, only those in the AFL group who presented in AFL or atrial fibrillation (AF) had significantly elevated CRP levels (odds ratio 1.26; P = .033). Levels of each marker were similar in the CS and peripheral blood in the SVT group; in the AFL group, both CRP and IL-6 were significantly lower in the CS than in the periphery (P = .0076 and P = .0021, respectively). CRP was significantly lower a median of 47 days after AFL ablation (from a median of 6.28 mg/L to a median of 2.92 mg/L; P = .028) and remained reduced at second follow-up. IL-6 decreased across three time points after AFL ablation (P = .002). No reduction in inflammatory biomarkers was observed after SVT ablation.
CONCLUSIONS: CRP and IL-6 levels are elevated in patients presenting in AFL. Given the lower CS values in these patients, their origin appears to be systemic rather than cardiac. Because these levels significantly fall after ablation of AFL, the atrial tachyarrhythmia appears to be the cause (not the effect) of the inflammation.
OBJECTIVE: The purpose of this study was to test the hypothesis that atrial tachyarrhythmias contribute to inflammation.
METHODS: We performed a prospective observational study wherein C-reactive protein (CRP) and interleukin-6 (IL-6) levels from the femoral vein and coronary sinus (CS) were compared before curative ablation for atrial flutter (AFL; n = 59) and paroxysmal supraventricular tachycardia (SVT; n = 110). Follow-up levels were obtained at 1 and 6 months.
RESULTS: Peripheral levels of both biomarkers were significantly higher in the AFL group. After multivariate adjustment, only those in the AFL group who presented in AFL or atrial fibrillation (AF) had significantly elevated CRP levels (odds ratio 1.26; P = .033). Levels of each marker were similar in the CS and peripheral blood in the SVT group; in the AFL group, both CRP and IL-6 were significantly lower in the CS than in the periphery (P = .0076 and P = .0021, respectively). CRP was significantly lower a median of 47 days after AFL ablation (from a median of 6.28 mg/L to a median of 2.92 mg/L; P = .028) and remained reduced at second follow-up. IL-6 decreased across three time points after AFL ablation (P = .002). No reduction in inflammatory biomarkers was observed after SVT ablation.
CONCLUSIONS: CRP and IL-6 levels are elevated in patients presenting in AFL. Given the lower CS values in these patients, their origin appears to be systemic rather than cardiac. Because these levels significantly fall after ablation of AFL, the atrial tachyarrhythmia appears to be the cause (not the effect) of the inflammation.