Background: Tachycardia induced cardiomyopathy (TIC), an etiology of growing interest, is caused by persistent tachyarrhythmia, and is characterized by reversible atrial/ventricular systolic dysfunction and dilation. The specific mechanisms involved in TIC pathophysiology remained largely unknown. In the present study we investigated inflammatory parameters that may accompany TIC.
Methods: Chronic tachycardia was induced by β-adrenoreceptor activation via isoprenaline systemic administration in female wistar rats (0.1mg/kg/daily, n=10 vs controls injected with saline, n=6). Echocardiography was performed after one month as well as after four months. The rats from both groups were sacrificed after four months and we evaluated the levels of different pro- and anti-inflammatory cytokines in the sera by ELISA. In addition, myocardial tissue was obtained from each rat and collagen content as well as macrophage occurrence was assessed by immunohistology.
Results: Isoprenaline induced significant tachycardia and after four month echocardiography revealed a significant decrease in the ejection fraction as well as in the fractional shortening, pointing at a cardiomyopathy. Masson's trichrome stain did not reveal myocardial scaring. ED-1 stain of myocardium showed a significantly increased macrophage infiltration in isoprenaline-treated rats. While no significant changes was noticed in the serum levels of interleukin (IL)-10, IL-13, MCP-1, IL-4 and IL-1 beta, a marked increase in the levels of IL-1 alpha, IL-2 and interferon (IFN)-gamma were found in TIC rats (3, 6 and 3.5 fold, respectively, p<0.05).
Conclusions: Our findings may point at a stimulated inflammatory state accompanying TIC, which might contribute to the associated myocardial dysfunction.
