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Atrial fibrillation (AF) is the most common progressive disease in patients with cardiac arrhythmia. AF is accompanied by complex atrial remodeling and changes in gene expression, but only a limited number of transcriptional regulators have been identified. Using a low-density cDNA array, we identified 31 genes involved in transcriptional regulation, signal transduction or structural components, which were either significantly upregulated or downregulated in porcine atria with fibrillation (induced by rapid atrial pacing at a rate of 400-600 bpm for 4 weeks that was then maintained without pacing for 2 weeks). The genes for four and a half LIM domains protein-1 (FHL1), transforming growth factor-beta (TGF-beta)-stimulated clone 22 (TSC-22), and cardiac ankyrin repeat protein (CARP) were significantly upregulated, and chromosome 5 open reading frame gene 13 (P311) was downregulated in the fibrillating atria. FHL1 and CARP play important regulatory roles in cardiac remodeling by transcriptional regulation and myofilament assembly. Induced mRNA expression of both FHL1 and CARP was also observed when cardiac H9c2 cells were treated with an adrenergic agonist. Increasing TSC-22 and marked P311 deficiency could enhance the activity of TGF-beta signaling and the upregulated TGF-beta1 and -beta2 expressions were identified in the fibrillating atria. These results implicate that observed alterations of underlying molecular events were involved in the rapid-pacing induced AF, possibly via activation of the beta-adrenergic and TGF-beta signaling.

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ObjectivesTo evaluate the relationship between the use of non-aristolochic acid (AA) prescribed Chinese herbal medicines (CHMs) and the risk of mortality in patients with chronic kidney disease (CKD).DesignNationwide population-based follow-up study.SettingLongitudinal health insurance database sampled from the Taiwan National Health Insurance Research Database.ParticipantsA total of 47 876 patients with CKD were identified. Participants who had ever used AA-containing CHMs, had cancer or HIV prior to the diagnosis of CKD, died within the first month of CKD diagnosis and who were not Taiwanese citizens were excluded. A total of 13 864 participants were eligible for final analysis.Primary and secondary outcome measuresAll-cause mortality among patients with CKD between 2000 and 2008.ResultsAfter controlling for potential confounders, we found that participants who started to receive non-AA prescribed CHMs after the diagnosis of CKD had a lower risk of mortality as compared with non-users of non-AA prescribed CHMs (adjusted HR (aHR) 0.6; 95% CI 0.4 to 0.7, p<0.001). Moreover, participants who had used non-AA prescribed CHMs prior to and after the diagnosis of CKD also had a lower risk of mortality than non-users (aHR 0.6; 95% CI 0.5 to 0.8, p<0.001). In subgroup analyses, we found that such an inverse association was present only among patients who were not eligible to receive erythropoietin therapy (ie, serum creatinine ≦6 mg/dL and/or haematocrit value ≧28%).ConclusionsPatients who received non-AA prescribed CHMs after the diagnosis of CKD, yet before the start of erythropoietin therapy had a lower risk of mortality than those who did not.