Increased pre-ablation level of ANP, BNP, NT-pro-BNP, IL-6, C-reactive protein, LDL, and TIMP-2 was associated with greater risk of AF recurrence after RFCA.
These results demonstrate that MMP‑7 and BAX were highly expressed, while TIMP‑2 and BCL‑2 were downregulated in a Beagle dog model of AF, indicating that MMP‑7 and apoptosis‑associated genes (TIMP‑2, BAX and BCL‑2) may be associated with the pathogenesis of AF.
This upregulated expression and activity were positively correlated with higher regulatory indicators of atrial structural remodeling as reflected by higher transcripts of tumor necrosis factor (TNF)-related apoptosis-inducing ligand, matrix metalloproteinase (MMP)-2 and MMP-9, pro-inflammatory factors TNF-α and interleukin-6, and higher ratios of MMP-9/tissue inhibitor of metalloproteinase (TIMP)-1 and MMP-2/TIMP-2 in AF.
Both genotype distribution and allele frequency of the TIMP-2 -418G>C polymorphism were significantly different between the AF and control group (P=0.005 and P=0.001, respectively).