Objective To investigate the effects of frequent premature atrial contraction (PAC) on atrial fibrillation susceptibility and cardiac remodeling in dogs. Methods Six beagle dogs were randomly divided into PAC group (n=3) or control group (n=3). A canine model of frequent PAC was established by implanting a dual⁃chamber pacemaker in the left atrial appendage through open‑chest surgery. Before intraoperative implantation of the dual‑chamber pacemaker, routine blood parameters, serum C‑reactive protein (CRP), and interleukin 6 (IL‑6) levels were measured in both groups. P‑wave duration and P‑wave amplitude were assessed by electrocardiography, and transthoracic echocardiography was performed. One week after dual⁃chamber pacemaker implantation, baseline pacemaker parameters were recorded, and routine blood parameters, and serum CRP and IL‑6 levels were measured in both groups. At 3 and 6 months post‑implantation, electrocardiography and transthoracic echocardiography were performed in both groups, and dual⁃chamber pacemaker parameters were documented. At 6 months post‑implantation, electrophysiological examinations were conducted to obtain atrial substrate maps and evaluate atrial fibrillation susceptibility. At the same time point, samples from the left atrium, left atrial appendage, left pulmonary veins, and right pulmonary veins were collected for Masson's staining to assess myocardial fibrosis in dogs. Peripheral blood expressions of brain natriuretic peptide (BNP), transforming growth factor β1 (TGF‑β1), and collagen type Ⅲ alpha 1 chain (COL3A1) protein were measured by ELISA. Protein expressions of TGF‑β1, α‑smooth muscle actin (α‑SMA), and COL3A1 in left atrial myocardial tissues were determined by Western blot. Results Before and at 1 week after dual⁃chamber pacemaker implantation, there was no statistically significant difference in routine blood parameters, CRP or IL‑6 levels between the two groups (P>0.05), and these parameters at 1 week post‑implantation did not differ significantly from pre‑implantation values within either group (P>0.05). At 3 months post‑implantation, there was no statistically significant difference in P‑wave amplitude or P‑wave duration between the two groups (P>0.05). At 6 months post‑implantation, the PAC group exhibited a longer P‑wave duration than the control group (P<0.05), but P‑wave amplitude did not differ significantly between the two groups (P>0.05). At 3 months post‑implantation, the left atrial end‑systolic volume was greater in the PAC group than in the control group (P<0.05). At 6 months post‑implantation, the PAC group interpreted greater left atrial end‑systolic volume, left atrial area, and higher E/A ratio, pulmonary artery pressure, as well as a lower left atrial ejection fraction compared with the control group (P<0.05). The successful PAC pacing rate in the PAC group ranged from 95.6% to 99.9% at 3 months and from 96.7% to 100.0% at 6 months post‑implantation. The duration of atrial fibrillation induced by stimulation at the coronary sinus, high right atrium, low right atrium was longer in the PAC group than in the control group, and the atrial fibrillation induction success rate at these sites was higher in the PAC group than in the control group (P<0.05). Atrial substrate mapping revealed increased low‑voltage areas in the PAC group compared with the control group. The fibrotic proportion in the left atrium, left atrial appendage, left pulmonary veins, and right pulmonary veins was higher in the PAC group than in the control group (P<0.05). Peripheral blood expressions of TGF‑β1 and COL3A1 were higher in the PAC group than in the control group (P<0.05), whereas BNP expressions indicated no statistically significant difference between the two groups (P>0.05). Compared with the control group, the PAC group exhibited elevated protein expressions of TGF‑β1, α‑SMA, and COL3A1 in left atrial myocardial tissues (P<0.05). Conclusion Stable PAC canine model can be established by implanting a dual‑chamber pacemaker in the left atrial appendage. Frequent PAC increases susceptibility to atrial fibrillation and leads to atrial and ventricular remodeling as well as functional deterioration.

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