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GW23-e2240
THE IMPACT OF CARDIAC RESYNCHRONISATION THERAPY ON TGF-β 1 SIGNAL PATHWAY IN ISCHAEMIC CARDIOMYOPATHY
  1. Yongle Chen,
  2. Leilei Cheng,
  3. Haohua Yao,
  4. Haiyan Chen,
  5. Cuizhen Pan,
  6. Xianhong Shu
  1. Department of Echocardiography, Zhongshan Hospital, Fudan University, Shanghai (200032), China

    Abstract

    Objectives To investigate the latent impact of cardiac resynchronisation therapy on TGF-β 1 signal pathway in Beagles with ischaemic cardiomyopathy.

    Methods Twenty adult Beagles were divided into group A (CRT group) and group B (non-CRT group). All of them were chest opened and had heart failure after a ligature in the first diagonal branch. A left ventricular epicardial lead, a right atrium and a right ventricle leads together with the pacemaker were implanted. The pacing was started in group A after myocardial infarction, but was not started in group B. After 4 weeks of CRT, group A was divided into group C (CRT response group) and group D (CRT non-response group). Myocardial tissues were collected from the marginal area of myocardial infarction. The expressions of TGF-β 1, p-Smad2/3, and Smad2/3 in group B, group C, and group D were investigated, respectively.

    Results The TGF-β 1, p-Smad2/3, and Smad2/3 were expressed at low levels in normal myocardial tissues. There showed a significant elevation of the expression of TGF-β 1, p-Smad2/3, and Smad2/3 at the marginal area of myocardial infarction after the first diagonal branch was ligatured. The expression of TGF-β 1, p-Smad2/3, and Smad2/3 in Group C and Group D were both higher than that in normal myocardial tissues. The collagen fibres of the marginal area of myocardial infarction in group C were significant less than that in group B or group D, meanwhile the expression of TGF-β 1, p-Smad2/3, and Smad2/3 in group C were also lower than that in group B and group D p<0.05).

    Conclusions In the responders of Beagles with ischaemic cardiomyopathy, CRT can inhibit the expression of TGF-β 1, p-Smad2/3, and Smad2/3 and reduce the deposition of collagen fibres, which leads to the improvement of cardiac function.

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