Effects of tirzepatide on circulatory overload and end-organ damage in heart failure with preserved ejection fraction and obesity: a secondary analysis of the SUMMIT trial.

• Tác giả: Seth J Baum, Barry A Borlaug, Karla Hurt, Christopher M Kramer, Sheldon E Litwin, Masahiro Murakami, Yang Ou, Milton Packer, Navneet Upadhyay, Michael R Zile
• Ngôn ngữ: eng
• Thông tin xuất bản: United States : Nature medicine , 2025
• Bộ sưu tập: NCBI
• ID: 188259

Tóm tắt

 Patients with obesity-related heart failure with preserved ejection fraction (HFpEF) display circulatory volume expansion and pressure overload contributing to cardiovascular-kidney end-organ damage. In the SUMMIT trial, patients with HFpEF and obesity were randomized to the long-acting glucose-dependent insulinotropic polypeptide receptor and glucagon-like peptide-1 receptor agonist tirzepatide (n = 364, 200 women) or placebo (n = 367, 193 women). As reported separately, tirzepatide decreased cardiovascular death or worsening heart failure. Here, in this mechanistic secondary analysis of the SUMMIT trial, tirzepatide treatment at 52 weeks, as compared with placebo, reduced systolic blood pressure (estimated treatment difference (ETD) -5 mmHg, 95% confidence interval (CI) -7 to -3
  P <
  0.001), decreased estimated blood volume (ETD -0.58 l, 95% CI -0.63 to -0.52
  P <
  0.001) and reduced C-reactive protein levels (ETD -37.2%, 95% CI -45.7 to -27.3
  P <
  0.001). These changes were coupled with an increase in estimated glomerular filtration rate (ETD 2.90 ml min