Aims: Metalloproteinases are proteolytic enzymes, which decompose the extracellular matrix, influence cardiac remodelling, and are inhibited by tissue inhibitor of metalloproteinases(TIMPs). Little is known about the ...Aims: Metalloproteinases are proteolytic enzymes, which decompose the extracellular matrix, influence cardiac remodelling, and are inhibited by tissue inhibitor of metalloproteinases(TIMPs). Little is known about the prognostic impact of the TIMP-1/matrix metalloproteinase complex in patients with future cardiovascular death. Methods and results: In 1979 patients with suspected coronary artery disease(CAD), TIMP-1 has been determined at baseline. Among 1945(98.4% ) patients with a mean follow-up period of 2.6± 1.2 years, 75 patients died because of cardiovascular causes. Mean concentrations of TIMP-1 were higher among patients who experienced a fatal cardiovascular event than among those who did not(820 vs. 692 ng/mL; P < 0.001). Age and sex adjusted hazard ratio of future cardiovascular death associated with one standard deviation of TIMP-1 level, was 1.37(95% CI: 1.17- 1.61; P < 0.001). The hazard ratio remained nearly identical after adjustment for clinical and therapeutic confounders. B-type natriuretic peptide(2.75, 95% CI: 1.94- 3.89; P < 0.001), C-reactive protein(1.79, 95% CI: 1.43- 2.24; P < 0.001), and TIMP-1(1.30, 95% CI: 1.07- 1.58; P=0.008) were independently associated with future cardiovascular death. Conclusion: In patients with CAD, TIMP-1 proves as an independent predictor for future cardiovascular death.展开更多
文摘Aims: Metalloproteinases are proteolytic enzymes, which decompose the extracellular matrix, influence cardiac remodelling, and are inhibited by tissue inhibitor of metalloproteinases(TIMPs). Little is known about the prognostic impact of the TIMP-1/matrix metalloproteinase complex in patients with future cardiovascular death. Methods and results: In 1979 patients with suspected coronary artery disease(CAD), TIMP-1 has been determined at baseline. Among 1945(98.4% ) patients with a mean follow-up period of 2.6± 1.2 years, 75 patients died because of cardiovascular causes. Mean concentrations of TIMP-1 were higher among patients who experienced a fatal cardiovascular event than among those who did not(820 vs. 692 ng/mL; P < 0.001). Age and sex adjusted hazard ratio of future cardiovascular death associated with one standard deviation of TIMP-1 level, was 1.37(95% CI: 1.17- 1.61; P < 0.001). The hazard ratio remained nearly identical after adjustment for clinical and therapeutic confounders. B-type natriuretic peptide(2.75, 95% CI: 1.94- 3.89; P < 0.001), C-reactive protein(1.79, 95% CI: 1.43- 2.24; P < 0.001), and TIMP-1(1.30, 95% CI: 1.07- 1.58; P=0.008) were independently associated with future cardiovascular death. Conclusion: In patients with CAD, TIMP-1 proves as an independent predictor for future cardiovascular death.
