Fig. 5: Incidence of the composite end-point and heart failure hospitalization, stroke, myocardial infarction, and death in the meta-cohort unadjusted.
From: Activated GDF11/8 subforms predict cardiovascular events and mortality in humans
A Stratified by quartile of active GDF11/8 [Q1 (0–2.70) n = 2,905, Q2 (2.71-2.76) n = 2904, Q3 (2.77-2.83) n = 2899, Q4 (2.84-3.53) n = 2,901]. P-Values for trend are p = 2.0e-60 for the composite endpoint, p = 2.5e-39 for death, p = 2.8e-32 for heart failure, p = 6.3e-03 for myocardial infarction, and p = 2.3e-02 for stroke. B Stratified by quartile of active GDF8 [Q1 (0–2.27) n = 2903, Q2 (2.28-2.32) n = 2,903, Q3 (2.33-2.37) n = 2,901, Q4 (2.38-4.17) n = 2,902]. P-Values for trend are p = 2.6e-32 for the composite endpoint, p = 1.3e-17 for death, p = 3.7e-26 for heart failure, p = 6.8e-01 for myocardial infarction, and p = 1.3e-02 for stroke. C Stratified by quartiles of active GDF11 [Q1 (0–1.86) n = 2,930, Q2 (1.87–1.91) n = 2,884, Q3 (1.92–2.00) n = 2894, Q4 (2.01–4.94) n = 2901]. There were no significant trend associations between active GDF11 quartiles with the composite endpoint of any of its individual components.Statistical analysis: Chi-squared test for trend in proportions (two-sided) was used to assess each event group distribution for each respective GDF quartile set. Data are presented as mean ± SEM. Sample size reflects independent biological replicates, each representing a unique patient from the meta-cohort. No technical replicates were used. The unit of study is the individual patient. Groups compared were stratified by quartiles of circulating ligand levels. No pooling of samples occurred. Source data are provided as a Source Data File.
