FigureĀ 3.
Analysis of secondary vascular risk and mortality according to CH status. (A) Kaplan-Meier analysis of the CEP (recurrent stroke, myocardial infarction, and all-cause death) stratified by CH status. (B) Kaplan-Meier analysis of the CEP, stratified by CH status and clone size. (C) HR for the CEP from univariable Cox regression with varying VAF cutoff and CH-negative patients as reference group. The shaded area visualizes the 95% CI. (D and E) HRs for the CEP from univariable Cox regression for different gene groups (D) and different genes (E). Point size visualizes patient number, color visualizes median age of the group, and bars visualize the 95% CI. DDR, mutations in DNA damage response pathway genes (TP53, PPM1D, CHEK2, ATM, and RAD21); DTA, mutations affecting the genes DNMT3A, TET2, and ASXL1; non-DNMT3A, mutation(s) in gene(s) other than DNMT3A; spliceosome, SF3B1, SRSF2, and U2AF1.

Analysis of secondary vascular risk and mortality according to CH status. (A) Kaplan-Meier analysis of the CEP (recurrent stroke, myocardial infarction, and all-cause death) stratified by CH status. (B) Kaplan-Meier analysis of the CEP, stratified by CH status and clone size. (C) HR for the CEP from univariable Cox regression with varying VAF cutoff and CH-negative patients as reference group. The shaded area visualizes the 95% CI. (D and E) HRs for the CEP from univariable Cox regression for different gene groups (D) and different genes (E). Point size visualizes patient number, color visualizes median age of the group, and bars visualize the 95% CI. DDR, mutations in DNA damage response pathway genes (TP53, PPM1D, CHEK2, ATM, and RAD21); DTA, mutations affecting the genes DNMT3A, TET2, and ASXL1; non-DNMT3A, mutation(s) in gene(s) other than DNMT3A; spliceosome, SF3B1, SRSF2, and U2AF1.

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