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1 SUPPLEMENTAL DATA METHODS (Supplemental Data) Study population Details of the LURIC baseline examination have been described previously (1). In brief, in the LURIC study clinically relevant CAD was defined as the occurrence of at least 1 stenosis ≥20% in at least 1 of 15 coronary segments of the 3 major coronary arteries. The angiographic severity of disease was reported as one-, two-, or three-vessel disease according to the number of vessels with stenosis ≥50% of the three major coronary arteries. Hypertension was diagnosed when systolic or diastolic blood pressure exceeded 140 or 90 mmHg, respectively, or in case of a known history of hypertension, evident through the use of antihypertensive drugs. Dyslipidemia was defined when one or more of the following criteria were present at baseline: total cholesterol ≥240 mg/dL (≥6.2 mmol/L), HDL-cholesterol <40 mg/dL (<1.0 mmol/L), LDL cholesterol >160 mg/dL (>4.1 mmol/L), triglycerides ≥150 mg/dL (≥1.6 mmol/L), and/or use of lipid-lowering medication. Diabetes mellitus was diagnosed when fasting glucose was ≥126 mg/dL (≥7.0 mmol/L), the 2 hour value from an oral glucose tolerance test was ≥200 mg/dL (≥11.1 mmol/L), and/or the glycosylated haemoglobin was ≥6.5%. Patients receiving antidiabetic medication were also classed as being diabetic. Current smoking, family history of cardiovascular disease (either fatal or non-fatal myocardial infarction or stroke) and medications from medical records and by self-reporting. Cerebrovascular disease was defined clinically by a documented previous cerebrovascular disease event (transient ischemic attack, prolonged ischemic neurologic deficit, and cerebral infarction with or without a permanent neurologic deficit) or by documented carotid stenosis with >50% luminal obstruction. Peripheral vascular disease was defined by a history of intermittent claudication, angiographic documentation of atherosclerotic luminal obstruction of the peripheral arteries, or a history of a peripheral arterial intervention for atherosclerotic disease (angioplasty, vascular surgery, and/or amputation). Left ventricular ejection fraction (LVEF) was estimated with echocardiography using the Simpson method and categorized into normal (≥55%), mildly reduced (45–54%), moderately reduced 2 (30–44%), and severely reduced (<30%). A clinical diagnosis of heart failure with reduced LVEF was defined by the combined presence of dyspnea on exertion and the echocardiographic finding LVEF<45% and the functional capacity for patients with heart failure was estimated according to New York Heart Association (NYHA) classification. Biochemical analysis Routine laboratory parameters were measured as described in detail previously (1). In Brief, Glucose was measured in serum enzymatically on a Hitachi 717 (Roche Diagnostics). Glycated hemoglobin was measured in EDTA whole blood with an immunoassay (hemoglobin A1c UNIMATE 5; Hoffmann-LaRoche) and the coefficients of variation (CVs) were 1.4-3.6% (1). Total cholesterol and triglycerides were quantified in serum with an enzymatic assay on a Hitachi 717 (Roche Diagnostics) (1). Lipoproteins (LDL- and HDL-cholesterol) were determined in plasma by a combined ultracentrifugation and precipitation method and measured with enzymatic reagents on a WAKO 30 R analyzer (WAKO Chemicals) as described previously (1). The CVs of all Lipids and Lipoproteins varied between 1-3% (1). Creatinine concentration was measured in serum by a kinetic colorimetric assay according to the Jaffé method on a Hitachi 717 (Roche Diagnostics) and estimated glomerular filtration rate (eGFR) was calculated according to the none-IDSMS traceable MDRD equation (2). Cholinesterase was measured in serum with a colorimetric assay on a Hitachi 717 (Roche Diagnostics) (1). High sensitivity Creactive protein (hs-CRP) was measured in serum by immunonephelometry on a Behring Nephelometer II (Dade Behring, Marburg) (1). Interleukin-6 was measured in plasma with a high sensitivity enzyme immunoassay (R&D Systems) (1). REFERENCES (Supplemental Data) 1. Winkelmann BR, März W, Boehm BO, Zotz R, Hager J, Hellstern P, et al. Rationale and design of the LURIC study--a resource for functional genomics, pharmacogenomics and long-term prognosis of cardiovascular disease. Pharmacogenomics. 2001;2:S1-S73. 2. Levey AS, Greene T, Kusek JW, Beck GJ. A simplified equation to predict glomerular filtration rate from serum creatinine. J Am Soc Nephrol 2000;11:A0828. 3 Table 1 (Supplemental Data). Baseline biochemical markers of all patients with stable CAD and according to all-cause mortality Total cholesterol, mmol/L LDL cholesterol, mmol/L HDL cholesterol, mmol/L Triglycerides, mmol/L Glycosylated haemoglobin, mmol/mol Glucose, mmol/L Creatinine, µmol/L eGFR, mL/min/1.73m2 Cholinesterase, µmol/sL hs-CRP, mg/L Interleukin-6, ng/L NT-proBNP, pmol/L hs-cTnT, ng/L Galectin-3, ng/mLb sST2, ng/mL All Survivors Decedents (n=1345) (n=868) (n=477) 5.0 (4.3-4.7) 2.95 (2.40-3.57) 0.98 (0.83-1.14) 1.69 (1.27-2.30) 43 (39-50) 5.2 (4.6-6.1) 80 (71-97) 81 (70-92) 97 (82-111) 2.8 (1.2-6.7) 3.0 (1.7-5.7) 35 (13-103) 10 (6-19) 14.7 (11.6-18.8) 19.4 (15.7-24.6) 5.0 (4.3-5.7) 2.97 (2.40-3.59) 0.98 (0.83-1.14) 1.71 (1.28-2.30) 42 (38-48) 5.1 (4.6-5.8) 80 (71-89) 83 (72-93) 99 (85-113) 2.3 (1.0-5.5) 2.6 (1.7-4.5) 24 (10-57) 8 (5-14) 14.2 (11.3-17.8) 18.5 (15.4-23.2) 4.9 (4.4-5.6) 2.92 (2.40-3.52) 0.96 (0.80-1.14) 1.68 (1.21-2.29) 45 (39-56) 5.4 (4.7-6.9) 89 (71-97) 78 (65-90) 91 (78-106) 4.1 (1.6-9.3) 4.3 (2.3-7.6) 89 (30-215) 17 (9-31) 15.6 (12.3-20.7) 21.4 (16.6-28.3) P value a 0.488 0.662 0.016 0.497 <0.001 <0.001 <0.001 <0.001 <0.001 <0.001 <0.001 <0.001 <0.001 <0.001 <0.001 Continuous variables are presented as median (interquartile range). a Univariate comparisons between survivors and decedents were performed with the the non-parametric Mann–Whitney U test for continuous variables. b Plasma concentrations for galectin-3 were available in 1025 patients. Respective P values were not adjusted for multiple comparisons and are therefore descriptive only.