Geometric Means and standard deviation of D-dimer (ng/mL) concentration at 45 years by the social class at three occasions in the 1958 British Birth cohort.

<p>SC indicates social class; SC1, professional & managerial; SC2, non-manual; SC3, manual; SC4, unskilled.</p><p>SD, standard deviation.</p

Change in the regression coefficient of Cumulative Indicator Score of SEP (CIS) in association with D-dimer without- and with-adjustments with risk factors in the 1958 British Birth Cohort.

<p>Model 1: Association between D-dimer and Cumulative Indicator Score of SEP (CIS).</p><p>Model 2: Model 1 plus smoking, physical activity and alcohol consumption.</p><p>Model 3: Model 1 plus fibrinogen, C-reactive protein and vWF.</p><p>Model 4: Model 1 plus Framingham risk score and BMI.</p><p>Model 5: Model 1 plus all the factors mentioned above.</p><p>* Each unstandardised regression coefficient (<i>β</i>) represents the amount of change in the logarithmic concentration of D-dimer for an increase in CIS.</p>†<p>This is the change in the regression coefficient of CIS in the regression models compared to Model 1 e.g., ((<i>β</i>_{Model 1} − <i>β</i>_{Model 2})/<i>β</i>_{Model 1})*10.</p

Characteristics of 21 published prospective studies of t-PA antigen, D-dimer and VWF.

<p><b>Abbreviations:</b><b>AmB</b>, American Bioproducts; <b>AmD</b>, American Diagnostica; <b>AP</b>, angina pectoris; <b>ARIC</b>, Atherosclerosis Risk in Communities Study; <b>BRHS</b>, British Regional Heart Study; <b>BWHHS</b>, British Women’s Heart and Health Study; <b>Caerphilly</b>, Caerphilly Prospective Study; <b>CHD</b>, coronary heart disease endpoint (composed of nonfatal myocardial infarction and coronary death); <b>CHS</b>, Cardiovascular Health Study; <b>CS</b>, coronary surgery; <b>DStago</b>, Diagnostica Stago; <b>EAS</b>, Edinburgh Artery Study; <b>ELISA</b>, enzyme-linked immunosorbent assay; <b>FHS</b>, Framingham Heart Study; <b>Fletcher</b>, Fletcher Challenge Study; <b>Glostrup</b>, Glostrup population studies; <b>IRE</b>, Ireland; <b>IT</b>, immunoturbidometry; <b>MESA</b>, Multi-Ethnic Study of Atherosclerosis; <b>MI</b>, myocardial infarction; <b>NPHS-I</b>, Northwick Park Heart Study I; <b>NSHDS</b>, Northern Sweden Health and Diseases Study cohort; <b>PHS</b>, Physicians’ Health Study; <b>PRIME</b>, Prospective Epidemiological Study of Myocardial Infarction; <b>PROSPER</b>, Prospective Study of Pravastatin in the Elderly at Risk; <b>NI</b>, Northern Ireland; <b>NL</b>, Netherlands; <b>NR</b>, not reported; <b>NZ</b>, New Zealand; <b>R&D Sys</b>, R&S Systems; <b>RE</b>, rocket electrophoresis; <b>Rotterdam</b>, Rotterdam Study; <b>SCO</b>, Scotland; <b>Speedwell</b>, Speedwell Study; <b>Three-City</b>, Three-City cohort study; <b>WHI</b>, Women’s Health Initiative; <b>WOSCOPS</b>, The West of Scotland Coronary Prevention Study.</p>*<p>Reports with two different study baselines and non-overlapping follow-up periods are available.</p>†<p>Median.</p>‡<p>Maximum.</p>§<p>Range.</p>||<p>Geometric mean.</p

Baseline characteristics of coronary heart disease cases and matched controls in the Reykjavik Study, and correlations with t-PA antigen, D-dimer and VWF.

<p>Abbreviations: ESR, erythrocyte sedimentation rate; IQR, inter-quartile range.</p>*<p>Means (SDs) of log_e transformed values in cases and controls were 0.2 (0.5) and 0.0 (0.4) for triglycerides; 4.4 (1.6) and 4.0 (1.7) for lipoprotein (a); 0.8 (0.8) and 0.7 (0.8) for interleukin 6; 0.5 (1.1) and 0.2 (1.1) for C-reactive protein; 2.0 (1.0) and 1.9 (1.0) for erythrocyte sedimentation rate; 2.6 (0.5) and 2.5 (0.5) for t-PA antigen; 4.8 (1.0) and 4.8 (1.0) for D-dimer; and 4.7 (0.4) and 4.6 (0.4) for VWF.</p>†<p>Percentage differences and 95% CIs were calculated per 1 SD higher level or compared to the reference category of variables shown in the left column (adjusted for age, sex and period of recruitment).</p

Associations of baseline t-PA antigen, D-dimer and VWF with coronary heart disease risk (Reykjavik Study).

<p>Odds ratios (95% CI) for coronary heart disease are shown by fifths of baseline t-PA antigen, D-dimer and VWF, plotted against the geometric mean level in each category on a log-doubling scale. *Adjusted for age, sex, period of recruitment, smoking status, body mass index, systolic blood pressure, history of diabetes, total cholesterol and log_e triglycerides.</p

Head-to-head comparison of associations of various baseline variables with coronary heart disease risk (Reykjavik Study).

<p>*Values were log_e transformed for analysis. †Adjusted for age, sex, period of recruitment, smoking status, body mass index, systolic blood pressure, history of diabetes, total cholesterol and log_e triglycerides.</p

Study flow diagram of the updated meta-analyses.

<p>The figure was designed based on the 2009 PRISMA flow diagram template (available from <a href="http://www.prisma-statement.org/statement.htm" target="_blank">http://www.prisma-statement.org/statement.htm</a>).</p

Association of baseline levels of t-PA antigen, D-dimer and VWF with coronary heart disease in the Reykjavik Study (1925 cases, 3616 controls).

*<p>Smoking status, body mass index, systolic blood pressure and any history of diabetes mellitus at baseline.</p>†<p>Total cholesterol and log_e triglycerides.</p><p>When analyses were restricted to participants with complete information on C-reactive protein (1906 cases, 3573 controls), the odds ratios (95% CI) per 1 SD higher value of t-PA antigen were 1.26 (1.18, 1.33) when adjusting for age, sex and period of recruitment, 1.15 (1.07, 1.22) when additionally adjusting for non-lipid risk factors, 1.07 (0.99, 1.14) when additionally adjusting for lipid risk factors and 1.04 (0.97, 1.11) when additionally adjusting for C-reactive protein. Corresponding odds ratios were 1.01 (0.95, 1.07), 1.04 (0.98, 1.11), 1.07 (1.00, 1.14) and 1.05 (0.99, 1.12) for D-dimer and 1.12 (1.05, 1.18), 1.09 (1.02, 1.15), 1.09 (1.03, 1.16) and 1.06 (1.00, 1.13) for VWF.</p

Meta-analyses of reported associations of t-PA antigen, D-dimer and VWF with coronary heart disease risk in prospective population-based studies.

<p>Study acronyms are explained in the legend of <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0055175#pone-0055175-t003" target="_blank"><b>Table 3</b></a>. Summary estimates were calculated using random effects models. *Degree of adjustment:+minimally adjusted (typically adjusted for age and sex only);++plus adjustment for at least one non-lipid marker;+++plus adjustment for at least one lipid marker;++++plus adjustment for at least one inflammatory marker. Where studies reported relative risks with more than one level of statistical adjustment, the most adjusted estimate was used (least adjusted estimates are reported in <b><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0055175#pone.0055175.s008" target="_blank">Figure S8</a></b>).</p

Thrombin generation.

<p>Data are presented as median [IQR] for lag time, normalized ETP (nETP), normalized peak height (nPeak Height) and the reduction on ETP upon addition of thrombomodulin (reduced ETP). Thrombin generation was assessed at a trigger of 1 or 2 pM tissue factor (TF) in the presence of 4 µM phospholipids, by means of the Calibrated Automated Thrombogram.</p