Hematological Parameters Outperform Plasma Markers in Predicting Long-Term Mortality After Coronary Angiography

High-sensitivity troponin I (hsTnI) and N-terminal pro-brain natriuretic peptide (NT-pro-BNP) are predictors of coronary artery disease. Recently, routine hematological parameters emerged as mortality predictors. We examined the predictive value of hematological parameters (from the Utrecht Patient Oriented Database) and hsTnI and NT-pro-BNP for mortality in a coronary angiography population (Utrecht Coronary Biobank n = 1913). Using Cox regression, receiver operating characteristics, integrated discrimination improvement (IDI), and continuous net reclassification improvement (cNRI) analysis, we compared the predictive properties of hematological parameters with hsTnI and NT-pro-BNP for mortality. During a median follow-up duration of 1.8 years, 77 deaths occurred. A panel of 7 hematological parameters (leukocyte count, reticulocyte mean corpuscular hemoglobin concentration, red blood cell [RBC] green (FL1) fluorescence, %neutrophils, %large [>120 fL] RBCs, %monocytes, and coefficient of variation of neutrophil complexity) was highly predictive. Added to clinical characteristics, hematological parameters (area under the curve [AUC]: 0.855, P < .001; IDI: 0.04, P = .02; cNRI: 0.41, P < .001) were better predictors than hsTnI (AUC: 0.818) or NT-pro-BNP (AUC: 0.834) alone or combined (AUC: 0.834). Hematological parameters may provide mortality risk information following coronary angiography and may be superior to hsTnI and/or NT-pro-BNP

Associations of Polymorphisms in the Peroxisome Proliferator-Activated Receptor Gamma Coactivator-1 Alpha Gene With Subsequent Coronary Heart Disease: An Individual-Level Meta-Analysis

Background: The knowledge of factors influencing disease progression in patients with established coronary heart disease (CHD) is still relatively limited. One potential pathway is related to peroxisome proliferator–activated receptor gamma coactivator-1 alpha (PPARGC1A), a transcription factor linked to energy metabolism which may play a role in the heart function. Thus, its associations with subsequent CHD events remain unclear. We aimed to investigate the effect of three different SNPs in the PPARGC1A gene on the risk of subsequent CHD in a population with established CHD. Methods: We employed an individual-level meta-analysis using 23 studies from the GENetIcs of sUbSequent Coronary Heart Disease (GENIUS-CHD) consortium, which included participants (n = 80,900) with either acute coronary syndrome, stable CHD, or a mixture of both at baseline. Three variants in the PPARGC1A gene (rs8192678, G482S; rs7672915, intron 2; and rs3755863, T528T) were tested for their associations with subsequent events during the follow-up using a Cox proportional hazards model adjusted for age and sex. The primary outcome was subsequent CHD death or myocardial infarction (CHD death/myocardial infarction). Stratified analyses of the participant or study characteristics as well as additional analyses for secondary outcomes of specific cardiovascular disease diagnoses and all-cause death were also performed. Results: Meta-analysis revealed no significant association between any of the three variants in the PPARGC1A gene and the primary outcome of CHD death/myocardial infarction among those with established CHD at baseline: rs8192678, hazard ratio (HR): 1.01, 95% confidence interval (CI) 0.98–1.05 and rs7672915, HR: 0.97, 95% CI 0.94–1.00; rs3755863, HR: 1.02, 95% CI 0.99–1.06. Similarly, no significant associations were observed for any of the secondary outcomes. The results from stratified analyses showed null results, except for significant inverse associations between rs7672915 (intron 2) and the primary outcome among 1) individuals aged ≥65, 2) individuals with renal impairment, and 3) antiplatelet users. Conclusion: We found no clear associations between polymorphisms in the PPARGC1A gene and subsequent CHD events in patients with established CHD at baseline

All-cause and cause-specific mortality of different migrant populations in Europe

This study aimed to examine differences in all-cause mortality and main causes of death across different migrant and local-born populations living in six European countries. We used data from population and mortality registers from Denmark, England & Wales, France, Netherlands, Scotland, and Spain. We calculated age-standardized mortality rates for men and women aged 0–69 years. Country-specific data were pooled to assess weighted mortality rate ratios (MRRs) using Poisson regression. Analyses were stratified by age group, country of destination, and main cause of death. In six countries combined, all-cause mortality was lower for men and women from East Asia (MRRs 0.66; 95 % confidence interval 0.62–0.71 and 0.76; 0.69–0.82, respectively), and Other Latin America (0.44; 0.42–0.46 and 0.56; 0.54–0.59, respectively) than local-born populations. Mortality rates were similar for those from Turkey. All-cause mortality was higher in men and women from North Africa (1.09; 1.08–1.11 and 1.19; 1.17–1.22, respectively) and Eastern Europe (1.30; 1.27–1.33 and 1.05; 1.01–1.08, respectively), and women from Sub-Saharan Africa (1.34; 1.30–1.38). The pattern differed by age group and country of destination. Most migrants had higher mortality due to infectious diseases and homicide while cancer mortality and suicide were lower. CVD mortality differed by migrant population. To conclude, mortality patterns varied across migrant populations in European countries. Future research should focus both on migrant populations with favourable and less favourable mortality pattern, in order to understand this heterogeneity and to drive policy at the European level

Association of Chromosome 9p21 with Subsequent Coronary Heart Disease events:A GENIUS-CHD study of individual participant data

BACKGROUND:Genetic variation at chromosome 9p21 is a recognized risk factor for coronary heart disease (CHD). However, its effect on disease progression and subsequent events is unclear, raising questions about its value for stratification of residual risk. METHODS:A variant at chromosome 9p21 (rs1333049) was tested for association with subsequent events during follow-up in 103,357 Europeans with established CHD at baseline from the GENIUS-CHD Consortium (73.1% male, mean age 62.9 years). The primary outcome, subsequent CHD death or myocardial infarction (CHD death/MI), occurred in 13,040 of the 93,115 participants with available outcome data. Effect estimates were compared to case/control risk obtained from CARDIoGRAMPlusC4D including 47,222 CHD cases and 122,264 controls free of CHD. RESULTS:Meta-analyses revealed no significant association between chromosome 9p21 and the primary outcome of CHD death/MI among those with established CHD at baseline (GENIUS-CHD OR 1.02; 95% CI 0.99-1.05). This contrasted with a strong association in CARDIoGRAMPlusC4D OR 1.20; 95% CI 1.18-1.22; p for interaction Conclusions: In contrast to studies comparing individuals with CHD to disease free controls, we found no clear association between genetic variation at chromosome 9p21 and risk of subsequent acute CHD events when all individuals had CHD at baseline. However, the association with subsequent revascularization may support the postulated mechanism of chromosome 9p21 for promoting atheroma development