Epidemiologic and Genetic Associations of Erythropoietin With Blood Pressure, Hypertension, and Coronary Artery Disease.
Ontology highlight
ABSTRACT:
SUBMITTER: Sun P
PROVIDER: S-EPMC8516734 | biostudies-literature | 2021 Nov
REPOSITORIES: biostudies-literature
Publications
Epidemiologic and Genetic Associations of Erythropoietin With Blood Pressure, Hypertension, and Coronary Artery Disease.
Sun Pengfei P Kumar Nitin N Tin Adrienne A Zhao Jing J Brown Michael R MR Lin Zesen Z Yang Min-Lee ML Zheng Qiwen Q Jia Jia J Bielak Lawrence F LF Yu Bing B Boerwinkle Eric E Hunker Kristina L KL Coresh Josef J Chen Y Eugene YE Huo Yong Y Kardia Sharon L R SLR Khoriaty Rami R Zhou Xiang X Morrison Alanna C AC Zhang Yan Y Ganesh Santhi K SK
Hypertension (Dallas, Tex. : 1979) 20210907 5
[Figure: see text]. ...[more]
Similar Datasets
Project description:Hypertension is a risk factor for coronary artery disease. Recent genome-wide association studies have identified 30 genetic variants associated with higher blood pressure at genome-wide significance (P<5 × 10(-8)). If elevated blood pressure is a causative factor for coronary artery disease, these variants should also increase coronary artery disease risk. Analyzing genome-wide association data from 22 233 coronary artery disease cases and 64 762 controls, we observed in the Coronary ARtery DIsease Genome-Wide Replication And Meta-Analysis (CARDIoGRAM) consortium that 88% of these blood pressure-associated polymorphisms were likewise positively associated with coronary artery disease, that is, they had an odds ratio >1 for coronary artery disease, a proportion much higher than expected by chance (P=4 × 10(-5)). The average relative coronary artery disease risk increase per each of the multiple blood pressure-raising alleles observed in the consortium was 3.0% for systolic blood pressure-associated polymorphisms (95% confidence interval, 1.8%-4.3%) and 2.9% for diastolic blood pressure-associated polymorphisms (95% confidence interval, 1.7%-4.1%). In substudies, individuals carrying most systolic blood pressure- and diastolic blood pressure-related risk alleles (top quintile of a genetic risk score distribution) had 70% (95% confidence interval, 50%-94%) and 59% (95% confidence interval, 40%-81%) higher odds of having coronary artery disease, respectively, as compared with individuals in the bottom quintile. In conclusion, most blood pressure-associated polymorphisms also confer an increased risk for coronary artery disease. These findings are consistent with a causal relationship of increasing blood pressure to coronary artery disease. Genetic variants primarily affecting blood pressure contribute to the genetic basis of coronary artery disease.
| S-EPMC3855241 | biostudies-literature
Project description:Background/objectivesTo investigate the associations between ophthalmic parameters, CYP4F2 (rs2108622) and ABCA1 (rs1883025) polymorphisms and coronary artery disease, considering the accessibility, non-invasive origin of retinal examination and its possible resemblance to coronary arteries.Subjects/methodsOverall 165 participants divided into groups based on the coronary angiography results and clinical status: control group (N = 73), MI group (N = 63), 3VD (three vessel disease) (N = 24). All the participants underwent total ophthalmic examination - optical coherence tomography (OCT) and OCT angiography of the macula region were performed and evaluated. Total cholesterol, high-density lipoprotein, low-density lipoprotein and triglyceride cholesterol (Tg-C) were tested. A standard manufacturer's protocol for CYP4F2 (rs2108622) and ABCA1 (rs1883025) was used for genotyping with TaqMan probes.ResultsGCL+ layer was thicker in control group vs. 3VD group (74.00; 62.67-94.67 (median; min.-max.) vs. 71.06; 51.33-78.44, p = 0.037). T allele carriers under ABCA1 rs1883025 dominant model were shown to have ticker retina and smaller foveal avascular zone in superficial capillary plexus and smaller Tg-C concentration. ABCA1 rs1883025 was associated with retinal thickness (OR = 0.575, 95% CI 0.348-0.948, p = 0.030). Univariate logistic regression showed that ABCA1 rs1883025 CT genotype is associated with decreased risk for coronary artery disease development under overdominant genetic model (OR = 0.498, 95% CI 0.254-0.976; p = 0.042) and codominant genetic model (OR = 0.468, 95% CI 0.232-0.945, p = 0.034).ConclusionsResults of this study confirmed that non-invasive methods such as OCT of eye might be used for identification of patients at risk of CAD.
| S-EPMC10810895 | biostudies-literature
Project description:The objective was to improve the management of patients with hypertension (HTN) and coronary artery disease (CAD), utilizing a model which integrates 3 determinants of coronary blood flow (CBF)-CAD severity, diastolic blood pressure (DBP), and left ventricular (LV) mass. We validated non-parametric equations for CBF estimation in a consecutive patient sample (N = 81) with HTN and CAD. There was a highly significant correlation (r = .565; P < .01) between clinical DBP and estimated CBF. Greater LV mass and more severe CAD shifted the relationship towards less CBF at the same DBP. LV mass was more critical when DBP >70 mm Hg. Estimated changes in CBF at different DBP considering the severity of CAD and LV mass can be calculated. In summary, the severity of CAD from coronary CT or coronary angiography combined with LV mass from echocardiography permits clinicians to guide the extent of, or target for, DBP to avoid seriously compromising CBF.
| S-EPMC8030961 | biostudies-literature
Project description:Objective- Arterial stiffness index (ASI) is independently associated with blood pressure (BP) and coronary artery disease (CAD) epidemiologically. However, it is unknown whether these associations represent causal relationships. Here, we assess whether genetic predisposition to increased ASI is associated with elevated BP and CAD risk. Approach and Results- We first performed a large-scale epidemiological association of finger photoplethysmography-derived ASI in the UK Biobank, finding significant associations with systolic BP (β=0.55 mm Hg; [95% CI, 0.45-0.65]; P=5.77×10-24; N=137 858), diastolic BP (β=1.05 mm Hg; [95% CI, 0.99-1.11]; P=7.27×10-272; N=137 862), and incident CAD (hazard ratio, 1.08; [95% CI, 1.04-1.11]; P=1.5×10-6; N=3692 cases, 126 615 controls) in multivariable models. We then performed an ASI genome-wide association study analysis in 131 686 participants from the UK Biobank. Across participants not in the ASI genome-wide association study, a 6-variant ASI polygenic risk score was calculated. Each SD increase in genetic ASI was associated with systolic BP (β=4.63 mm Hg; [95% CI, 2.1-7.2]; P=3.37×10-4; N=208 897), and diastolic BP (β=2.61 mm Hg; [95% CI, 1.2-4.0]; P=2.85×10-4; N=208 897); however, no association was observed with incident CAD (hazard ratio, 1.12; [95% CI, 0.55-2.3]; P=0.75; N=223 061; 7534 cases). The lack of CAD association observed was replicated among 184 305 participants (60 810 cases) from the CARDIOGRAMplusC4D (Coronary Artery Disease Genetics Consortium; odds ratio, 0.56; [95% CI, 0.26-1.24]; P=0.15). Conclusions- Our data support the conclusion that finger photoplethysmography-derived ASI is an independent, genetically causal risk factor for BP, but do not support the notion that ASI is a suitable surrogate for CAD risk.
| S-EPMC6531323 | biostudies-literature
Project description:Background and aimsHypertension is associated with increased clinical and subclinical coronary artery disease (CAD); however, the relationship between blood pressure and coronary plaque volume is unclear. We examined the effect of systolic blood pressure (SBP) and diastolic blood pressure (DBP) on coronary artery plaque volume.Methods285 subjects with stable CAD on statin therapy underwent coronary computed tomographic angiography to measure volume of fatty, fibrous, noncalcified, calcified and total coronary plaque.ResultsMean (SD) age was 63.1 (7.7); mean (SD) LDL-C, 78.7 mg/dL (28.5). Compared to the highest DBP tertile (>76 mmHg), those in the lowest DBP tertile (≤68 mmHg) had lower volumes of fatty: 10.0 vs. 7.7 mm3/mm, (p trend = 0.042), fibrous: 19.6 vs. 13.8 mm3/mm (p trend = 0.011), non-calcified: 29.7 vs. 22.5 mm3/mm (p trend = 0.017) and total plaque: 37.8 vs. 25.1 mm3/mm (p trend = 0.010) whereas there was no relationship with SBP tertiles. Similarly, when examined as a continuous variable, higher DBP was a significant independent predictor of higher plaque volume after multivariate adjustment: for every 1 mmHg increase in DBP, fibrous plaque increased 0.128 mm3/mm (p = 0.022), noncalcified plaque increased 0.176 mm3/mm (p = 0.045), calcified plaque increased 0.096 mm3/mm (p = 0.001) and total plaque increased 0.249 mm3/mm (p = 0.019) whereas SBP ranging from 95 to 154 mmHg did not predict plaque volume.ConclusionsLevel of DBP predicts coronary plaque with a DBP tertile ≤68 mmHg associated with the least amount of coronary plaque in subjects with LDL-C < 80 mg/dL.
| S-EPMC7963403 | biostudies-literature
Project description:It has been postulated that multiple-marker methods may have added ability, over single-marker methods, to detect genetic variants associated with disease. The Wellcome Trust Case Control Consortium (WTCCC) provided the first successful large genome-wide association studies (GWAS) which included single-marker association analyses for seven common complex diseases. Of those signals detected, only one was associated with coronary artery disease (CAD), and none were identified for hypertension (HTN). Our objective was to find additional genetic associations and pathways for cardiovascular disease by examining the WTCCC data for variants associated with CAD and HTN using two-marker testing methods. We applied two-marker association testing to the WTCCC dataset, which includes ~2,000 affected individuals with each disorder, and a shared pool of ~3,000 controls, all genotyped using Affymetrix GeneChip 500 K arrays. For CAD, we detected single nucleotide polymorphisms (SNP) pairs in three genes showing genome-wide significance: HFE2, STK32B, and DIPC2. The most notable SNP pairs in a non-protein-coding region were at 9p21, a known major CAD-associated region. For HTN, we detected SNP pairs in five genes: GPR39, XRCC4, MYO6, ZFAT, and MACROD2. Four further associated SNP pair regions were at least 70 kb from any known gene. We have shown that novel, multiple-marker, statistical methods can be of use in finding variants in GWAS. We describe many new, associated variants for both CAD and HTN and describe their known genetic mechanisms.
| S-EPMC3576836 | biostudies-literature
Project description:BackgroundBlood pressure (BP) control among coronary artery disease patients remains suboptimal in clinical practice, potentially due to gaps in treatment intensification and medication adherence. However, longitudinal studies evaluating these relationships and outcomes are limited.Methods and resultsWe assessed BP trajectories among health maintenance organization patients with hypertension and incident coronary artery disease. BP trajectories were modeled over the year after coronary artery disease diagnosis, stratified by target BP goal. Treatment intensification (increase in BP therapies in the setting of an elevated BP), medication adherence (percentage of days covered with BP therapies), and outcomes (all-cause mortality, myocardial infarction, and revascularization) were evaluated in multivariable models: 9569 patients had a <140/90 mm Hg BP target and 12,861 had a <130/80 mm Hg BP target. Within each group, 4 trajectories were identified: good, borderline, improved, and poor control. After adjustment, increasing BP treatment intensity was significantly associated with better BP trajectories in both groups. Medication adherence had inconsistent effects. There were no significant differences in combined outcomes by BP trajectory, but among the diabetes and renal disease cohort, borderline control patients were less likely to have myocardial infarction (odds ratio, 0.61; 95% confidence interval, 0.40-0.93), and good control patients were less likely to have myocardial infarction (odds ratio, 0.53; 95% confidence interval, 0.34-0.84) or a revascularization procedure (odds ratio, 0.66; 95% confidence interval, 0.47-0.93) compared with poor control patients.ConclusionsIn this health maintenance organization population, treatment intensification but not medication adherence significantly affects BP trajectories in the year after coronary artery disease diagnosis. Better BP trajectories are associated with lower rates of myocardial infarction and revascularization.
| S-EPMC3069553 | biostudies-literature
Project description:To investigate the optimal blood pressure (BP) in patients with coronary artery disease (CAD), we conducted subgroup analysis using SPRINT data. The study sample included 1206 participants with CAD (of whom 692 underwent coronary revascularization) and 8127 participants without CAD. Participants were randomized into two groups (systolic BP target of 140 mm Hg vs. 120 mm Hg). The primary outcome was a composite of cardiovascular events. After a median follow-up of 3.9 years, the hazard ratios (HRs) for the primary outcome were 0.65 (95% confidence interval (CI) 0.53-0.79) and 1.05 (95% CI 0.76-1.46) among those in the non-CAD and CAD subgroups, respectively (P value for interaction 0.02). Intensive BP treatment was a protective factor for all-cause death (HR 0.60, 95% CI 0.37-0.96) in the CAD subgroup, compared with standard BP treatment. The HRs (95% CI) for stroke were 3.57 (1.17-10.85) and 1.03 (0.29-3.62) among those in the coronary revascularization and non-revascularization subgroups, respectively (P value for interaction 0.13). For safety events, intensive BP treatment increased the risk of hypotension (HR 2.00, 95% CI 1.06-3.79) and electrolyte abnormalities (HR 2.38, 95% CI 1.25-4.56) in the CAD subgroup, while the risk of serious adverse events did not increase (HR 1.03, 95% CI 0.88-1.20). These results suggest that positive benefits from intensive BP treatment might be attenuated in patients with CAD who are under better secondary prevention. The risk of stroke might increase at the systolic BP target of 120 mm Hg in case of coronary revascularization, although the confidence interval was wide.
| S-EPMC8766284 | biostudies-literature
Project description:The dipping variations of circadian blood pressure (BP) correlate closely with target-organ damages and cardiovascular events. The aim of this study was to investigate the relationship between BP reverse dipping and the prevalence of stable coronary artery disease (sCAD) in hypertensive patients. Clinical data and the results of 24-hour ambulatory BP monitoring (ABPM) were obtained from 718 hypertensive patients (390 males, mean age 59.6 ± 13.8 years) in a single centre in Northern China. Reverse dipping pattern was defined as nocturnal systolic BP (SBP) was higher than daytime SBP. A logistic regression model was applied to explore the independent risk factors of sCAD. The patients with BP reverse dipping accounted for 31.5% in sCAD group and 19.5% in control group (P < 0.05). In multivariate analysis, BP reverse dipping remained significantly associated with the prevalence of sCAD (Odds ratio [OR], 1.772; p = 0.027). Furthermore, the circadian decline rate of SBP was independently associated with sCAD (OR, 0.975; p = 0.043). The hypertensive patients with reverse BP dipping were found to be more frequently suffering from sCAD. BP reverse dipping examined with 24-hour ABPM may indicate sCAD.
| S-EPMC4853743 | biostudies-literature
Project description:Office blood pressure (OBP) is used for diagnosing and treating hypertension but ambulatory blood pressure measurement (ABPM) associates more accurately with patient outcome. BP control is important in secondary prevention but it is unknown whether the use of APBM improves BP-control in this setting. Our objective was to investigate whether physician awareness of ABP after percutaneous coronary intervention (PCI) improved BP-control. Methods: A total of 200 patients performed ABPM before and after their PCI follow-up visit. Patients were randomized to open (O) or concealed (C) ABPM results for the physician at the follow-up visit. The change in ABP and antihypertensive medication in relation to baseline ABP was compared between the two groups. Results: The average OBP (O and C: 128/76 mmHg) and ABP (O: 123/73 mmHg, C: 127/74 mmHg) was well controlled and did not change between the first and second measurement. A slight increase in systolic ABP during night time was observed in the open arm compared to the concealed arm. Among patients with high ABP (>130/80 mm Hg) at baseline more patients in the C compared to O group remained with a high ABP at the end of study 34/44 (77%) vs 19/34 (56%), p = 0.045. There was a positive correlation between baseline systolic ABP and ABP change in both the O (r = 0.41, p < 0.001) and the C (r = 0.24, p = 0.014) groups but the association was steeper in the open group (p = 0.035). In patients with low ABP an increase and in patients with high ABP a decrease in ABP was observed in the O group where more changes in medication were done. Conclusions: ABPM did not lower blood pressure in patients with CAD apart from in those with elevated ABP but led to more relevant changes in antihypertensive treatments. Further studies are needed to answer whether patient outcome is affected.
| S-EPMC7803061 | biostudies-literature