scholarly journals Relationship Between Blood Pressure and Incident Cardiovascular Disease

Hypertension ◽  
2021 ◽  
Author(s):  
Rainer Malik ◽  
Marios K. Georgakis ◽  
Marijana Vujkovic ◽  
Scott M. Damrauer ◽  
Paul Elliott ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Diastolic Blood Pressure ◽  
Genetic Variants ◽  
Mendelian Randomization ◽  
Hazard Ratio ◽  
European Ancestry ◽  
Artery Disease

Observational studies exploring whether there is a nonlinear effect of blood pressure on cardiovascular disease (CVD) risk are hindered by confounding. This limitation can be overcome by leveraging randomly allocated genetic variants in nonlinear Mendelian randomization analyses. Based on their association with blood pressure traits in a genome-wide association study of 299 024 European ancestry individuals, we selected 253 genetic variants to proxy the effect of modifying systolic and diastolic blood pressure. Considering the outcomes of incident coronary artery disease, stroke and the combined outcome of CVD, linear and nonlinear Mendelian randomization analyses were performed on 255 714 European ancestry participants without a history of CVD or antihypertensive medication use. There was no evidence favoring nonlinear relationships of genetically proxied systolic and diastolic blood pressure with the cardiovascular outcomes over linear relationships. For every 10-mm Hg increase in genetically proxied systolic blood pressure, risk of incident CVD increased by 49% (hazard ratio, 1.49 [95% CI, 1.38–1.61]), with similar estimates obtained for coronary artery disease (hazard ratio, 1.50 [95% CI, 1.38–1.63]) and stroke (hazard ratio, 1.44 [95% CI, 1.22–1.70]). Genetically proxied blood pressure had a similar relationship with CVD in men and women. These findings provide evidence to support that even for individuals who do not have elevated blood pressure, public health interventions achieving persistent blood pressure reduction will be of considerable benefit in the primary prevention of CVD.

scholarly journals MR-Clust: Clustering of genetic variants in Mendelian randomization with similar causal estimates

2019 ◽  
Author(s):  
Christopher N Foley ◽  
Paul D W Kirk ◽  
Stephen Burgess
Keyword(s):  
Blood Pressure ◽  
Coronary Artery Disease ◽  
Risk Factor ◽  
Coronary Artery ◽  
Genetic Variants ◽  
Mendelian Randomization ◽  
Disease Risk ◽  
Causal Effect ◽  
Coronary Artery Disease Risk ◽  
Artery Disease

AbstractMotivationMendelian randomization is an epidemiological technique that uses genetic variants as instrumental variables to estimate the causal effect of a risk factor on an outcome. We consider a scenario in which causal estimates based on each variant in turn differ more strongly than expected by chance alone, but the variants can be divided into distinct clusters, such that all variants in the cluster have similar causal estimates. This scenario is likely to occur when there are several distinct causal mechanisms by which a risk factor influences an outcome with different magnitudes of causal effect. We have developed an algorithm MR-Clust that finds such clusters of variants, and so can identify variants that reflect distinct causal mechanisms. Two features of our clustering algorithm are that it accounts for uncertainty in the causal estimates, and it includes ‘null’ and ‘junk’ clusters, to provide protection against the detection of spurious clusters.ResultsOur algorithm correctly detected the number of clusters in a simulation analysis, outperforming the popular Mclust method. In an applied example considering the effect of blood pressure on coronary artery disease risk, the method detected four clusters of genetic variants. A hypothesis-free search suggested that variants in the cluster with a negative effect of blood pressure on coronary artery disease risk were more strongly related to trunk fat percentage and other adiposity measures than variants not in this cluster.Availability and ImplementationMR-Clust can be downloaded from https://github.com/cnfoley/[email protected] or [email protected] InformationSupplementary Material is included in the submission.

scholarly journals MR-Clust: clustering of genetic variants in Mendelian randomization with similar causal estimates

2020 ◽  
Author(s):  
Christopher N Foley ◽  
Amy M Mason ◽  
Paul D W Kirk ◽  
Stephen Burgess
Keyword(s):  
Blood Pressure ◽  
Coronary Artery Disease ◽  
Risk Factor ◽  
Coronary Artery ◽  
Genetic Variants ◽  
Mendelian Randomization ◽  
Disease Risk ◽  
Causal Effect ◽  
Coronary Artery Disease Risk ◽  
Artery Disease

Abstract Motivation Mendelian randomization is an epidemiological technique that uses genetic variants as instrumental variables to estimate the causal effect of a risk factor on an outcome. We consider a scenario in which causal estimates based on each variant in turn differ more strongly than expected by chance alone, but the variants can be divided into distinct clusters, such that all variants in the cluster have similar causal estimates. This scenario is likely to occur when there are several distinct causal mechanisms by which a risk factor influences an outcome with different magnitudes of causal effect. We have developed an algorithm MR-Clust that finds such clusters of variants, and so can identify variants that reflect distinct causal mechanisms. Two features of our clustering algorithm are that it accounts for differential uncertainty in the causal estimates, and it includes ‘null’ and ‘junk’ clusters, to provide protection against the detection of spurious clusters. Results Our algorithm correctly detected the number of clusters in a simulation analysis, outperforming methods that either do not account for uncertainty or do not include null and junk clusters. In an applied example considering the effect of blood pressure on coronary artery disease risk, the method detected four clusters of genetic variants. A post hoc hypothesis-generating search suggested that variants in the cluster with a negative effect of blood pressure on coronary artery disease risk were more strongly related to trunk fat percentage and other adiposity measures than variants not in this cluster. Availability and implementation MR-Clust can be downloaded from https://github.com/cnfoley/mrclust. Supplementary information Supplementary data are available at Bioinformatics online.

scholarly journals Increased response of diastolic blood pressure to exercise in patients with coronary artery disease: an index of latent ventricular dysfunction?

Heart ◽  
1993 ◽  
Vol 69 (6) ◽  
pp. 507-511 ◽  
Author(s):  
I A Paraskevaidis ◽  
D T Kremastinos ◽  
A S Kassimatis ◽  
G K Karavolias ◽  
G D Kordosis ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Diastolic Blood Pressure ◽  
Ventricular Dysfunction ◽  
Artery Disease

scholarly journals Genetically Predicted Type 2 Diabetes Mellitus Liability, Glycated Hemoglobin and Cardiovascular Diseases: A Wide-Angled Mendelian Randomization Study

Genes ◽  
2021 ◽  
Vol 12 (10) ◽  
pp. 1644
Author(s):  
Bowen Liu ◽  
Amy M. Mason ◽  
Luanluan Sun ◽  
Emanuele Di Angelantonio ◽  
Dipender Gill ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Cardiovascular Diseases ◽  
General Population ◽  
Mendelian Randomization ◽  
Causal Effects ◽  
Disease Outcomes ◽  
Artery Disease ◽  
Diagnosed Diabetes

(1) Aim: To investigate the causal effects of T2DM liability and glycated haemoglobin (HbA1c) levels on various cardiovascular disease outcomes, both in the general population and in non-diabetic individuals specifically. (2) Methods: We selected 243 variants as genetic instruments for T2DM liability and 536 variants for HbA1c. Linear Mendelian randomization analyses were performed to estimate the associations of genetically-predicted T2DM liability and HbA1c with 12 cardiovascular disease outcomes in 367,703 unrelated UK Biobank participants of European ancestries. We performed secondary analyses in participants without diabetes (HbA1c < 6.5% with no diagnosed diabetes), and in participants without diabetes or pre-diabetes (HbA1c < 5.7% with no diagnosed diabetes). (3) Results: Genetically-predicted T2DM liability was positively associated (p < 0.004, 0.05/12) with peripheral vascular disease, aortic valve stenosis, coronary artery disease, heart failure, ischaemic stroke, and any stroke. Genetically-predicted HbA1c was positively associated with coronary artery disease and any stroke. Mendelian randomization estimates generally shifted towards the null when excluding diabetic and pre-diabetic participants from analyses. (4) Conclusions: This genetic evidence supports causal effects of T2DM liability and HbA1c on a range of cardiovascular diseases, suggesting that improving glycaemic control could reduce cardiovascular risk in a general population, with greatest benefit in individuals with diabetes.

Cardiovascular Prognosis in Drug-Resistant Hypertension Stratified by 24-Hour Ambulatory Blood Pressure: The JAMP Study

Hypertension ◽  
2021 ◽  
Author(s):  
Kazuomi Kario ◽  
Satoshi Hoshide ◽  
Keisuke Narita ◽  
Yukie Okawara ◽  
Hiroshi Kanegae ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Coronary Artery Disease ◽  
Risk Factor ◽  
Coronary Artery ◽  
Ambulatory Blood Pressure ◽  
Resistant Hypertension ◽  
Cardiovascular Events ◽  
Atherosclerotic Cardiovascular Disease ◽  
Artery Disease

Resistant hypertension is an important cardiovascular risk factor. This analysis of the JAMP study (Japan Ambulatory Blood Pressure Monitoring Prospective) data investigated the effects of uncontrolled resistant hypertension diagnosed using ambulatory blood pressure (BP) monitoring on the risk of heart failure (HF) and overall cardiovascular events. The JAMP study patients with hypertension and no HF history were included. They had true resistant hypertension (24-hour BP ≥130/80 mm Hg), pseudoresistant hypertension (24-hour BP <130/80 mm Hg), well-controlled nonresistant hypertension (24-hour BP <130/80 mm Hg), or uncontrolled nonresistant hypertension (24-hour BP ≥130/80 mm Hg). The primary end point was total cardiovascular events, including atherosclerotic cardiovascular disease (fatal/nonfatal stroke and fatal/nonfatal coronary artery disease), and HF. During 4.5±2.4 years of follow-up the overall incidence per 1000 person-years was 10.1 for total cardiovascular disease, 4.1 for stroke, 3.5 for coronary artery disease, and 2.6 for HF. The adjusted risk of total cardiovascular and HF events was significantly increased in patients with true resistant versus controlled nonresistant hypertension (hazard ratio, 1.66 [95% CI, 1.12–2.48]; P =0.012 and 2.24 [95% CI, 1.17–4.30]; P =0.015, respectively) and versus uncontrolled nonresistant hypertension (1.51 [1.03–2.20]; P =0.034 and 3.03 [1.58–5.83]; P <0.001, respectively). The findings were robust in a sensitivity analysis using a slightly different definition of resistant hypertension. True resistant hypertension diagnosed using ambulatory BP monitoring is a significant independent risk factor for cardiovascular disease events, especially for HF. This highlights the importance of diagnosing and effectively treating resistant hypertension. Registration: URL: https://www.umin.ac.jp/ctr ; Unique identifier: UMIN000020377.

scholarly journals THE ASSOCIATION BETWEEN LOW DIASTOLIC BLOOD PRESSURE AND HIGH ATHEROSCLEROTIC VASCULAR BURDEN IN PATIENTS WITH CORONARY ARTERY DISEASE

2019 ◽  
Vol 6 (14) ◽  
pp. 1109-1112
Author(s):  
Kavirayani P. Hemamalini ◽  
Bitra Veera Raghavulu ◽  
Akula Annapurna ◽  
Gadamsetty Rajkumar ◽  
Challapalli Narasimha Raju
Keyword(s):  
Blood Pressure ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Diastolic Blood Pressure ◽  
Artery Disease ◽  
Vascular Burden

scholarly journals Associations of Systolic Blood Pressure and Diastolic Blood Pressure With the Incidence of Coronary Artery Disease or Cerebrovascular Disease According to Glucose Status

2021 ◽  
Author(s):  
Mayuko Harada Yamada ◽  
Kazuya Fujihara ◽  
Satoru Kodama ◽  
Takaaki Sato ◽  
Taeko Osawa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Cerebrovascular Disease ◽  
Systolic Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Proportional Hazards Model ◽  
Cox Proportional Hazards Model ◽  
Artery Disease ◽  
Glucose Status

<b>Aims: </b>To determine associations of systolic blood pressure (SBP) and diastolic blood pressure (DBP) with new-onset coronary artery disease (CAD) or cerebrovascular disease (CVD) according to glucose status. <p><b>Research Design and Methods: </b>Examined was a nationwide claims database from 2008 – 2016<b> </b>on 593,196 individuals. Cox proportional hazards model identified risks of CAD and CVD events among 5 levels of SBP and DBP. </p> <p><b>Results:</b> During the study period 2,240 CAD and 3,207 CVD events occurred. Compared with SBP ≤119 mmHg, which was the lowest quintile of SBP, hazard ratios (HRs) (95% confidence interval) for CAD/CVD in the 4 higher quintiles (120-129, 130-139, 140-149, ≥150 mmHg) gradually increased from 2.10 (1.73 to 2.56)/ 1.46 (1.27 to 1.68) in quintile 2 to 3.21 (2.37 to 4.34)/4.76 (3.94 to 5.75) in quintile 5 for normoglycemia; from 1.39 (1.14 to 1.69)/1.70 (1.44 to 2.10) in quintile 2 to 2.52 (1.95 to 3.26)/4.12 (3.38 to 5.02) in quintile 5 for borderline glycemia; and from 1.50 (1.19 to 1.90)/1.72 (1.31 to 2.26) in quintile 2 to 2.52 (1.95 to 3.26)/3.54 (2.66 to 4.70) in quintile 5 for diabetes. A similar trend was observed for DBP across 4 quintiles (75-79, 80-84, 85-89, ≥90 mmHg) compared with ≤74 mmHg, which was the lowest quintile. </p> <p><b>Conclusions: </b>Results indicated that cardiovascular risks gradually increased with increases in SBP and DBP regardless of the presence of and degree of a glucose abnormality. Further interventional trials are required to apply findings from this cohort study to clinical practice. </p>

Genetically rheumatoid arthrits and risk of comorbidities: a Mendelian randomization study

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Fokina ◽  
J Fill ◽  
G Klappacher
Keyword(s):  
Rheumatoid Arthritis ◽  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Mendelian Randomization ◽  
Funding Source ◽  
Artery Disease ◽  
Genetically Determined ◽  
Genetic Instruments

Abstract Background Ample observational evidence indicates that patients with rheumatoid arthritis (RA) are at increased risk of developing comorbid conditions, in particular cardiovascular disease. The pathogenesis of these comorbidities is still largely unknown. For effective preventive measures, it would however be important to discriminate between those that are causally linked with rheumatoid arthritis and those that are the results of concomitant treatments or other confounding factors. Purpose Our objective was to explore whether genetically determined manifestation of RA was associated with any comorbidities, in particular cardiovascular disease, by conducting a 2-sample Mendelian randomization (MR) study on publicly available summary statistics from genome-wide association study (GWAS) consortia. Methods Genetic instruments for RA were obtained from a GWAS of 14,361 autoantibody-positive individuals with RA and 43,923 controls of European descent (Okada et al. 2014). The CARDIoGRAMplusC4D consortium comprising 60,801 cases with coronary artery disease and 123,504 controls was used to evaluate the associations with cardiovascular outcomes applying inverse variance–weighted meta-analysis, weighted-median analysis, Mendelian randomization–Egger regression, and multivariable Mendelian randomization. Genetic instruments for RA were further tested for association with other etiologically related traits by using publicly available GWAS data. Results Genetic predisposition to RA was not associated with higher risk of coronary artery disease (beta coefficient [b] ± standard error [se] = 0.02±0.03; P=0.4913), and myocardial infarction (b ± se = 0.03±0.03; P=0.3338). In contrast, IgA nephropathy (b ± se = 0.47±0.18; P=0.0225) and triglyceride levels were significantly related as outcomes to genetically determined RA as exposure. Other significantly related outcomes were the manifestation of squamous cell lung cancer (b ± se = 0.17±0.08; P=0.0496), serous ovarian cancer (b ± se = 0.13±0.05; P=0.0202), and prostate cancer (b ± se = 0.06±0.02; P=0.0041). Conclusions Despite the high prevalence of coronary artery disease and myocardial infarction among RA patients in observational studies, cardiovascular outcomes were not significantly associated with RA by Mendelian randomization. This paradox might partly be explained by the traits such as IgA nephropathy and elevated triglyceride levels that could act as mediators for the increased cardiovascular risk by their causal link with genetically determined RA. Funding Acknowledgement Type of funding source: Public hospital(s). Main funding source(s): Medical University of Vienna, Austria

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