Prospective Study of Fibrinolytic Factors and Incident Coronary Heart Disease

Folsom, Aaron R.; Aleksic, Nena; Park, Eunsik; Salomaa, Veikko; Juneja, Harinder S.; Wu, Kenneth K.

doi:10.1161/01.atv.21.4.611

Cited by 223 publications

(178 citation statements)

References 54 publications

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“…A pooled meta‐analysis shows the highest quantile (ie, tertile, quartile, or quintile) of blood PAI‐1 levels is associated with higher risk of CHD incidence compared with the lowest quantile (OR=2.17; 95% CI: 1.53, 3.07; Figure 2A) in an age‐and sex‐adjusted model 11, 12, 13, 14, 15, 16, 17, 18, 19, 22. The overall heterogeneity across studies is high (I 2 =71.5%, P <0.001; Figure 2A).…”

Section: Resultsmentioning

confidence: 99%

“…The overall heterogeneity across studies is high (I 2 =71.5%, P <0.001; Figure 2A). The association estimate is reduced but remains significant in studies using a multivariable‐adjusted model (OR=1.46; 95% CI: 1.13, 1.88; Figure 2B),11, 12, 13, 14, 16, 17, 18, 19, 20, 21, 22, 23, 31 with a lower overall heterogeneity compared with studies applying only an age‐and sex‐adjusted model (I 2 =55.7%, P =0.008; Figure 2B). In the subgroup meta‐analysis based on different PAI‐1 quantile scales, heterogeneity is observed most strongly in the quartile subgroup in both age‐ and sex‐adjusted model (I 2 =81.6%, P <0.001; Figure 2A) and the multivariable‐adjusted model (I 2 =61.7%, P <0.016; Figure 2B).…”

Section: Resultsmentioning

confidence: 99%

“…The association of elevated plasma PAI‐1 levels with CHD incidence has been reported in longitudinal studies 11, 12, 13, 14, 15, 16, 17, 18, 19. However, this association did not always remain consistent after adjusting for cardiovascular risk factors 11, 12, 13, 14, 16, 17, 18, 19, 20, 21, 22, 23. On the one hand, these inconsistencies could be due to small sample sizes and/or restricted study populations (eg, type 2 diabetes mellitus patients, obese individuals, or HIV patients) 20, 24.…”

Section: Introductionmentioning

confidence: 84%

“…Ten studies that adjusted only for age and sex reported association between PAI‐1 and CHD incidence (Table S1), while 13 studies found the same association following adjustment for multiple covariates (eg, BMI, blood glucose, blood lipids, and blood pressure; Table S1). 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 31 Covariates used in each study that included multivariable‐adjusted models are shown in Table S1. Detailed literature screening procedure is presented in Figure 1.…”

Section: Methodsmentioning

confidence: 99%

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Causal Effect of Plasminogen Activator Inhibitor Type 1 on Coronary Heart Disease

Song

Burgess

Eicher

et al. 2017

JAHA

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101

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BackgroundPlasminogen activator inhibitor type 1 (PAI‐1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI‐1 levels are associated with increased risk of coronary heart disease (CHD). However, it is unclear whether the association reflects a causal influence of PAI‐1 on CHD risk.Methods and ResultsTo evaluate the association between PAI‐1 and CHD, we applied a 3‐step strategy. First, we investigated the observational association between PAI‐1 and CHD incidence using a systematic review based on a literature search for PAI‐1 and CHD studies. Second, we explored the causal association between PAI‐1 and CHD using a Mendelian randomization approach using summary statistics from large genome‐wide association studies. Finally, we explored the causal effect of PAI‐1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta‐analysis, the highest quantile of blood PAI‐1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age‐ and sex‐adjusted model. The effect size was reduced in studies using a multivariable‐adjusted model (odds ratio=1.46; 95% CI: 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI‐1 level on CHD risk (odds ratio=1.22 per unit increase of log‐transformed PAI‐1; 95% CI: 1.01, 1.47). In addition, we also detected a causal effect of PAI‐1 on elevating blood glucose and high‐density lipoprotein cholesterol.ConclusionsOur study indicates a causal effect of elevated PAI‐1 level on CHD risk, which may be mediated by glucose dysfunction.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 84%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Causal Effect of Plasminogen Activator Inhibitor Type 1 on Coronary Heart Disease

Song

Burgess

Eicher

et al. 2017

JAHA

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101

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“…Additionally, plasminogen-activator inhibitor-1 (PAI-1), a marker of fibrinolysis, is thought to be a risk factor for cardiovascular events [17]. PAI-1 gene transcription was reported to be stimulated by hypoxia in an experimental model [18].…”

Section: Introductionmentioning

confidence: 99%

Increased low-grade inflammation and plasminogen-activator inhibitor-1 level in nondippers with sleep apnea syndrome

Ishikawa¹,

Hoshide²,

Eguchi³

et al. 2008

Journal of Hypertension

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Objective-Patients with sleep apnea syndrome (SAS) have an increased risk of cardiovascular events and frequently show a non-dipper pattern (blunted nocturnal decline <10%) of systolic blood pressure (BP). We investigated neurohumoral activation and risk factors in relation to nocturnal BP dipping pattern and SAS.Methods-We conducted sleep polysomnography and ambulatory BP monitoring, and measured high-sensitivity C-reactive protein (hsCRP), tissue-type plasminogen activator inhibitor-1 (PAI-1), and neurohumoral factors in 121 outpatients with suspected SAS, who were classified in 4 groups depending on the presence or absence of dipping/non-dipping and SAS.Results-Non-dippers with SAS had higher hsCRP (overall P<0.001), PAI-1 (overall P=0.004), and aldosterone levels (overall P=0.010) than any of the other 3 groups. After adjustment for significant covariates such as age, sex, body mass index, waist circumference, smoking, alcohol drinking, aspirin use, presence of DM, and insulin, non-dippers with SAS still had a higher hsCRP level than non-dippers without SAS (geometric mean: 1.47 vs. 0.37 mg/L, P=0.001). In multiple linear regression analysis controlling for confounding factors that related with SAS, hsCRP was significantly correlated with 3% oxygen desaturation index (P=0.047). PAI-1 was also highest in the non-dippers with SAS, but this was not independent of obesity. PAI-1 was correlated with insulin (r=0.32, P=0.002) and hsCRP levels (r=0.26, P=0.005).Conclusion-Non-dipper status was associated with an increased hsCRP in patients who also had SAS, but not in those who did not, and hsCRP was closely affected by the desaturation level. PAI-1 is also increased in non-dippers with SAS, and is related to insulin and hsCRP.

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An Assessment of Incremental Coronary Risk Prediction Using C-Reactive Protein and Other Novel Risk Markers

Folsom¹,

Chambless²,

Ballantyne³

et al. 2006

Arch Intern Med

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183

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Prospective Study of Fibrinolytic Factors and Incident Coronary Heart Disease

Cited by 223 publications

References 54 publications

Causal Effect of Plasminogen Activator Inhibitor Type 1 on Coronary Heart Disease

Causal Effect of Plasminogen Activator Inhibitor Type 1 on Coronary Heart Disease

Increased low-grade inflammation and plasminogen-activator inhibitor-1 level in nondippers with sleep apnea syndrome

An Assessment of Incremental Coronary Risk Prediction Using C-Reactive Protein and Other Novel Risk Markers

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