Association of Impaired Fasting Glucose with Cardiovascular Disease in the Absence of Risk Factor

Author(s):  
Yingting Zuo ◽  
Xinsheng Han ◽  
Xue Tian ◽  
Shuohua Chen ◽  
Shouling Wu ◽  
...  

Abstract Background The association between impaired fasting glucose (IFG) and cardiovascular disease (CVD) in participants without atherosclerotic cardiovascular disease (ASCVD) risk factors based on current definitions is unclear. The study aimed to examine the association of fasting glucose levels with CVD and its subtypes in persons without ASCVD risk factors. Methods This study included 38,297 participants (men, 62.1%; mean age, 47.9 [12.9] years) who were free of a history of CVD, absent of ASCVD risk factors, and had a fasting plasma glucose (FPG) level between 70 to 125 mg/dl at baseline from Kailuan Study during 2006 to 2007, participants were followed up until new-onset CVD event, death or December 31, 2017. Cox proportional hazards models were performed to evaluate the associations. Results During a median follow-up of 11.0 years (interquartile range, 10.7-11.2 years), we observed 1,217 incident CVD events. Compared with participants with FPG 70 to 99 mg/dl, the multivariable adjusted hazard ratios for CVD among participants with FPG 100 to 109 mg/dl and 110 to 125 mg/dl were 1.18 (95% confidence interval [CI], 1.02-1.38) and 1.27 (95%CI, 1.03-1.55), respectively. Multivariable-adjusted spline regression model showed a J-shaped association between FPG and the risk of CVD. Conclusions We found that among individuals without diabetes or other traditional ASCVD risk factors, there is an increased risk of incident CVD with increasing abnormal FPG levels. These results highlight the importance of primordial prevention for FPG level increases along with other traditional ASCVD risk factors.

RMD Open ◽  
2021 ◽  
Vol 7 (2) ◽  
pp. e001618
Author(s):  
Gulsen Ozen ◽  
Sofia Pedro ◽  
Rebecca Schumacher ◽  
Teresa Simon ◽  
Kaleb Michaud

ObjectiveVenous thromboembolism (VTE) is an increasing concern in rheumatoid arthritis (RA) with little known about risk factors. We aimed to compare risk factors for unprovoked VTE and atherosclerotic cardiovascular disease (ASCVD) in patients with RA and to assess subsequent ASCVD risk after an unprovoked VTE.MethodsPeople with RA participating in a US-wide longitudinal observational registry from 1998 to 2018 were assessed for incident unprovoked VTE (deep venous thrombosis and pulmonary emboli not associated with cancer, recent surgery, hospitalisation, fracture and pregnancy) and ASCVD (myocardial infarction and stroke) validated from hospital/death records. Risk factors for VTE and ASCVD and the risk of ASCVD after an unprovoked VTE were determined using Cox proportional hazards models.ResultsDuring median (IQR) 4 (1.5–7) years of follow-up in 31 366 patients with RA, 539 unprovoked VTE and 1648 ASCVD events were identified. The adjusted models showed increased VTE and ASCVD risk with older age, male sex, comorbidities, prior fracture, worse disability, higher disease activity and glucocorticoids. Traditional cardiovascular disease risk factors were common in both ASCVD and VTE but only increased ASCVD risk with obesity as the exception (VTE HR (95% CI), 1.46 (1.13–1.87)) and ASCVD, 0.58 (0.50–0.68)). ASCVD risk doubled after an unprovoked VTE (HR (95% CI), 2.05 (1.43–2.95)).ConclusionOur findings suggest that unprovoked VTE is mediated by inflammation of RA and may be considered a spectrum of pan-cardiovascular syndrome.


2021 ◽  
Vol 10 (3) ◽  
Author(s):  
Rebecca C. Thurston ◽  
Helen E. Aslanidou Vlachos ◽  
Carol A. Derby ◽  
Elizabeth A. Jackson ◽  
Maria Mori Brooks ◽  
...  

Background Cardiovascular disease (CVD) in women has unique features, including associations with reproductive factors that are incompletely understood. Vasomotor symptoms (VMS), the classic menopausal symptom, are linked to CVD risk factors and subclinical CVD. Evidence linking VMS to CVD events is limited. We tested whether frequent and/or persistent VMS were associated with increased risk for fatal and nonfatal CVD events in SWAN (Study of Women’s Health Across the Nation). Methods and Results A total of 3083 women, aged 42 to 52 years at baseline, underwent up to 16 in‐person visits over 22 years. Assessments included questionnaires on VMS frequency (0, 1–5, or ≥6 days/2 weeks), physical measures, phlebotomy, and reported CVD events (myocardial infarction, stroke, heart failure, and revascularization). A subset of events was adjudicated via medical record. Death certificates were obtained. Relationships between baseline VMS or persistent VMS over the follow‐up (proportion of visits with frequent VMS) with combined incident nonfatal and fatal CVD were tested in Cox proportional hazards models adjusted for demographics, medication use, and CVD risk factors. Participants experienced 231 CVD events over the follow‐up. Women with frequent baseline VMS had an elevated risk of subsequent CVD events (relative to no VMS; ≥6 days: hazard ratio [HR] [95% CI], 1.51 [1.05–2.17], P =0.03; 1–5 days: HR [95% CI], 1.02 [0.75–1.39], P =0.89, multivariable). Women with frequent VMS that persisted over time also had an increased CVD event risk (>33% versus ≤33% of visits: HR [95% CI], 1.77 [1.33–2.35], P <0.0001, multivariable). Conclusions Frequent and persistent VMS were associated with increased risk of later CVD events. VMS may represent a novel female‐specific CVD risk factor.


Gerontology ◽  
2021 ◽  
pp. 1-9
Author(s):  
Feng Cheng Lin ◽  
Chih Yin Chen ◽  
Chung Wei Lin ◽  
Ming Tsang Wu ◽  
Hsuan Yu Chen ◽  
...  

<b><i>Introduction:</i></b> Dementia is one of the major causes of disability and dependency among older people worldwide. Alz­heimer’s disease (AD), the most common cause of dementia among the elderly, has great impact on the health-care system of developed nations. Several risk factors are suggestive of an increased risk of AD, including APOE-ε4, male, age, diabetes mellitus, hypertension, and low social engagement. However, data on risk factors of AD progression are limited. Air pollution is revealed to be associated with increasing dementia incidence, but the relationship between air pollution and clinical AD cognitive deterioration is unclear. <b><i>Methods:</i></b> We conducted a case-control and city-to-city study to compare the progression of AD patients in different level of air-polluted cities. Clinical data of a total of 704 AD patients were retrospectively collected, 584 residences in Kaohsiung and 120 residences in Pingtung between 2002 and 2018. An annual interview was performed with each patient, and the Clinical Dementia Rating score (0 [normal] to 3 [severe stage]) was used to evaluate their cognitive deterioration. Air pollution data of Kaohsiung and Pingtung city for 2002–2018 were retrieved from Taiwan Environmental Protection Administration. Annual Pollutant Standards Index (PSI) and concentrations of particulate matter (PM<sub>10</sub>), sulfur dioxide (SO<sub>2</sub>), ozone (O<sub>3</sub>), nitrogen dioxide (NO<sub>2</sub>), and carbon monoxide (CO) were obtained. <b><i>Results:</i></b> The PSI was higher in Kaohsiung and compared with Pingtung patients, Kaohsiung patients were exposed to higher average annual concentrations of CO, NO<sub>2</sub>, PM<sub>10</sub>, and SO<sub>2</sub>. AD patients living in Kaohsiung suffered from faster cognitive deterioration in comparison with Pingtung patients (log-rank test: <i>p</i> = 0.016). When using multivariate Cox proportional hazards regression analysis, higher levels of CO, NO<sub>2</sub>, PM<sub>10</sub>, and SO<sub>2</sub> exposure were associated with increased risk of AD cognitive deterioration. Among all these air pollutants, high SO<sub>2</sub> exposure has the greatest impact while O<sub>3</sub> has a neutral effect on AD cognitive deterioration. <b><i>Conclusions:</i></b> Air pollution is an environment-related risk factor that can be controlled and is associated with cognitive deterioration of AD. This finding could contribute to the implementation of public intervention strategies of AD.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Christina M Parrinello ◽  
Pamela L Lutsey ◽  
Christie M Ballantyne ◽  
Aaron R Folsom ◽  
James S Pankow ◽  
...  

Background: High levels of C-reactive protein (CRP) are associated with cardiovascular disease, diabetes and mortality. It is unclear whether changes in CRP or persistently high CRP are associated with these outcomes beyond the baseline measure. Methods: We conducted a prospective cohort analysis of 10,229 participants from the ARIC Study with two measurements of CRP six years apart (at visits 2 and 4, 1990-92 and 1996-98, respectively). CRP was categorized into two groups using a standard cut-point for defining high levels (≥3 vs. <3 mg/L). Six-year change in CRP was categorized as: persistently not high (<3 mg/L), decreasing (≥3 to <3 mg/L), increasing (<3 to ≥3 mg/L), and persistently high (≥3 mg/L). Cox proportional hazards models were used to assess the association between visit 2 CRP, visit 4 CRP and six-year change in CRP and each of the following outcomes from visit 4 through 2010: diabetes, coronary heart disease, ischemic stroke, heart failure and all-cause mortality. Models were adjusted for traditional risk factors at visit 2. Sensitivity analyses additionally adjusted for visit 4 covariates. Results: Persons with CRP ≥3 mg/L at visit 2 or 4 had higher risk of each outcome compared to those with CRP <3 mg/L ( Table ). We observed higher risk of all outcomes in persons with persistently high CRP, and of all outcomes except stroke in persons with increasing CRP, compared to those with CRP <3 mg/L at both visits ( Table ). Persons whose CRP decreased from high to <3 mg/L did not have significantly increased risk of cardiovascular outcomes or diabetes compared to those with CRP persistently <3 mg/L. Results were similar after adjusting for visit 4 covariates. Conclusions: Persons with sustained high levels of CRP or whose CRP increased to high levels had higher risk of diabetes, cardiovascular disease, and death, while those whose levels decreased from high to moderate or low were at lower risk. Multiple measures of CRP may better characterize inflammatory status and provide more comprehensive information regarding long-term risk.


Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Gabriel S Tajeu ◽  
Monika M Safford ◽  
George Howard ◽  
Rikki M Tanner ◽  
Paul Muntner

Introduction: Black Americans have higher rates of cardiovascular disease (CVD) mortality compared with whites. Differences in sociodemographic, psychosocial, CVD, and other risk factors may explain increased mortality risk. Methods: We analyzed data from 29,015 REasons for Geographic and Racial Differences in Stroke study participants to determine factors that may explain the higher hazard ratio for CVD and non-CVD mortality in blacks compared with whites. Cause of death was adjudicated by trained investigators. Within age-sex sub-groups, we used Cox proportional hazards regression with progressive adjustment to estimate black:white hazard ratios. Results: Overall, 41.0% of participants were black, and 54.9% were women. Over a mean follow-up of 7.1 years (maximum 12.3 years), 5,299 participants died (1,797 CVD and 3,502 non-CVD deaths). Among participants < 65 years of age, the age and region adjusted black:white hazard ratio for CVD mortality was 2.28 (95% CI: 1.68-3.10) and 2.32 (95% CI: 1.80-3.00) for women and men, respectively, and for participants ≥ 65 was 1.54 (95% CI: 1.30-1.82) and 1.35 (95% CI: 1.16-1.57) for women and men, respectively ( Table ). The higher black:white hazard ratios for CVD mortality were no longer statistically significant after multivariable adjustment, with the largest attenuation occurring with sociodemographic and CVD risk factor adjustment. Among participants < 65 years of age, the age and region adjusted black:white hazard ratios for non-CVD mortality were 1.51 (95% CI: 1.24-1.85) and 1.76 (95% CI: 1.46-2.13) for women and men, respectively, and for participants ≥ 65 was 1.12 (95% CI: 1.00-1.26) and 1.34 (95% CI: 1.20-1.49) for women and men, respectively. The higher black:white hazard ratios for non-CVD mortality were attenuated after adjustment for sociodemographics. Conclusions: Black:white differences are larger for CVD than non-CVD causes of death. The increased CVD mortality for blacks compared with whites is primarily explained by sociodemographic and CVD risk factors.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Wei Zhang ◽  
Jaime L Speiser ◽  
Miguel Cainzos Achirica ◽  
Khurram Nasir ◽  
Michael Tsai ◽  
...  

Introduction: Lipoprotein (a) (Lp(a)) and inflammation, as represented by elevated high-sensitivity C-reactive protein (hsCRP) concentration, are both considered as risk-enhancers in the 2018 AHA/ACC Cholesterol guidelines. However, little is known as to whether the association of Lp(a) with atherosclerotic cardiovascular disease (ASCVD) risk is modified by inflammation. Objective: We assessed whether hsCRP modifies the association of Lp(a) with ASCVD risk. Methods: MESA participants with baseline hsCRP and Lp(a) levels were included. Incident ASCVD events were ascertained from baseline through 2017. Time to incident ASCVD was analyzed using Kaplan Meir curves. Cox proportional hazards models were used to assess the association between Lp(a), hsCRP, and time to ASCVD events adjusting for covariates. Results: The study included 4,654 participants with mean age of 62 and 52.5% females (1,702 Caucasians, 557 Chinese Americans, 1,336 African Americans and 1,059 Hispanics). With a mean 13.6-year follow-up, 676 ASCVD events occurred among 4,609 participants (Figure 1). In participants with hsCRP <2mg/L, the association of Lp(a) (per 1 Log unit increase) and risk for ASCVD as represented by hazard ratio (HR) and 95%CI was 1.01 (0.79, 1.28). In subjects with hsCRP ≥2mg/L, the risk increased to 1.26 (1.01, 1.58). When compared to the reference group with Lp(a) <50mg/dL and hsCRP <2mg/L, the risk for ASCVD in participants with Lp(a) ≥50mg/dL and hsCRP <2mg/L was 1.13 (0.85, 1.50) and in those with Lp(a) <50mg/dL and hsCRP ≥2mg/L was 1.09 (0.92, 1.31). The risk increased significantly to 1.62 (1.26, 2.07) in participants with Lp(a) ≥50mg/dL and hsCRP ≥2mg/L. Conclusions: Lp(a)-related ASCVD risk is modified by hsCRP levels. The findings of this analysis suggest that Lp(a) may serve as a risk enhancing factor in individuals with hsCRP level ≥2mg/L. Future studies are needed to determine whether Lp(a) is associated with risk of ASCVD in the absence of subclinical inflammation.


Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Hiroaki Ikezaki ◽  
Elise Lim ◽  
Ching-Ti Liu ◽  
L Adrienne Cupples ◽  
Bela F Asztalos ◽  
...  

Introduction: Elevated plasma low-density lipoprotein cholesterol (LDL-C), small-dense LDL-C (sdLDL-C), LDL-triglyceride (LDL-TG), triglycerides (TG), remnant-lipoprotein cholesterol (RLP-C), triglyceride-rich lipoprotein-C (TRL-C), very low-density lipoprotein cholesterol (VLDL-C), and lipoprotein(a) [Lp(a)] levels have been associated with increased atherosclerotic cardiovascular disease (ASCVD) risk. However, these parameters have not been included in risk factors for ASCVD in the pooled cohort equation (PCE). Hypothesis: We assessed the hypothesis that these atherogenic lipoprotein parameters add significant information for ASCVD risk prediction in the Framingham Offspring Study. Methods: We evaluated 3,147 subjects without ASCVD at baseline (mean age 58 years) from participants of Framingham Offspring Study cycle 6, 677 (21.5%) of whom developed inclusive ASCVD over 16 years. Biomarkers of risk were assessed in frozen plasma samples. Total cholesterol, TG, HDL-C, direct LDL-C, sdLDL-C, LDL-TG, Lp(a), RLP-C, and TRL-C were measured by standardized automated analysis. Calculated LDL-C, large buoyant low-density lipoprotein cholesterol (lbLDL-C), VLDL-C, and non-HDL-C values were calculated. Data were analyzed using Cox proportional regression analysis and net reclassification improvement (NRI) analysis to identify parameters significantly associated with the incidence of ASCVD after controlling for standard ASCVD risk factor and applying the PCE model. Results: All specialized lipoprotein parameters were significant ASCVD risk factors on univariate analysis, but only direct LDL-C, sdLDL-C, and Lp(a) were significant on multivariate analysis with standard risk factors in the model. Together these parameters significantly improved the model c statistic (0.716 vs 0.732, P < 0.05) and net risk reclassification (mean NRI 0.104, P < 0.01) for ASCVD risk. Using the ASCVD risk pooled cohort equation, sdLDL-C, TG, LDL-TG, LDL-C, RLP-C, and TRL-C individually added significant information, but no other parameter added significant information with sdLDL-C (hazard ratio 1.30 for 75th vs 25th percentile, P < 0.0001) in the model. Conclusions: In multivariate analysis, sdLDL-C, direct LDL-C, and Lp(a) contributed significantly to ASCVD risk, but only sdLDL-C added significant risk information to the PCE model, indicating that sdLDL-C may be the most atherogenic lipoprotein particle.


2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Romona D. Govender ◽  
Saif Al-Shamsi ◽  
Elpidoforos S. Soteriades ◽  
Dybesh Regmi

Abstract Background Individuals with established cardiovascular disease (CVD) and risk factors such as age, smoking, hypertension, and diabetes mellitus are at an increased risk of recurrent cardiovascular events and death. The incidence rate of recurrent CVD events varies between countries and populations. The United Arab Emirates (UAE) has one of the highest age-standardized death rates for CVD worldwide. The aim of our study was to estimate the incidence rates and determine the predictors of recurrent CVD events among UAE nationals. Methods We investigated an outpatient-based cohort of patients with a history of CVD visiting Tawam Hospital between April 1, 2008 and December 31, 2008. They were followed-up until July 31, 2018. Univariable and multivariable Cox proportional hazards regression models were used to determine the association between major CVD risk factors and the risk of CVD recurrence. Results A total of 216 patients (167 males, 49 females) with a history of CVD were included. They were followed for a median (interquartile range) of 8.1 (5.5–9.3) years, with a total of 1184 patient-years of follow-up. The overall incidence rate of recurrent CVD events was 92.1 per 1000 patient-years. The 8-year cumulative incidence was 73.7%. Age, female sex, and diabetes mellitus were significant predictors of recurrent CVD events, where females had a 1.96 times higher risk of recurrent CVD events than males. Conclusion Significant predictors of recurrent CVD events are older age, female sex, and diabetes mellitus. The incidence rate of recurrent CVD events was 92.1 per 1000 patient-years. Preventive measures, based on international guidelines for CVD management, may improve CVD morbidity and mortality in the UAE population.


2019 ◽  
Vol 149 (8) ◽  
pp. 1451-1459 ◽  
Author(s):  
Emiko Okada ◽  
Toru Shirakawa ◽  
Nitin Shivappa ◽  
Kenji Wakai ◽  
Koji Suzuki ◽  
...  

ABSTRACT Background The Dietary Inflammatory Index (DII) is a comprehensive, literature-derived index for assessing the effect of dietary constituents on inflammatory biomarkers. Several studies have shown an association between DII score and mortality, but there are limited prospective studies in Asian populations. Objectives The aim of this study was to investigate the association between DII score and risk of all-cause, total cardiovascular disease (CVD), stroke, coronary heart disease (CHD), total cancer, digestive cancer, and noncancer/non-CVD mortality in the Japanese population. Methods A total of 58,782 Japanese participants aged 40–79 y who were enrolled in the Japan Collaborative Cohort Study during 1988–1990 were included in the analysis. DII scores were calculated based on a food-frequency questionnaire. HRs and 95% CIs for mortality according to DII quintiles were estimated using Cox proportional hazards models. Results During the median follow-up period of 19.3 y, a total of 11,693 participants died. The multivariable HR for all-cause mortality for the highest compared with the lowest DII quintiles was 1.13 (95% CI: 1.05, 1.21). For CVD mortality, the highest multivariable HRs were 1.30 (95% CI: 1.13, 1.49), 1.29 (95% CI: 1.05, 1.59), and 1.30 (95% CI: 0.96, 1.76) for total CVD, stroke, and CHD, respectively. No significant associations were observed between DII and risk of total cancer, digestive cancer, and noncancer/non-CVD mortality. Conclusion Our findings suggest that a higher DII was associated with an increased risk of all-cause and CVD mortality among Japanese adults.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1508-1508
Author(s):  
Mengjie Yuan ◽  
R Taylor Pickering ◽  
Martha Singer ◽  
Lynn l Moore

Abstract Objectives Few studies have estimated the independent effects of butter and margarine on risk of cardiovascular disease (CVD). Our goal was to examine these effects as well as that of other fats and oils on risk of CVD and markers of cardiometabolic risk in subjects in the prospective Framingham Offspring Study. Methods Data from 2038 adults, who were free of CVD and diabetes through exam 5 were included. Intakes of butter, margarine, mayonnaise, oils, and shortening were assessed using 3-day diet records at exams 3 and 5. Concentrations of low-density lipoproteins (LDL), high-density lipoproteins (HDL), and their particle sizes were analyzed cross-sectionally at exam 5. Subjects were followed from exam 5 to 9 for incident CVD and type 2 diabetes (T2DM) (median follow-up, 16.9 years). Cox proportional hazards models were used to estimate risk of CVD and T2DM and generalized linear models were used to evaluate effects on other cardiometabolic outcomes, while adjusting for age, sex, pack-years of smoking, BMI, physical activity, intakes of other fats, hypertension and use of lipid-lowering medication. Intake of each type of dietary fat was categorized as low, moderate, or high using sensitivity analyses. Results Intake of &gt;5 g/day of butter (vs. non-consumers) had no effect on CVD risk but was associated with a non-statistically significant 24% lower risk of T2DM. In men, higher butter intake was linked with larger LDL and HDL particles sizes (P &lt; 0.01 for both) and a lower LDL: HDL ratio (P &lt; 0.01). Consuming &gt;7 g/day (vs. ≤2) of margarine was associated with a 48% (95% CI: 1.03–2.13) increased risk of CVD and a 68% (95% CI: 1.00–2.82) higher risk of T2DM in women. In men, higher margarine intake was associated with much weaker, non-statistically significant increased risks of CVD and T2DM. Finally, total intake of oils (&gt;7 vs. ≤2 g/day) was associated with a strong reduced risk of T2DM (HR: 0.55; 95% CI: 0.36–0.85) in men but not women. There was no effect of margarine or oils on lipid particle sizes in either men or women. Conclusions While butter intake had no adverse effect on risk of CVD in either men or women, it was beneficially associated with lipid profiles in men. In women, higher intakes of margarine but not butter were associated with increased risks of both CVD and T2DM. Finally greater oil consumption led to lower risks of T2DM in men. Funding Sources NHLBI National Dairy Council.


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