Risk Of Vascular Disease Research Articles

Progression of conventional cardiovascular risk factors and vascular disease risk in individuals: insights from the PROG-IMT consortium.

AimsAveraged measurements, but not the progression based on multiple assessments of carotid intima-media thickness, (cIMT) are predictive of cardiovascular disease (CVD) events in individuals. Whether this is true for conventional risk factors is unclear.Methods and resultsAn individual participant meta-analysis was used to associate the annualised progression of systolic blood pressure, total cholesterol, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol with future cardiovascular disease risk in 13 prospective cohort studies of the PROG-IMT collaboration (n = 34,072). Follow-up data included information on a combined cardiovascular disease endpoint of myocardial infarction, stroke, or vascular death. In secondary analyses, annualised progression was replaced with average. Log hazard ratios per standard deviation difference were pooled across studies by a random effects meta-analysis. In primary analysis, the annualised progression of total cholesterol was marginally related to a higher cardiovascular disease risk (hazard ratio (HR) 1.04, 95% confidence interval (CI) 1.00 to 1.07). The annualised progression of systolic blood pressure, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol was not associated with future cardiovascular disease risk. In secondary analysis, average systolic blood pressure (HR 1.20 95% CI 1.11 to 1.29) and low-density lipoprotein cholesterol (HR 1.09, 95% CI 1.02 to 1.16) were related to a greater, while high-density lipoprotein cholesterol (HR 0.92, 95% CI 0.88 to 0.97) was related to a lower risk of future cardiovascular disease events.ConclusionAveraged measurements of systolic blood pressure, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol displayed significant linear relationships with the risk of future cardiovascular disease events. However, there was no clear association between the annualised progression of these conventional risk factors in individuals with the risk of future clinical endpoints.

Association between CPR-related genetic variants and risk of ischemic stroke: a nested case-control study

ABSTRACTBackground: Serum C-reactive protein (CRP) has been reported to be associated with risk of ischemic vascular disease including ischemic stroke. Genome-wide association studies have revealed several gene variants related to CRP concentration.Methods: We investigated genetic variants in CRP-related genes associated with ischemic stroke in a nested case-control study with 138 ischemic stroke cases and 276 controls. We sequenced the whole coding region of six CPR-related genes and selected eligible SNPs. Three genetic models (additive, dominant and recessive) were calculated by a multivariable conditional logistic regression to estimate the association between SNPs and risk of ischemic stroke. We also calculated gene–environment interactions by using a crossover analysis.Results: Three out of 10 eligible SNPs were shown to be associated with risk of ischemic stroke. rs1800947 in CRP gene (additive model: OR = 2.08, 95% CI: 1.00–4.23) and rs1169288 in HNF1A gene (additive model: OR = 1.45, 95% CI: 1.03–2.06) were associated with an increased risk of ischemic stroke. rs440446 in APOE gene (additive model: OR = 0.63, 95%CI: 0.44–0.88) was associated with a decreased risk of ischemic stroke. Genetic risk scores models including SC-GRS and OR-GRS both showed a significant association with risk of ischemic stroke. These three SNPs interacted with smoking and red meat intake.Conclusions: Our study showed genetic variants of CRP-related genes were associated with risk of ischemic stroke. Our findings could provide useful data for the etiology of ischemic stroke.

Associations Between Midlife (but Not Late-Life) Elevated Coronary Heart Disease Risk and Lower Cognitive Performance: Results From the Framingham Offspring Study.

It is unclear how coronary heart disease (CHD) risk across the adult life span affects late-life cognition. We estimated associations of midlife and late-life elevated CHD risk with cognitive trajectories (general cognitive performance, processing speed/executive function, memory) in later life (after age 55 years or age 70 years) among 2,892 Framingham Offspring Study participants who had completed CHD risk assessments approximately every 4 years since 1971 and had undergone neuropsychological testing between 1999 and 2014. We stratified analyses by apolipoprotein E gene (APOE) Ɛ4 allele carrier status. Using linear mixed-effects models, elevated CHD risk in midlife (age 55 years) was associated with lower levels of general cognitive performance (β=-0.560 standard deviation (SD) units, 95% confidence interval (CI): -0.874, -0.246), executive function (β=-0.624 SD units, 95% CI: -0.916, -0.332), and memory (β=-0.560 SD units, 95% CI: -0.907, -0.213) at age 70 years but not with rates of cognitive change. Late-life (age 70 years) elevated CHD risk, however, was associated with somewhat better levels of general cognitive performance and memory. There were associations between duration of elevated CHD risk during midlife and levels (but not trajectories) of later-life cognitive outcomes. Associations were not modified by APOE-ɛ4 status. These findings suggest that midlife elevated CHD risk is associated with lower cognition, independently of APOE-ɛ4 status, suggesting that risk of vascular disease may not contribute a "second hit" to AD risk.

Associations between Peripheral Thromboembolic Vascular Disease and Androgen Deprivation Therapy in Asian Prostate Cancer Patients

This study aimed to investigate the risks of thromboembolic vascular disease following androgen deprivation therapy (ADT) administered to prostate cancer (PCa) patients. A total of 24,464 men with newly diagnosed PCa during 2000–2008 were recruited through a longitudinal health insurance database in Taiwan. All PCa patients were stratified into two: ADT and non-ADT groups. Patients with ADT treatment were grouped into three: surgical castration, chemical castration, and anti-androgen alone. The risks of pulmonary embolism (PE), peripheral arterial occlusion disease (PAOD), and deep vein thrombosis (DVT) were assessed in multiple Cox proportional-hazards regression with time-dependent covariates. During the 12-year follow-up period, incidence rates per 1000 person-years in ADT and non-ADT groups were 2.87 and 1.62 for DVT, 1.00 and 0.52 for PE, and 1.03 and 0.70 for PAOD, respectively. The DVT and PE risks were significantly increased in patients receiving combined androgen blockade (CAB) compared with the counterpart ADT non-recipients. After adjusting for potential risk factors, PCa patients receiving CAB had the highest PE risk (HR = 3.11), followed by DVT risk (HR = 2.53). The DVT risk remained elevated throughout the entire duration of chemical castration. However, high PE risk was observed in patients with ≤720-day treatment duration. No association was found between ADT and PAOD risks. Overall, the risks of PE and DVT were considerably heightened in Asian men subjected to CAB for PCa, whereas PAOD risk was unrelated to such treatments.

P1228Impact of history of vascular disease on lipoprotein(a) associations with cardiovascular outcomes: a Mendelian randomisation study in 283,658 UK Biobank participants

Abstract Background Mendelian randomisation (MR) studies have been widely used to assess the causal relevance of risk factors for disease and to elucidate the likely effects of novel drug targets. MR studies have confirmed the causal relevance of lipoprotein(a) [Lp(a)] for risk of coronary heart disease (CHD), but the impact of prior vascular disease on these associations remains unclear, and is potentially important when testing the effects of Lp(a) lowering therapies. Purpose To examine the associations of LPA variants, as a proxy for Lp(a) levels, with risk of CHD, ischaemic stroke and peripheral vascular disease (PVD), by history of vascular disease in UK Biobank (UKB). Methods An LPA genotype score was constructed in 283,658 unrelated white British UKB participants, using 2 SNPs (rs3798220 and rs10455872) previously shown to be independently associated with, and explain ∼40% of the variance in, Lp(a) levels. The LPA score was tested for association with hospitalisation for CHD (n=23,165), presumed ischaemic stroke (n=2,579) and PVD (n=3,780) using Cox PH models. Estimated hazard ratios (per LPA variant) for cardiovascular outcomes are reported both overall and by history of vascular disease (CHD, ischaemic stroke or PVD) at baseline. Results As observed in previous studies, LPA was associated with a higher risk of CHD (Hazard ratio [HR] 1.27 per LPA variant; 95% CI: 1.24–1.31). However, the effect was substantially attenuated in participants with versus without prior vascular disease (p-interaction = 3x10–5; Figure). The effect of the LPA score on PVD was comparable to that for CHD (p-heterogeneity = 0.25), whilst the effect on ischaemic stroke was significantly weaker than that for CHD (p-heterogeneity = 6x10–3). As for CHD, the effects of the LPA score on both ischaemic stroke and PVD were weaker in those with versus those without prior vascular disease. Furthermore, the heterogeneity between the effects on cardiovascular outcomes was more extreme when stratified by history of CHD. Conclusions This MR study shows that the effects of LPA on risk of CHD, ischaemic stroke and PVD are weaker in individuals with a history of vascular disease, perhaps reflecting the effects of medications used in this setting. Therefore, MR studies in the general population may overestimate the anticipated effects of Lp(a)-lowering therapies in randomised trials, which are typically conducted in individuals with prior vascular disease. Acknowledgement/Funding British Heart Foundation

MAPPING THE HEART-BRAIN CONNECTION IN CARDIOVASCULAR DISEASE

While it is known that cardiovascular diseases and vascular brain disorders share common medical and lifestyle risk factors, the degree to which having one cardiovascular disease or vascular brain disorder may increase the risk of developing others has not been systematically examined. This study mapped the associated risk between a broad set of cardiovascular diseases and vascular brain disorders to better understand their interconnectedness. We conducted a structured review of the literature to determine and classify the strength of the associated risk between nine cardiovascular diseases and vascular brain disorders. The seven cardiovascular diseases included atrial fibrillation, cardiac arrest, congenital heart disease, coronary artery and vascular disease, heart failure, myocardial infarction, and valvular heart disease (acquired). The two vascular brain disorders included stroke and vascular cognitive impairment. The strength of the associated risk between diseases/conditions was classified as strong, moderate, weak, or no known association based on a review and quality assessment of the existing evidence. All nine conditions were associated with increased risk of at least one other cardiovascular disease or vascular brain disorder. Heart failure and congenital heart disease had the greater number of associations classified as strong – both were strongly associated with increased risk of five other cardiovascular diseases or vascular brain disorders. Six of the seven cardiovascular diseases were associated with increased risk of at least one other cardiovascular disease. Stroke was strongly associated with increased risk of vascular cognitive impairment and vascular cognitive impairment was moderately associated with increased risk of stroke. All seven cardiovascular diseases were associated with increased risk of vascular cognitive impairment. Atrial fibrillation, heart failure, congenital heart disease, and myocardial infarction were each strongly associated with increased risk of stroke. Stroke was strongly associated with increased risk of coronary artery and vascular disease and weakly associated with increased risk of myocardial infarction. This systematic mapping of the associated risk between a broad set of cardiovascular diseases and vascular brain disorders revealed a complex pattern of heart-brain interconnectedness. These connections may have broad impact on healthcare policy, prevention strategy, and systems change in Canada - preventing one disease may prevent many others and reduce the burden on people experiencing these conditions and the healthcare system.

Incident cardiovascular disease in patients diagnosed with multiple sclerosis: A multi-database study

BackgroundRecent data on rates of cardiovascular disease (CVD) in patients after MS diagnosis are sparse. ObjectiveTo describe incident CVD in MS patients after diagnosis compared with a matched non-MS population. MethodsWe conducted a matched cohort study in two separate electronic medical databases, the United States Department of Defense military health care system and the United Kingdom's Clinical Practice Research Datalink GOLD. The study population included all patients with a first recorded diagnosis of MS and no history of CVD or selected measurable comorbidities associated with CVD and matched non-MS patients who were also free of CVD and the CVD associated comorbidities. We identified incident CVD outcomes first recorded after the MS diagnosis / matched date and calculated incidence rates and incidence rate ratios by type of CVD. ResultsRates of venous thromboembolism and peripheral vascular disease were 2-fold higher among MS than non-MS patients in both databases and the risk of myocardial infarction was 2.5 times higher among female MS patients compared with non-MS females in both databases. Other CVD outcomes were not consistent between databases. ConclusionMS patients in the UK and the US have increased risk of venous thromboembolism and peripheral vascular disease. The risk of myocardial infarction is increased among female MS patients.

P656Risk of major gastrointestinal bleed in relation to vascular disease risk in 0.5M UK Biobank participants

Abstract Background Low-dose aspirin is of established benefit for secondary prevention of cardiovascular events but in primary prevention the benefit is finely balanced with the hazard of major bleeds, and in particular gastrointestinal (GI) bleeds. Purpose To investigate non-vascular, non-genetic risk factors for major GI bleeds and derive a score for GI bleed risk which may help identify who will receive most net benefit from aspirin. Methods In the UK Biobank prospective study of 0.5M participants aged 40–69 at recruitment, prior history of cardiovascular disease, bleeds and other medical conditions was ascertained from self-reported diagnoses and electronic heath records (EHR) prior to recruitment. Major GI bleed during 6 years of follow-up was defined based on coded diagnoses and duration of hospital stay. Non-vascular risk factors for bleed were identified from amongst 100 baseline and prior disease factors using a stepwise regression with adjustment for established vascular risk factors, aspirin and warfarin use. 10-way cross-validation was used when making risk scores. Results Among the primary prevention population without prior intracranial bleed, serious extracranial bleed or gastrointestinal ulcer in the 6 months prior to recruitment, 1682 (0.06%/y) participants had a major GI bleed (1006 upper GI, 676 lower GI) with a mean stay in hospital of 3.2 days. Antiplatelet use (in 11%) and anticoagulant use (in 1%), were associated with 1.5 and 4 fold risks of GI bleed, respectively. Stepwise regression identified a non-vascular risk score for major bleed with a 4-fold risk ratio across fifths (Figure). But the score was also associated with a 2-fold risk ratio for major vascular events. Conclusions Major GI bleeds cause substantial morbidity. A 4-fold difference in bleed risk across quintiles was distinguishable by a score based largely on EHR prior disease information and frailty measures. This score is applicable in other contexts and will be applied in the ASCEND randomised trial of daily aspirin to provide randomized evidence of the net benefit of aspirin in different risk categories. However, vascular risk factors predicted risk of GI bleeds, and non-vascular risk factors for GI bleed predicted risk of major vascular events; so the net benefit from aspirin may vary only modestly across categories by vascular and bleed risks.

MHealth nutrition and lifestyle intervention (mHENAL) to reduce cardiovascular disease risk in a middle-aged, overweight and obese population in Sri Lanka: Study protocol for a randomized controlled trial

Mobile phone-based health interventions (mHealth) are viewed as an attractive approach to foster behaviour change, and found to be effective in promoting physical activity and healthy diets. The present study aims to investigate whether mHealth with advice for dietary and lifestyle modifications would reduce 10-year cardio vascular disease (CVD) risk among overweight or obese adults aged 35–64 years in Sri Lanka. A two-group parallel-arm randomized controlled trial (RCT) was conducted in Colombo district, recruiting 1200 individuals aged 35–64 years with a body mass index (BMI) of ≥25 kgm−2. Participants were randomly assigned either to mHealth package (intervention arm, n = 600) or usual care (control arm, n = 600). The intervention package contains a series of dietary and lifestyle improvement messages, a mobile application to register participants, and a web application to deliver these messages. Participants in the intervention arm receive 2 voice and 2 text messages per week to their mobile phones for a period of 12 months. The primary outcome (10-year CVD risk) will be assessed according to sex, age, smoking status, blood pressure, serum cholesterol and glycaemic status. Data are collected at enrollment and after 12 months of intervention on: dietary practices, physical activity, smoking, anthropometry, body composition, blood pressure, fasting plasma glucose, HbA1c and lipid profile. Analysis of effect will be performed by intention-to-treat principle, comparing the outcomes between intervention and control arms. The study resulted in a comprehensive mHealth nutrition and lifestyle package (mHENAL) and successfully completed recruitment and baseline assessment of participants. The message delivery is in progress.

Physical Activity, Sedentary Leisure Time, Circulating Metabolic Markers, and Risk of Major Vascular Diseases.

Physical inactivity and sedentary behavior are associated with higher risk of cardiovascular disease (CVD). Little is known about the relevance of circulating metabolites for these associations. A nested case-control study within the prospective China Kadoorie Biobank included 3195 incident CVD cases (2057 occlusive CVD and 1138 intracerebral hemorrhage) and 1465 controls aged 30 to 79 years without prior CVD or statin use at baseline. Nuclear magnetic resonance spectroscopy was used to measure 225 metabolic markers and derived traits in baseline plasma samples. Linear regression was used to relate self-reported physical activity and sedentary leisure time to biomarkers, adjusting for potential confounders. These were contrasted with associations of biomarkers with occlusive CVD risk. Physical activity and sedentary leisure time were associated with >100 metabolic markers, with patterns of associations generally mirroring each other. Physical activity was inversely associated with very low and low-density and positively with large and very large HDL (high-density lipoprotein) particle concentrations. Physical activity was also inversely associated with alanine, glucose, lactate, acetoacetate, and the inflammatory marker glycoprotein acetyls. In general, associations of physical activity and sedentary leisure time with specific metabolic markers were directionally consistent with the associations of these metabolic markers with occlusive CVD risk. Overall, metabolic markers potentially explained ≈70% of the protective associations of physical activity and ≈50% of the positive associations of sedentary leisure time with occlusive CVD. Among Chinese adults, physical activity and sedentary behavior have opposing associations with a diverse range of circulating metabolites, which may partially explain their associations with CVD risk.

Abstract P1116: Early Life Stress Induces HDAC-Dependent Expression of Pro-Oxidant Genes in the Aorta

Childhood adversity or early life stress (ELS) is an understudied risk factor for cardiovascular disease (CVD). The mouse ELS model, maternal separation with early weaning (MSEW), generates robust effects on anxiety as well as immunological consequences in adulthood. Previous studies from our laboratory showed that MSEW induces a pro-oxidant vascular phenotype in adulthood. Early in life or during development, epigenetic mechanisms such as the cellular balance of histone acetylation and deacetylation (HDACs) critically influences gene expression. We hypothesized that MSEW induces HDAC-dependent expression of pro-oxidant genes in the vasculature. Thoracic aortae were isolated from male adult (12 wk) normally-reared (NR) or MSEW mice. Histone 3 lysine acetylation (H3K27) status was found to be significantly decreased in aorta from MSEW compared to NR mice, indicating MSEW induced increased HDAC activity. The MSEW-induced increased in aortic NADPH oxidase (NOX) 2, NOX4, and toll-like receptor (TLR) 4 expression and was significantly blunted with ex vivo trichostatin A (TSA) treatment with no changes in NR mice (relative mRNA; NOX2: MSEW+VEH 1.55±0.12 vs MSEW+TSA 1.24±0.16, NOX4: MSEW+VEH 1.68±0.14 vs MSEW+TSA 1.25±0.07, TLR4: MSEW+VEH 1.65±0.16 vs MSEW+TSA 0.79±0.09, N=4-8, p<0.05). Further, MSEW-induced endothelial dysfunction was reversed with ex vivo TSA treatment with no changes observed in NR mice (E max NR+VEH 86.3±3.5, NR+TSA 82.8±6.3, MSEW+VEH 64.1±8.2 vs MSEW+TSA 85.9±1.7, N=8-12, p<0.05). Reports show that HDAC9 is associated with increased risk for vascular diseases. Aorta from MSEW mice had a significant increase in HDAC9 abundance compared to NR mice (rel. mRNA; NR: 1.02±0.1 vs MSEW: 1.67±0.2, N=6, p<0.05). To determine whether HDAC9 directly induces NOX2, NOX4, and/or TLR4 expression, we utilized HDAC9 over-expressing (HDAC9-OE) mice. Aortic tissue from HDAC9-OE mice revealed a 10-fold NOX4 and 13-fold TLR4 increase, with no change in NOX2 expression. Our results indicate that HDACs, especially HDAC9, are ELS-sensitive mediator(s) of pro-oxidant gene expression. We conclude, that activation of HDAC-dependent pro-oxidant genes, specifically NOX4 and TLR4 pathways, contribute to increased CVD risk following ELS.

Nanofibrous vildagliptin-eluting stents enhance re-endothelialization and reduce neointimal formation in diabetes: in vitro and in vivo.

BackgroundThe high lifetime risk of vascular disease is one of the important issues that plague patients with diabetes mellitus. Systemic oral vildagliptin administration favors endothelial recovery and inhibits smooth muscle cell (SMC) proliferation. However, the localized release of vildagliptin in the diabetic vessel damage has seldom been investigated.Research design and methodsIn this work, nanofiber-eluting stents that loaded with vildagliptin, a dipeptidyl peptidase-4 enzyme (DPP-4) inhibitor, was fabricated to treat diabetic vascular disease. To prepare nanofibers, the poly (D,L)-lactide-co-glycolide (PLGA) and vildagliptin were mixed using hexafluoroisopropanol and electrospinning process. In vitro and in vivo release rates of the vildagliptin were characterized using high-performance liquid chromatography.ResultsEffective vildagliptin concentrations were delivered for more than 28 days from the nanofibrous membranes coating on the surface of the stents in vitro and in vivo. The vildagliptin-eluting PLGA membranes greatly accelerated the recovery of diabetic endothelia and reduced SMC hyperplasia. The type I collagen content of the diabetic vascular intimal area that was treated by vildagliptin-eluting stents was lower than that of the non-vildagliptin-eluting group.ConclusionThe experimental results revealed that stenting with vildagliptin-eluting PLGA membranes could potentially promote healing for diabetic arterial diseases.

Serious Adverse Effects of Extended-release Niacin/Laropiprant: Results From the Heart Protection Study 2–Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE) Trial

PurposeThe Heart Protection Study 2–Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE) trial of patients at high risk of vascular disease found that adding extended-release niacin-laropiprant to intensive statin-based LDL-lowering therapy had no benefit on cardiovascular outcomes. However, the trial also identified previously unrecognized serious adverse effects (including new-onset diabetes, bleeding, and infection). Our objective was to explore the safety profile of niacin-laropiprant and examine whether any patients were at lower (or higher) risk of its adverse effects. MethodsHPS2-THRIVE was a randomized, double-blind trial of niacin-laropiprant (2000/40 mg/d) versus placebo among 25,673 patients at high risk of vascular disease. Information on all serious adverse events was collected during a median of 3.9 years of study treatment. Effects of niacin-laropiprant on new-onset diabetes, disturbances of diabetes control, bleeding, infection, and gastrointestinal upset were estimated by (1) time after randomization, (2) severity, (3) baseline characteristics, (4) baseline risk of the adverse event of interest, and (5) risk of major vascular event. FindingsThe hazard ratio (HR) for new-onset diabetes with niacin/laropiprant was 1.32 (95% CI, 1.16–1.51; P < .001), which corresponded to an absolute excess of 4 people (95% CI, 2–6) developing diabetes per 1000 person-years in the study population as a whole. Among the 8299 participants with diabetes at baseline, the HR for serious disturbances in diabetes control was 1.56 (95% CI, 1.35–1.80), corresponding to an absolute excess of 12 (95% CI, 8–16) per 1000 person-years. The HR was 1.38 (95% CI, 1.17–1.63; P < .001) for serious bleeding, corresponding to an absolute excess of 2 (95% CI, 1–3) per 1000 person-years and 1.22 (95% CI, 1.11–1.34; P < .001) for serious infection, corresponding to an absolute excess of 4 (95% CI, 2–6) per 1000 person-years. The excess risks of these serious adverse events were larger in the first year after starting niacin-laropiprant therapy than in later years (except for the excess of infection, which did not appear to attenuate with time), and the risks of nonfatal and fatal events were similarly increased. The absolute excesses of each of these adverse effects were similar regardless of the baseline risk of the outcome. ImplicationsPractitioners or patients considering the use of niacin (in addition to, or instead of, a statin) despite the lack of evidence of cardiovascular benefits (at least when added to effective statin therapy) should take account of the significant risks of these serious adverse effects when making such decisions. ClinicalTrials.gov identifier: NCT00461630.

Increased Vascular Pathology in Older Veterans With a Purple Heart Commendation or Chronic Post-Traumatic Stress Disorder.

The goal of this retrospective cohort study was to determine whether stressors related to military service, determined by a diagnosis of chronic post-traumatic stress disorder (cPTSD) or receiving a Purple Heart (PH), are associated with an increased risk of vascular risk factors and disease, which are of great concern for veterans, who constitute a significant portion of the aging US population. The Veterans Integrated Service Network (VISN) 16 administrative database was searched for individuals 65 years or older between October 1, 1997 to September 30, 1999 who either received a PH but did not have cPTSD (PH+/cPTSD-; n = 1499), had cPTSD without a PH (PH-/cPTSD+; n = 3593), had neither (PH-/cPTSD-; n = 5010), or had both (PH+/cPTSD+; n = 153). In comparison to the control group (PH-/cPTSD-), the PH+/cPTSD- group had increased odds ratios for incidence and prevalence of diabetes mellitus, hypertension, and hyperlipidemia. The PH-/cPTSD+ group had increased odds ratios for prevalence of diabetes mellitus and for the incidence and prevalence of hyperlipidemia. The PH-/cPTSD+ and PH+/cPTSD- groups were associated with ischemic heart disease and cerebrovascular disease, but not independently of the other risk factors. The PH+/cPTSD+ group was associated only with an increase in the incidence and prevalence of hyperlipidemia, though this group's much smaller sample size may limit the reliability of this finding. We conclude that certain physical and psychological stressors related to military service are associated with a greater incidence of several vascular risk factors in veterans aged 65 years or older, which in turn are associated with greater rates of ischemic heart disease and cerebrovascular disease.

Predictors of heart failure development in type 2 diabetes: a practical approach.

Purpose of reviewAlthough type 2 diabetes (T2D) is one of the most important risk factors that leads to the development of de novo heart failure, there are limited data, particularly from a practical/qualitative standpoint, about predictors of heart failure in this population.Recent findingsSodium-glucose cotransporter-2 (SGLT-2) inhibitors have been shown to prevent the development of heart failure and the composite of heart failure and cardiovascular death in patients with T2D without known heart failure who have either established atherosclerotic vascular disease or multiple risk factors. The concept of primary prevention of heart failure has led many clinicians to inquire if there are specific risk/enrichment factors that may predict an increased risk of heart failure.SummaryIn this review, we identify some general and diabetes-specific risk factors that are associated with an increased risk of developing heart failure in people with T2D.

High Glucose Levels And Risk Of Vascular Diseases – Observational And Mendelian Randomization Studies Of The General Population

Background and Aims: To investigate the observational and causal associations between glucose levels and risk of vascular diseases across the prediabetic spectrum in the general population.

Loss-Of-Function Mutations In Abca1, Hdl-Cholesterol, Metabolomic Profiles And Risk Of Vascular Disease And Dementia – A Cohort Study Of Up To 100,000 Individuals

Background and Aims: The adenosine triphosphate-binding cassette transporter A1 (ABCA1) is a major cholesterol transporter highly expressed in liver and brain. ABCA1 mediates cholesterol and phospholipid efflux to lipid-poor apolipoproteins, and is essential for the biogenesis of high-density lipoprotein (HDL) cholesterol in the circulation and HDL-like particles in the brain. We therefore investigated the impact of two well-known HDL-deficiency loss-of-function mutations in ABCA1 on lipid levels, metabolomic profiles, and on risk of vascular disease and dementia.

Outcomes of the V-Healthy Awareness Campaign That Empowers High-School Students to Understand and Diagnose Vascular Disease Risk Factors

Just imagine the impact of empowering young high-school students to become the Sherlock Holmes of vascular health and disease. V-Healthy is a grassroots vascular education and awareness campaign that educates high-school students of the importance of vascular disease risks they face today and its impact decades later. Since 2016, >300 volunteer educators including vascular surgeons, primary care physicians, allied health care providers, and teachers have participated in the V-Healthy campaign that educated >12,000 students in 40 high schools on the implications of vascular disease risks. Students participated in didactics and hands-on workshops focused on the impact of vascular disease risk factors on peripheral artery disease, venous disease, aortic aneurysms and dissections, and stroke. In 3 years, 1210 students have participated in a Diagnosing Hypertension (HTN) study, which included monitoring daily blood pressures in their parents for a week, and participated in creating a public service announcement focused on vascular health education and awareness in their communities. An additional 2950 students participated in a survey questionnaire on the impact of the V-Healthy campaign. Of the previously undiagnosed 1210 parents who participated in the Diagnosing HTN study, >50% were hypertensive; 10% had pre-HTN (120-129/<80 mm Hg), 31% had stage 1 HTN (130-139/80-89 mm Hg), and an additional 20% had stage 2 HTN (≥140/≥90 mm Hg). Of the 2950 students who participated in the V-Healthy survey, 99% reported that they had a better understanding of vascular health; 90% recognized HTN, diabetes, smoking, obesity, and family history as risk factors; 84% would discuss vascular health with their families; and 76% were interested in learning more about their vascular health. V-Healthy is a grassroots campaign that allows vascular surgeons to lead community vascular health education and awareness and to have an impact on change. HTN is prevalent and an under-recognized vascular disease risk factor that can be used as a focal point for public vascular health education and awareness. The V-Healthy project identifies a process that can be used to develop outreach programs that empower high-school students to understand the implications of vascular disease risks and promote vascular health in our communities.

Cardiovascular risk factors associated with polymyalgia rheumatica and giant cell arteritis in a prospective cohort: EPIC-Norfolk Study.

PMR and GCA are associated with increased risk of vascular disease. However, it remains unclear whether this relationship is causal or reflects a common underlying propensity. The aim of this study was to identify whether known cardiovascular risk factors increase the risk of PMR and GCA. Clinical records were examined using key word searches to identify cases of PMR and GCA, applying current classification criteria in a population-based cohort. Associations between cardiovascular risk factors and incident PMR and GCA were analysed using Cox proportional hazards. In 315 022 person years of follow-up, there were 395 incident diagnoses of PMR and 118 incident diagnoses of GCA that met the clinical definition. Raised diastolic blood pressure (>90 mmHg) at baseline/recruitment was associated with subsequent incident PMR [hazard ratio=1.35 (95% CI 1.01, 1.80) P=0.045], and ever-smoking was associated with incident GCA [hazard ratio=2.01 (95% CI 1.26, 3.20) P=0.003]. Estimates were similar when the analysis was restricted to individuals whose diagnoses satisfied the current classification criteria sets. PMR and GCA shares common risk factors with vascular disease onset, suggesting a common underlying propensity. This may indicate a potential for disease prevention strategies through modifying cardiovascular risk.

Association of prevalent vascular disease with allograft failure and mortality in live-donor kidney transplant recipients - a retrospective cohort study.

Limited data exist regarding the impact of prevalent vascular disease after live-donor kidney transplantation. We aimed to determine the associations between the number of prevalent vascular diseases, allograft, and patient outcomes following live-donor transplantation. This cohort study used data from the Australia and New Zealand Dialysis and Transplant Registry. Rates between recipients of live-donor kidney transplants±prevalent vascular disease prior to transplantation were calculated. The associations between vascular disease, allograft failure, and all-cause mortality were assessed using Cox regression modeling. Kaplan-Meier proportions were used to calculate all-cause mortality and death with a function graft stratified by vascular disease burden. Of 4742 live-donor recipients, 428 (9%) and 84 (2%) had prevalent vascular disease at 1 and ≥2 sites, respectively. Compared to recipients without vascular disease, the respective adjusted hazard ratios (95% confidence intervals) for patients with vascular disease at 1 and ≥2 sites were 1.78 (1.41-2.25) and 3.02 (2.03-4.50) for all-cause mortality; and 1.54 (1.26-1.88) and 2.28 (1.54-3.38) for allograft failure. All-cause mortality in recipients with vascular disease at 0, 1 and ≥2 sites was 0.028 (0.025, 0.031), 0.090 (0.073, 0.106) and 0.247 (0.196, 0.282) over the first 5-year post-transplant. There was an incremental association between the number of prevalent vascular disease sites and risk of allograft failure and all-cause mortality in live-donor kidney transplant recipients.