Computational framework for dynamic cardiovascular risk assessment with cluster-specific Cox models and cumulative risk analysis

Recognizing Pregnancy-Associated Cardiovascular Risk Factors

Are We There Yet? Pediatric Screening for Inflammatory Biomarkers and Low Cardiorespiratory Fitness to Identify Youth at Increased Risk of Cardiovascular Disease

Impact of psychological status on cardiovascular diseases: Is it time for upgrading risk score charts?

AimsTo describe change in self-reported diet and plasma vitamin C, and to examine associations between change in diet and cardiovascular disease risk factors and modelled 10-year cardiovascular disease risk in the year following diagnosis of Type 2 diabetes.MethodsEight hundred and sixty-seven individuals with screen-detected diabetes underwent assessment of self-reported diet, plasma vitamin C, cardiovascular disease risk factors and modelled cardiovascular disease risk at baseline and 1 year (n = 736) in the ADDITION-Cambridge trial. Multivariable linear regression was used to quantify the association between change in diet and cardiovascular disease risk at 1 year, adjusting for change in physical activity and cardio-protective medication.ResultsParticipants reported significant reductions in energy, fat and sodium intake, and increases in fruit, vegetable and fibre intake over 1 year. The reduction in energy was equivalent to an average-sized chocolate bar; the increase in fruit was equal to one plum per day. There was a small increase in plasma vitamin C levels. Increases in fruit intake and plasma vitamin C were associated with small reductions in anthropometric and metabolic risk factors. Increased vegetable intake was associated with an increase in BMI and waist circumference. Reductions in fat, energy and sodium intake were associated with reduction in HbA1c, waist circumference and total cholesterol/modelled cardiovascular disease risk, respectively.ConclusionsImprovements in dietary behaviour in this screen-detected population were associated with small reductions in cardiovascular disease risk, independently of change in cardio-protective medication and physical activity. Dietary change may have a role to play in the reduction of cardiovascular disease risk following diagnosis of diabetes.

Introduction Cardiovascular disease (CVD) is the leading cause of mortality in people with type 2 diabetes (T2D). CAPTURE, a non-interventional, cross-sectional study conducted across 13 countries in 2019, collected demographic and clinical characteristics in almost 10,000 adults with T2D in primary or secondary care. Less than 25% of patients with established CVD treated with a glucose-lowering agent received an agent with demonstrated benefit in cardiovascular (CV) risk reduction, such as a glucagon-like peptide-1 receptor agonist (GLP-1 RA) or a sodium–glucose co-transporter-2 inhibitor (SGLT-2i).1 It is not known whether this is linked to estimated 10-year and lifetime CV risk. Purpose To estimate the CV risk distribution in the CAPTURE population using the Diabetes Lifetime-perspective prediction (DIAL) model, and to assess treatment patterns by CV risk. Methods The DIAL model is an externally validated competing risk adjusted model for predicting CV risk in patients with T2D, calculating absolute 10-year and lifetime risk of myocardial infarction, stroke or cardiovascular death, and life-expectancy free of a CVD event. Patient-level data from CAPTURE (age, sex, body mass index, smoking status, HbA1c, CVD history, T2D duration, clinical parameters and treatment history) were used in the DIAL model. Missing data were imputed by region using predicted mean matching. High risk was defined as 10-year risk >10%, and lifetime risk >50%. Results Data from 9457 patients with T2D aged 30–85 years were included in the analyses. There was a wide distribution of both 10-year and lifetime risk, with higher risk in patients with a history of CVD (n=2914) than in those without (n=6543). Among patients with a history of CVD, 96% had a 10-year risk of CVD >10% and 81% had a lifetime risk of CVD >50% (Figure). In patients with CVD and a high 10-year risk of recurrent CVD, 81% had a lifetime risk of recurrent CVD >50%. In patients without history of CVD, 14% had a 10-year risk >10% and only 1% had a lifetime risk >50% (Figure). Among patients without previous CVD but with a high 10-year risk of CVD, only 4% had a lifetime risk >50%. Of the patients with CVD, 10% received a GLP-1 RA and 18% received an SGLT-2i. Similarly, of patients with CVD and a high 10-year risk of recurrent CVD, 10% received a GLP-1 RA and 17% received an SGLT-2i. Among patients without CVD, 11% received a GLP-1 RA and 16% received an SGLT-2i, and among patients without current CVD but at a high 10-year risk of CVD, 12% received a GLP-1 RA and 16% received an SGLT-2i. Conclusion There is a wide distribution of CVD risk in the CAPTURE population, and only a minority of patients at high risk of CVD received a glucose-lowering agent with demonstrated benefit in CV risk reduction. Discussing with patients the 10-year and lifetime risks, and the CV benefit to be gained from interventions, can enhance shared decision making. Funding Acknowledgement Type of funding sources: Private company. Main funding source(s): Funded by Novo Nordisk A/S

Cardiovascular disease in HIV-positive patients

Heart rate variability, but not heart rate, is associated with handgrip strength and mortality in older Africans at very low cardiovascular risk: A population-based study

BackgroundTreatment of patients with type 2 diabetes mellitus (T2DM) and a history of cardiovascular (CV) disease or CV risk factors may present clinical challenges due to the presence of comorbid conditions and the use of concomitant medications. The sodium glucose co-transporter 2 inhibitor, canagliflozin, has been shown to improve glycaemic control and reduce body weight and blood pressure (BP) with a favourable tolerability profile in a broad range of patients with T2DM. This post hoc analysis assessed the efficacy and safety of canagliflozin in patients with T2DM based on CV disease history or CV risk factors.MethodsAnalyses were based on pooled data from four 26-week, placebo-controlled, Phase 3 studies that evaluated canagliflozin 100 and 300 mg in patients with T2DM (N = 2313; mean HbA1c, 8.0%; body weight, 89 kg; systolic BP, 128 mmHg). Changes from baseline to week 26 in HbA1c, body weight, and systolic BP were assessed based on history of CV disease, history of hypertension, baseline statin use, and number of CV risk factors. Safety was assessed based on adverse event (AE) reports.ResultsAt week 26, both canagliflozin doses lowered HbA1c, body weight, and systolic BP compared with placebo in patients with and without CV disease history or risk factors. Placebo-subtracted HbA1c reductions with canagliflozin 100 and 300 mg were similar in patients with a history of CV disease (−0.95 and −1.07%) versus no history of CV disease (−0.71 and −0.90%), history of hypertension (−0.72 and −0.89%) versus no history of hypertension (−0.73 and −0.95%), baseline statin use (−0.77 and −0.99%) versus no statin use (−0.69 and −0.85%), and 0–1 CV risk factor (−0.72 and −0.87%) versus ≥2 CV risk factors (−0.74 and −1.02%). Similar body weight and systolic BP reductions were seen with canagliflozin versus placebo across subgroups. The incidence of AEs, AEs leading to discontinuation, and serious AEs was similar across subgroups.ConclusionsThe efficacy and safety of canagliflozin were generally consistent across subgroups of patients with T2DM and varying degrees of CV disease history or risk factors.Trial registration numbers and dates ClinicalTrials.gov: NCT01081834, 4 March 2010; NCT01106625, 1 April 2010; NCT01106677, 1 April 2010; NCT01106690, 1 April 2010

Nonalcoholic Fatty Liver Disease and Cardiovascular Disease Risk

WHITE MATTER VULNERABILITY AND CARDIOVASCULAR RISK IN OLDER HISPANICS/LATINOS: EVIDENCE FOR EARLIER NEURODEGENERATION?

With successful antiretroviral therapy, patients infected with the human immunodeficiency virus (HIV) are living longer; however, recent reports suggest increased rates of coronary heart disease (CHD) among HIV-infected patients,1 and cardiovascular disease has become an important cause of morbidity and mortality in this population.2 Increased CHD rates in the HIV population may relate to traditional risk factors, including advancing age, higher smoking rates, dyslipidemia, insulin resistance, and impaired glucose tolerance. Cardiovascular disease may also be due to nontraditional factors, including changes in body composition with loss of subcutaneous fat and/or accumulation of visceral fat in some patients, inflammation, and direct effects of the virus on the vasculature, as well as to direct effects of specific antiretroviral drugs. Important questions remain as to the pathogenesis, detection, and treatment of cardiovascular disease and related risk factors in HIV-infected patients. These questions concern, among other things, the design of adequate trials to determine CHD incidence and the utility of existing CHD guidelines for screening, prevention, treatment, and risk stratification. To ascertain the state of the science with respect to these and related questions, a multidisciplinary conference with interested HIV specialists, cardiologists, endocrinologists, primary care physicians, National Institutes of Health representatives, and patient advocates was convened June 28–30, 2007, in Chicago, Ill, and chaired by Drs Steven Grinspoon and Robert Eckel. The discussions focused on 6 areas of interest, each with its own working group, including the following: (1) the contribution of metabolic and anthropometric abnormalities to cardiovascular disease risk factors (chaired by Drs Carl Grunfeld and Donald Kotler); (2) the epidemiological evidence for cardiovascular disease and its relationship to highly active antiretroviral therapy (HAART; chaired by Drs Judy Currier and Jens Lundgren); (3) the effects of HIV infection and antiretroviral therapy on the heart and vasculature (chaired by Drs Michael Dube …

As reports show cardiovascular (CV) risks in first-degree relatives (FDR) of type2 diabetics, and autonomic imbalance predisposing to CV risks, in the present study we have assessed the contribution of sympathovagal imbalance (SVI) to CV risks in these subjects. Body mass index (BMI), waist-to-hip ratio (WHR), basal heart rate (BHR), blood pressure (BP), rate pressure product (RPP), and spectral indices of heart rate variability (HRV) were reordered and analyzed in FDR of type2 diabetics (study group, n=293) and in subjects with no family history of diabetes (control group, n=405). The ratio of low-frequency (LF) to high-frequency (HF) power of HRV (LF-HF), a sensitive marker of SVI, was significantly increased (P<0.001) in the study group compared with the control group. The SVI in the study group was due to concomitant sympathetic activation (increased LF) and vagal inhibition (decreased HF). In the study group, the LF-HF ratio was significantly correlated with BMI, WHR, BHR, BP and RPP. Multiple regression analysis showed an independent contribution of LF-HF to hypertension status (P=0.000), and bivariate logistic regression showed significant prediction (odds ratio 2.16, confidence interval 1.130-5.115) of LF-HF to increased RPP, the marker of CV risk, in the study group. Sympathovagal imbalance in the form of increased sympathetic and decreased parasympathetic activity is present in FDR of type2 diabetics. Increased resting heart rate, elevated hypertension status, decreased HRV and increased RPP in these subjects make them vulnerable to CV risks. SVI in these subjects contributes to CV risks independent of the degree of adiposity.

Cardiovascular Protection in People With Diabetes.

Atherosclerosis and Vascular Biology

To assess the suitability of Australian community pharmacies as cardiovascular disease risk profile screening centres and evaluate whether community pharmacists can play an important role in detecting, educating and referring screened individuals at high risk of cardiovascular disease. 14 Australian community pharmacies. Opportunistic cardiovascular disease risk profiling for members of the public aged greater than 30 years with no existing cardiovascular diseases was performed. All major cardiovascular risk factors were measured. Exercise habits, existing conditions and therapy, and family history were also assessed. The results were used to calculate each subject's 10-year risk of developing cardiovascular events, based on Framingham Risk Equations (New Zealand tables). Each subject's knowledge of cardiovascular risk factors was assessed using a multiple-choice questionnaire. Written educational materials and verbal counselling were provided. Referral to a doctor for further assessment was recommended as appropriate. The screened individuals were followed up via mailed out questionnaire. A random sample of individuals at elevated risk was phoned to assess for outcomes of the screening and referral process. Risk of developing cardiovascular disease and knowledge of cardiovascular risk factors. A total of 655 individuals (71.4% female) were screened for cardiovascular disease risk factors. Ages ranged from 30 to 90 years (median: 54 years) and 14.2% were smokers. Of the individuals screened, 28.1% had a 10-year risk of developing cardiovascular disease greater than 15%, including 6.9% who had a 10-year risk above 30%. The median calculated 10-year risk of developing cardiovascular disease was 9.5%. Approximately one-third of the individuals had elevated blood pressure, and almost two-thirds were either overweight or obese. The mean total serum cholesterol was 5.31 mmol/l, with 40% of individuals having a level above 5.5 mmol/l and 20% having a high-density lipoprotein cholesterol level below 1.0 mmol/l. There was a statistically significant improvement in the knowledge of cardiovascular disease risk factors at follow-up. Almost half of the contacted high-risk subjects reported lifestyle changes or started drug therapy following re-testing by their general practitioner. A pharmacy-based cardiovascular disease risk profile screening and education program has the potential to identify and refer many undiagnosed individuals at high risk of cardiovascular events, and help contain the burden of heart disease.