It's about time: The association between abacavir and cardiovascular disease.

High hemoglobin A1c (HbA1c) levels are strongly associated with an increased risk of cardiovascular disease (CVD) in people with and without diabetes. However, information regarding the relationship between low HbA1c levels and the risk of CVD among people without known diabetes is limited. The aim of this large-scale, prospective, population-based cohort study was to clarify the association between HbA1c levels and CVD risk among people without known diabetes.We followed-up 10,980 men and 18,079 women (46–80 years old and free of CVD and cancer at baseline) in the Japan Public Health Center-based Prospective Study. Using Cox models, we estimated the hazard ratios for CVD risk with adjustments for age, sex, geographic areas, body mass index, smoking status, sports and physical exercise, alcohol intake, systolic blood pressure, non-high-density lipoprotein cholesterol, and high-density lipoprotein cholesterol.During the median follow-up of 9.4 years, 935 CVD events (770 strokes and 165 coronary heart diseases) occurred. We observed a nonlinear association between HbA1c levels and CVD risk in participants without known diabetes. Compared with HbA1c levels of 5.0 to 5.4% (31–36 mmol/mol), the hazard ratios for CVD in participants without known diabetes were 1.50 (95% confidence interval: 1.15–1.95), 1.01 (0.85–1.20), 1.04 (0.82–1.32), and 1.77 (1.32–2.38) for HbA1c levels of <5.0% (<31 mmol/mol), 5.5 to 5.9% (37–41 mmol/mol), 6.0 to 6.4% (42–47 mmol/mol), and ≥6.5% (≥48 mmol/mol), respectively (P value for nonlinear trend: <0.001). In addition, the hazard ratio for CVD was 1.81 (1.43–2.29) in patients with known diabetes compared with participants with HbA1c levels of 5.0 to 5.4% and without known diabetes. This nonlinear relation persisted after excluding people with kidney dysfunction, liver dysfunction, anemia, body mass index <18.5 kg/m2, or early events within 3 years of follow-up (P value for nonlinear trend: <0.01 for all tests).In conclusion, both low and high levels of HbA1c were associated with a higher risk of CVD in a Japanese general population without known diabetes.

ESC/EASD guideline sheds light on diabetes and cardiovascular disease management

A spinal cord injury (SCI) is an extremely complex condition and is associated with numerous adverse health complications. One concern in particular is an increased prevalence and risk of cardiovascular disease (CVD). Cardiovascular disease, which encompasses pathologies of the heart and vascular tree, is one of the leading causes of morbidity and premature mortality in this population. Current clinical practice guidelines for CVD risk estimation in SCI use traditional cardiovascular risk factors and risk algorithms validated in able-bodied populations. However, despite the increased prevalence of CVD in people with SCI, research has demonstrated no difference in traditional cardiovascular risk factors when compared to the able-bodied population. The aim of Chapter 3 was to explore whether traditional models of CVD risk prediction are accurate in estimating CVD events in people with SCI. Firstly, this study used retrospective data from 200 individuals with a SCI to prospectively estimate their 5-year risk of developing CVD using the FRS. The difference in clinical outcomes of individuals with a below median FRS (1.36%) were compared to individuals with an above median FRS (&gt;1.36%) using Kaplan-Meier curves and log-rank test. The end point was defined as either a CVD event or CVD mortality. Across the 5-year period, 39 (19.5%) participants developed a CVD event, 10 of which were fatalities. The log-rank test demonstrated that individuals with &gt;median FRS vs.

There may be an association between periodontitis and cardiovascular disease (CVD); however, the evidence so far has been uncertain about whether periodontal therapy can help prevent CVD in people diagnosed with chronic periodontitis. This is the second update of a review originally published in 2014, and first updated in 2017. Although there is a new multidimensional staging and grading system for periodontitis, we have retained the label 'chronic periodontitis' in this version of the review since available studies are based on the previous classification system. To investigate the effects of periodontal therapy for primary or secondary prevention of CVD in people with chronic periodontitis. Cochrane Oral Health's Information Specialist searched the Cochrane Oral Health's Trials Register, CENTRAL, MEDLINE, Embase, and CINAHL, two trials registries, and the grey literature to September 2019. We placed no restrictions on the language or date of publication. We also searched the Chinese BioMedical Literature Database, the China National Knowledge Infrastructure, the VIP database, and Sciencepaper Online to August 2019. We included randomised controlled trials (RCTs) that compared active periodontal therapy to no periodontal treatment or a different periodontal treatment. We included studies of participants with a diagnosis of chronic periodontitis, either with CVD (secondary prevention studies) or without CVD (primary prevention studies). Two review authors carried out the study identification, data extraction, and 'Risk of bias' assessment independently and in duplicate. They resolved any discrepancies by discussion, or with a third review author. We adopted a formal pilot-tested data extraction form, and used the Cochrane tool to assess the risk of bias in the studies. We used GRADE criteria to assess the certainty of the evidence. We included two RCTs in the review. One study focused on the primary prevention of CVD, and the other addressed secondary prevention. We evaluated both as being at high risk of bias. Our primary outcomes of interest were death (all-cause and CVD-related) and all cardiovascular events, measured at one-year follow-up or longer. For primary prevention of CVD in participants with periodontitis and metabolic syndrome, one study (165 participants) provided very low-certainty evidence. There was only one death in the study; we were unable to determine whether scaling and root planning plus amoxicillin and metronidazole could reduce incidence of all-cause death (Peto odds ratio (OR) 7.48, 95% confidence interval (CI) 0.15 to 376.98), or all CVD-related death (Peto OR 7.48, 95% CI 0.15 to 376.98). We could not exclude the possibility that scaling and root planning plus amoxicillin and metronidazole could increase cardiovascular events (Peto OR 7.77, 95% CI 1.07 to 56.1) compared with supragingival scaling measured at 12-month follow-up. For secondary prevention of CVD, one pilot study randomised 303 participants to receive scaling and root planning plus oral hygiene instruction (periodontal treatment) or oral hygiene instruction plus a copy of radiographs and recommendation to follow-up with a dentist (community care). As cardiovascular events had been measured for different time periods of between 6 and 25 months, and only 37 participants were available with at least one-year follow-up, we did not consider the data to be sufficiently robust for inclusion in this review. The study did not evaluate all-cause death and all CVD-related death. We are unable to draw any conclusions about the effects of periodontal therapy on secondary prevention of CVD. For primary prevention of cardiovascular disease (CVD) in people diagnosed with periodontitis and metabolic syndrome, very low-certainty evidence was inconclusive about the effects of scaling and root planning plus antibiotics compared to supragingival scaling. There is no reliable evidence available regarding secondary prevention of CVD in people diagnosed with chronic periodontitis and CVD. Further trials are needed to reach conclusions about whether treatment for periodontal disease can help prevent occurrence or recurrence of CVD.

There may be an association between periodontitis and cardiovascular disease (CVD); however, the evidence so far has been uncertain about whether periodontal therapy can help prevent CVD in people diagnosed with chronic periodontitis. This is the third update of a review originally published in 2014, and most recently updated in 2019. Although there is a new multidimensional staging and grading system for periodontitis, we have retained the label 'chronic periodontitis' in this version of the review since available studies are based on the previous classification system. To investigate the effects of periodontal therapy for primary or secondary prevention of CVD in people with chronic periodontitis. An information specialist searched five bibliographic databases up to 17 November 2021 and additional search methods were used to identify published, unpublished, and ongoing studies. We also searched the Chinese BioMedical Literature Database, the China National Knowledge Infrastructure, the VIP database, and Sciencepaper Online to March 2022. We included randomised controlled trials (RCTs) that compared active periodontal therapy to no periodontal treatment or a different periodontal treatment. We included studies of participants with a diagnosis of chronic periodontitis, either with CVD (secondary prevention studies) or without CVD (primary prevention studies). Two review authors carried out the study identification, data extraction, and 'Risk of bias' assessment independently and in duplicate. They resolved any discrepancies by discussion, or with a third review author. We adopted a formal pilot-tested data extraction form, and used the Cochrane tool to assess the risk of bias in the studies. We used GRADE criteria to assess the certainty of the evidence. There are no new completed RCTs on this topic since we published our last update in 2019. We included two RCTs in the review. One study focused on the primary prevention of CVD, and the other addressed secondary prevention. We evaluated both as being at high risk of bias. Our primary outcomes of interest were death (all-cause and CVD-related) and all cardiovascular events, measured at one-year follow-up or longer. For primary prevention of CVD in participants with periodontitis and metabolic syndrome, one study (165 participants) provided very low-certainty evidence. There was only one death in the study; we were unable to determine whether scaling and root planning plus amoxicillin and metronidazole could reduce incidence of all-cause death (Peto odds ratio (OR) 7.48, 95% confidence interval (CI) 0.15 to 376.98), or all CVD-related death (Peto OR 7.48, 95% CI 0.15 to 376.98). We could not exclude the possibility that scaling and root planning plus amoxicillin and metronidazole could increase cardiovascular events (Peto OR 7.77, 95% CI 1.07 to 56.1) compared with supragingival scaling measured at 12-month follow-up. For secondary prevention of CVD, one pilot study randomised 303 participants to receive scaling and root planning plus oral hygiene instruction (periodontal treatment) or oral hygiene instruction plus a copy of radiographs and recommendation to follow-up with a dentist (community care). As cardiovascular events had been measured for different time periods of between 6 and 25 months, and only 37 participants were available with at least one-year follow-up, we did not consider the data to be sufficiently robust for inclusion in this review. The study did not evaluate all-cause death and all CVD-related death. We are unable to draw any conclusions about the effects of periodontal therapy on secondary prevention of CVD. For primary prevention of cardiovascular disease (CVD) in people diagnosed with periodontitis and metabolic syndrome, very low-certainty evidence was inconclusive about the effects of scaling and root planning plus antibiotics compared to supragingival scaling. There is no reliable evidence available regarding secondary prevention of CVD in people diagnosed with chronic periodontitis and CVD. Further trials are needed to reach conclusions about whether treatment for periodontal disease can help prevent occurrence or recurrence of CVD.

With advances in antiretroviral therapy, most deaths in people with HIV are now attributable to noncommunicable illnesses, especially cardiovascular disease. We determine the association between HIV and cardiovascular disease, and estimate the national, regional, and global burden of cardiovascular disease attributable to HIV. We conducted a systematic review across 5 databases from inception to August 2016 for longitudinal studies of cardiovascular disease in HIV infection. A random-effects meta-analysis across 80 studies was used to derive the pooled rate and risk of cardiovascular disease in people living with HIV. We then estimated the temporal changes in the population-attributable fraction and disability-adjusted life-years (DALYs) from HIV-associated cardiovascular disease from 1990 to 2015 at a regional and global level. National cardiovascular DALYs associated with HIV for 2015 were derived for 154 of the 193 United Nations member states. The main outcome measure was the pooled estimate of the rate and risk of cardiovascular disease in people living with HIV and the national, regional, and global estimates of DALYs from cardiovascular disease associated with HIV. In 793 635 people living with HIV and a total follow-up of 3.5 million person-years, the crude rate of cardiovascular disease was 61.8 (95% CI, 45.8-83.4) per 10 000 person-years. In comparison with individuals without HIV, the risk ratio for cardiovascular disease was 2.16 (95% CI, 1.68-2.77). Over the past 26 years, the global population-attributable fraction from cardiovascular disease attributable to HIV increased from 0.36% (95% CI, 0.21%-0.56%) to 0.92% (95% CI, 0.55%-1.41%), and DALYs increased from 0.74 (95% CI, 0.44-1.16) to 2.57 (95% CI, 1.53-3.92) million. There was marked regional variation with most DALYs lost in sub-Saharan Africa (0.87 million, 95% CI, 0.43-1.70) and the Asia Pacific (0.39 million, 95% CI, 0.23-0.62) regions. The highest population-attributable fraction and burden were observed in Swaziland, Botswana, and Lesotho. People living with HIV are twice as likely to develop cardiovascular disease. The global burden of HIV-associated cardiovascular disease has tripled over the past 2 decades and is now responsible for 2.6 million DALYs per annum with the greatest impact in sub-Saharan Africa and the Asia Pacific regions. URL: https://www.crd.york.ac.uk/prospero . Unique identifier: CRD42016048257.

Tofacitinib is a Janus kinase inhibitor for the treatment of psoriatic arthritis (PsA) and has been investigated for psoriasis (PsO). This post hoc analysis examined baseline cardiovascular (CV) disease risk and its association with the occurrence of major adverse cardiovascular events (MACE) and malignancies in tofacitinib-treated patients with PsA and PsO. Included three phase III/long-term extension (LTE) PsA trials and seven phase II/phase III/LTE PsO trials of patients receiving ⩾ 1 dose of tofacitinib. Incidence rates (IRs: patients with events/100 patient-years) for MACE and malignancies (excluding non-melanoma skin cancer) were determined in subgroups according to history of atherosclerotic CV disease (ASCVD), baseline 10-year risk of ASCVD (in patients without history of ASCVD), and baseline metabolic syndrome (MetS). For patients with PsA (N = 783) and PsO (N = 3663), respectively, tofacitinib exposure was 2038 and 8950 patient-years (median duration: 3.0 and 2.4 years), and 40.9% and 32.7% had MetS. Excluding missing CV risk profile data, 51/773 (6.6%) and 144/3629 (4.0%) patients had history of ASCVD, and in patients without history of ASCVD, around 20.0% had intermediate/high baseline 10-year ASCVD risk. For PsA and PsO, IRs of MACE were greatest in those with history of ASCVD or high baseline 10-year ASCVD risk. For PsA, five of six patients with MACE had baseline MetS. Malignancy IRs in patients with PsA were greatest in those with intermediate/high baseline 10-year ASCVD risk. Of these, eight of nine patients with malignancies had baseline MetS. In the PsO cohort, IR of malignancies was notably greater with high versus low/borderline/intermediate baseline 10-year ASCVD risk. In tofacitinib-treated patients with PsA/PsO, increased ASCVD risk and baseline MetS were associated with higher IRs for MACE and malignancies. Our results support assessing CV risk in patients with PsA/PsO and suggest enhanced cancer monitoring in those with increased ASCVD risk. NCT01877668/NCT01882439/NCT01976364/NCT00678210/NCT01710046/NCT01241591/NCT01186744/NCT01276639/NCT01309737/NCT01163253. People who have psoriatic arthritis or psoriasis may have more heart-related problems and cancer if they have a higher risk of cardiovascular disease: A study in people with psoriatic arthritis or psoriasis receiving tofacitinib Why was this study done? • People with psoriatic arthritis (PsA) and psoriasis (PsO) are more likely than the general population to have a disease affecting the heart and blood vessels [cardiovascular (CV) disease].• People who are more likely to have CV disease may also be more likely to have certain types of cancer.• Tofacitinib is a medicine to treat people with PsA and has been tested in people with PsO.• We wanted to know if the risk of CV disease affects the number of heart-related problems (including heart attack, stroke, or death) and cancer in people with PsA and PsO. What did the researchers do? • We used results from 10 clinical trials.• In these trials, people with PsA and PsO were taking tofacitinib 5 or 10 mg twice a day.• After the trials had ended, we measured people's risk of CV disease using a risk calculator. This risk calculator showed if they had a low, borderline, intermediate, or high risk of CV disease over the next 10 years. We also checked if they had had CV disease before treatment.• We checked if people had a group of conditions linked to CV disease: diabetes, high blood pressure, and obesity.• We counted the cases of heart-related problems and cancer in people once they started taking tofacitinib. What did the researchers find? In people with PsA and PsO taking tofacitinib:• There were more cases of heart-related problems and cancer in people who had intermediate or high risk of CV disease.• There were more cases of heart-related problems in people who had had CV disease before.• More people with diabetes, high blood pressure, and obesity had heart-related problems and cancer than people without those conditions. What do the findings mean? • It is important to measure risk and assess history of CV disease in people with PsA and PsO, including those taking tofacitinib.• We should test for cancer in people with high risk of CV disease.

Risk of Cardiovascular Disease, Chronic Kidney Disease, Cerebrovascular Disease, and Cardiovascular Mortality According to Blood Pressure Categories in Diabetes Patients: A Population-Based Study

Cardiovascular (CV) disease (CVD) risk is greater in patients with diabetes mellitus and is the major contributor to disability and premature mortality compared to those who do not have diabetes. The clinical implications of CVD in people with type 2 diabetes mellitus (T2DM) have increased the emphasis on concurrent treatment to prevent the onset of CVD through personalized management for glycemic control and CVD risk management. Key opinion leaders, comprising 98 cardiologists from across India, participated in seven advisory board meetings held in various cities to explore the challenges and strategies for the early initiation of fixed-dose combinations (FDCs) of sodium-glucose co-transporter-2 inhibitors (SGLT2i) and dipeptidyl peptidase-4 inhibitors (DPP4i) with a focus on the combination of dapagliflozin and sitagliptin in addressing the CVD risks in patients with T2DM and high risk for CV complications. The expert group discussed the available literature evidence from the clinical trials, systematic reviews, and real-world studies on the benefits of FDC of SGLT2i and DPP4i and FDC of dapagliflozin and sitagliptin to provide rational and practical guidance for its optimal use in addressing the CVD risks in patients with T2DM. The expert group emphasized the importance of timely glycemic control and early initiation of combination therapy of FDC of SGLT2i + DPP4i in T2DM with CVD risks. Addressing multiple pathophysiological aspects of T2DM is crucial, and considering combination therapy with SGLT2i and DPP4i may be pertinent in this context. Combining dapagliflozin and sitagliptin in FDC to target multiple pathophysiological pathways for T2DM appears to have several glycemic and extra-glycemic benefits. This practical guidance document provides valuable insights from leading cardiologists that would support clinicians in selecting the synergistic combination SGLT2i + DPP4i (dapagliflozin + sitagliptin) FDC as an appropriate treatment choice in early intensive therapy in managing people with T2DM and CVD risk for better patient outcomes. The expert opinion in this guidance builds on the established guideline recommendations on FDC of SGLT2i and DPP4i.

Background and Aims American College of Cardiology/American Heart Association (ACC/AHA) guidelines and cardiovascular disease (CVD) and chronic kidney disease (CKD) in diabetes patients remain unclear. We aimed to examine the effects of BP categories defined by the 2017 ACC/AHA guidelines in diabetes patients on the risk of CVD and CKD. Method In this population-based cohort study we analyzed data from the National Health Information Database in Korea during 2009-2017. The BP categories were defined as per the 2017 ACC/AHA guidelines: level 1 (systolic &amp;lt;120 mmHg and diastolic &amp;lt;80 mmHg), level 2 (systolic 120-129 mmHg and diastolic &amp;lt;80 mmHg), level 3 (systolic 130-139 mmHg or diastolic 80-89 mmHg), and level 4 (systolic ≥140 mmHg or diastolic ≥90 mmHg). We obtained the risk of CVD, CKD, cerebrovascular disease and CVD mortality. Results Overall, 490,352 diabetes patients (men 313,752 [64·0%], women 176,599 [36·0%]) were included in the analysis. Over a mean follow-up of 5 years, 6,508 CVD events occurred. Compared to people with BP levels 1, the adjusted hazard ratios (HRs) for CVD in people with BP levels 2, 3, and 4 were 1·07 (95% confidence interval [CI], 0·98-1·16), 1·12 (95% CI, 1·04-1·20) and 1·17 (95% CI, 1·08-1·26), respectively. There were also increased risks of CKD [1·18 (95% CI, 1·12-1·24) and 1·22 (95% CI, 1·15-1·29)], cerebrovascular disease [1·21 (95% CI, 1·14-1·29) and 1·52 (95% CI, 1·42-1·63)], and CVD mortality [1·31 (95% CI, 1·09-1·56) and 1·91 (95% CI, 1·58-2·32)] among subjects with BP levels 3 and 4 compared with those with BP level 1. Moreover, among people not taking antihypertensive medications, there were higher risks of CVD, CKD, cerebrovascular disease, and CVD mortality in those with BP levels 3 and 4 than in those with BP level 1. The risks of CVD, CKD, cerebrovascular disease, and CVD mortality significantly increased in patients with a systolic BP of 130 mmHg and diastolic BP of 80 mmHg. These findings provide evidence supporting the 2017 ACC/AHA guidelines for BP targets in diabetes patients. Conclusion The risks of CVD, CKD, cerebrovascular disease, and CVD mortality significantly increased in patients with a systolic BP of 130 mmHg and diastolic BP of 80 mmHg. These findings provide evidence supporting the 2017 ACC/AHA guidelines for BP targets in diabetes patients.

The association between obesity and cardiovascular disease (CVD) in people without traditional CVD risk factors is unclear. This study aimed to investigate the association of obesity with CVD and its subtypes in people without traditional CVD risk factors. Based on the Kailuan cohort study, the included participants were divided into different groups according to levels of body mass index (BMI) and waist height ratio (WHtR), respectively. Multivariate Cox proportional hazard models were used to evaluate the associations. This study included 31,955 participants [men 63.99%; mean age (48.14 ± 3.33) years]. During a median follow-up period of 12.97 (interquartile range: 12.68-13.17) years, 1298 cases of CVD were observed. Compared with the normal BMI group, the hazard ratios (HRs) for CVD, stroke, and myocardial infarction (MI) in the BMI obese group were 1.31 (95% confidence interval [CI] 1.11-1.55), 1.21 (95%CI 1.01-1.46), 1.62 (95%CI 1.13-2.33), respectively. Compared with the WHtR non-obese group, the HRs for CVD, stroke, and MI in the obese group were 1.25(95%CI 1.11-1.41), 1.18 (95%CI 1.03-1.34), 1.57 (95%CI 1.18-2.09), respectively. There was an interaction between age and WHtR (P for interaction was 0.043). The association between WHtR and CVD was stronger in people under 60 years old, with a HR of 1.44 (95%CI 1.24-1.67). We found that obesity increased the risk of CVD in people without traditional CVD risk factors. The association of WHtR with CVD was stronger in people under 60 years old.

Cardiovascular disease (CVD) is the most frequent cause of death in people with type 1 diabetes (T1D), despite modern advances in glycemic control and CVD risk factor modification. CVD risk identification is essential in this high-risk population, yet remains poorly understood. This review discusses the risk factors for CVD in young people with T1D, including hyperglycemia, traditional CVD risk factors (dyslipidemia, smoking, physical activity, hypertension), as well as novel risk factors such as insulin resistance, inflammation, and hypoglycemia. We present evidence that adverse changes in cardiovascular function, arterial compliance, and atherosclerosis are present even during adolescence in people with T1D, highlighting the need for earlier intervention. The methods for investigating cardiovascular risk are discussed and reviewed. Finally, we discuss the observational studies and clinical trials which have thus far attempted to elucidate the best targets for early intervention in order to reduce the burden of CVD in people with T1D.

This study was undertaken to investigate the distribution of social, lifestyle/behavior, and chronic disease risk factors for cardiovascular disease (CVD) in people with epilepsy as compared to the general population. We also measured the cross-sectional association between epilepsy and CVD in older adults, with and without adjustments for a history of stroke. We analyzed data for 44817 participants in the Canadian Longitudinal Study on Aging, including 751 individuals with a lifetime history of epilepsy. We modeled associations using ordinal and binomial logistic regression, as well as log-binomial regression, with multiple imputation for missing data. We measured the attributable fraction of CVD burden due to stroke. The majority of the CVD risk factors were significantly more prevalent in people with epilepsy as compared to the general population without epilepsy, independent of age and sex. After adjusting for a history of stroke, people with epilepsy had a significantly higher prevalence of heart disease (prevalence ratio [PR]=1.27, 95% confidence interval [CI] = 1.02-1.57) and peripheral vascular disease (PR=1.88, 95% CI = 1.50-2.36). Stroke accounted for 36% (95% CI = 19.85-48.76) of the increased prevalence of any CVD among people with epilepsy, similar to the 32% (95% CI = 27.82-36.25) among people without epilepsy. After adjustment for all other CVD risk factors, peripheral vascular disease remained significantly more prevalent (PR=1.65, 95% CI = 1.28-2.12) in people with epilepsy as compared to those without. CVD risk factors are more prevalent in people with epilepsy, independent of age and sex, and the association between epilepsy and CVD is independent of the association between epilepsy and stroke. The association between peripheral vascular disease and epilepsy may differ from the associations with other types of CVD. These findings are important steps in more comprehensively understanding the origins of CVD in people with epilepsy.

Despite inflammation being implicated in cardiovascular disease (CVD) in people with human immunodeficiency virus (PWH), considerable heterogeneity within populations of PWH exists. Stratifying CVD risk based on inflammatory phenotype could play an important role. Using principal component analyses and unsupervised hierarchical clustering, we examined 38 biomarkers to identify inflammatory phenotypes in 2 independent cohorts of PWH. We identified 3 distinct inflammatory clusters present in both cohorts that were associated with altered risk of both subclinical CVD (cohort 1) and prevalent clinical CVD (cohort 2) after adjusting for CVD risk factors. These data support precision medicine approaches to enhance CVD risk assessment in PWH.

Vascular Protection in People with Diabetes