Importance: Whether people infected with human immunodeficiency virus (HIV) are at an increased risk of acute myocardial infarction (AMI) compared with uninfected people is not clear. Without demographically and behaviorally similar uninfected comparators and without uniformly measured clinical data on risk factors and fatal and nonfatal AMI events, any potential association between HIV status and AMI may be confounded.Objective: To investigate whether HIV is associated with an increased risk of AMI after adjustment for all standard Framingham risk factors among a large cohort of HIV-positive and demographically and behaviorally similar (ie, similar prevalence of smoking, alcohol, and cocaine use) uninfected veterans in care.

As early and effective antiretroviral therapy has become more widespread, HIV has transitioned from a progressive, fatal disease to a chronic, manageable disease marked by elevated risk of chronic comorbid diseases, including cardiovascular diseases (CVDs). Rates of myocardial infarction, heart failure, stroke, and other CVD manifestations, including pulmonary hypertension and sudden cardiac death, are significantly higher for people living with HIV than for uninfected control subjects, even in the setting of HIV viral suppression with effective antiretroviral therapy. These elevated risks generally persist after demographic and clinical risk factors are accounted for and may be partly attributed to chronic inflammation and immune dysregulation. Data on long-term CVD outcomes in HIV are limited by the relatively recent epidemiological transition of HIV to a chronic disease. Therefore, our understanding of CVD pathogenesis, prevention, and treatment in HIV relies on large observational studies, randomized controlled trials of HIV therapies that are underpowered to detect CVD end points, and small interventional studies examining surrogate CVD end points. The purpose of this document is to provide a thorough review of the existing evidence on HIV-associated CVD, in particular atherosclerotic CVD (including myocardial infarction and stroke) and heart failure, as well as pragmatic recommendations on how to approach CVD prevention and treatment in HIV in the absence of large-scale randomized controlled trial data. This statement is intended for clinicians caring for people with HIV, individuals living with HIV, and clinical and translational researchers interested in HIV-associated CVD.

Background There is growing concern that racial and ethnic minority communities around the world are experiencing a disproportionate burden of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and coronavirus disease 2019 (COVID-19). We investigated racial and ethnic disparities in patterns of COVID-19 testing (i.e., who received testing and who tested positive) and subsequent mortality in the largest integrated healthcare system in the United States. Methods and findings This retrospective cohort study included 5,834,543 individuals receiving care in the US Department of Veterans Affairs; most (91%) were men, 74% were non-Hispanic White (White), 19% were non-Hispanic Black (Black), and 7% were Hispanic. We evaluated

OBJECTIVE -The aim of this study was to examine the relations of alcohol consumption to the prevalence of the metabolic syndrome and its components in the U.S. population. RESEARCH DESIGN AND METHODS-We performed a cross-sectional analysis on data from 8,125 participants from the Third National Health and Nutrition Examination Survey who were evaluated for each component of the metabolic syndrome, using the National Cholesterol Education Program criteria, fasting insulin, and alcohol consumption. Current alcohol consumption was defined as Ն1 alcoholic drink per month.RESULTS -After adjustment for age, sex, race/ethnicity, education, income, tobacco use, physical activity, and diet, subjects who consumed 1-19 and Ն20 drinks of alcohol per month had odds ratios (ORs) for the prevalence of the metabolic syndrome of 0.65 and 0.34, respectively (P Ͻ 0.05 for all), compared with current nondrinkers. These findings were particularly noteworthy for beer and wine drinkers. The association of Ն20 alcoholic drinks per month with the prevalence of the metabolic syndrome was consistent across ethnicities but was most striking in white men and women (ORs 0.35 and 0.22, respectively; P Ͻ 0.05). Alcohol consumption was significantly and inversely associated with the prevalence of the following three components of the metabolic syndrome: low serum HDL cholesterol, elevated serum triglycerides, high waist circumference, as well as hyperinsulinemia (P Ͻ 0.05 for all).CONCLUSIONS -Mild to moderate alcohol consumption is associated with a lower prevalence of the metabolic syndrome, with a favorable influence on lipids, waist circumference, and fasting insulin. This association was strongest among whites and among beer and wine drinkers. Diabetes Care 27:2954 -2959, 2004L ight to moderate alcohol consumption is associated with lower cardiovascular mortality (1) and a reduced risk of developing type 2 diabetes (2). Some of the biological mechanisms reported to explain this observation include an improvement of the lipid profile, especially HDL cholesterol (3) and increasing insulin sensitivity (4,5).The metabolic syndrome is a clustering of low serum HDL cholesterol, elevated serum triglycerides, hyperglycemia, central obesity, and elevated blood pressure, mediated in part by insulin resistance (6,7). The metabolic syndrome is associated with an increased risk of developing diabetes (8) and cardiovascular disease (9).The favorable influence of alcohol consumption on select components of the metabolic syndrome (3,10) raises the possibility that alcohol intake may reduce the risk of the metabolic syndrome. Few studies have examined the association between alcohol consumption and the metabolic syndrome as defined by the National Cholesterol Education Program (11-13), and data are limited on how the relation may be modified by type of alcohol, sex, or race/ethnicity (14,15).We investigated the relations of the quantity and the type of alcohol consumed to the prevalence of the metabolic syndrome (and its components) in men and women of dif...

IMPORTANCE With improved survival, heart failure (HF) has become a major complication for individuals with human immunodeficiency virus (HIV) infection. It is unclear if this risk extends to different types of HF in the antiretroviral therapy (ART) era. Determining whether HIV infection is associated with HF with reduced ejection fraction (HFrEF), HF with preserved ejection fraction (HFpEF), or both is critical because HF types differ with respect to underlying mechanism, treatment, and prognosis. OBJECTIVES To investigate whether HIV infection increases the risk of future HFrEF and HFpEF and to assess if this risk varies by sociodemographic and HIV-specific factors. DESIGN, SETTING, AND PARTICIPANTS This study evaluated 98 015 participants without baseline cardiovascular disease from the Veterans Aging Cohort Study, an observational cohort of HIV-infected veterans and uninfected veterans matched by age, sex, race/ethnicity, and clinical site, enrolled on or after April 1, 2003, and followed up through September 30, 2012. The dates of the analysis were October 2015 to November 2016. EXPOSURE Human immunodeficiency virus infection. MAIN OUTCOMES AND MEASURES Outcomes included HFpEF (EF≥50%), borderline HFpEF (EF 40%–49%), HFrEF (EF<40%), and HF of unknown type (EF missing). RESULTS Among 98 015 participants, the mean (SD) age at enrollment in the study was 48.3 (9.8) years, 97.0% were male, and 32.2% had HIV infection. During a median follow-up of 7.1 years, there were 2636 total HF events (34.6% were HFpEF, 15.5% were borderline HFpEF, 37.1% were HFrEF, and 12.8% were HF of unknown type). Compared with uninfected veterans, HIV-infected veterans had an increased risk of HFpEF (hazard ratio [HR], 1.21; 95% CI, 1.03–1.41), borderline HFpEF (HR, 1.37; 95% CI, 1.09–1.72), and HFrEF (HR, 1.61; 95% CI, 1.40–1.86). The risk of HFrEF was pronounced in veterans younger than 40 years at baseline (HR, 3.59; 95% CI, 1.95–6.58). Among HIV-infected veterans, time-updated HIV-1 RNA viral load of at least 500 copies/mL compared with less than 500 copies/mL was associated with an increased risk of HFrEF, and time-updated CD4 cell count less than 200 cells/mm3 compared with at least 500 cells/mm3 was associated with an increased risk of HFrEF and HFpEF. CONCLUSIONS AND RELEVANCE Individuals who are infected with HIV have an increased risk of HFpEF, borderline HFpEF, and HFrEF compared with uninfected individuals. The increased risk of HFrEF can manifest decades earlier than would be expected in a typical uninfected population. Future research should focus on prevention, risk stratification, and identification of the mechanisms for HFrEF and HFpEF in the HIV-infected population.

Peripheral artery disease (PAD) is a leading cause of cardiovascular morbidity and mortality1; however, the extent to which genetic factors increase risk for PAD is largely unknown. Using electronic health record data, we performed a genome-wide association study in the Million Veteran Program testing ~32 million DNA sequence variants with PAD (31,307 cases and 211,753 controls) across veterans of European, African, and Hispanic ancestry. The results were replicated in an independent sample of 5,117 PAD cases and 389,291 controls from UK Biobank. We identified 19 PAD loci, 18 of which have not been previously reported. 11 of the 19 loci were associated with disease in three vascular beds (coronary, cerebral, peripheral), including LDLR, LPL, and LPA, suggesting that therapeutic modulation of LDL cholesterol, the LPL pathway or circulating lipoprotein(a) may be efficacious for multiple atherosclerotic disease phenotypes. Conversely, 4 of the variants appeared to be specific for PAD, including F5 p.R506Q, highlighting the pathogenic role of thrombosis in the peripheral vascular bed and providing genetic support for Factor Xa inhibition as a therapeutic strategy for PAD. Our results highlight mechanistic similarities and differences among coronary, cerebral, and peripheral atherosclerosis and provide therapeutic insights.

Objective: To examine dose-response relationships between the cumulative number of months women lactated and postmenopausal risk factors for cardiovascular disease. Methods:We examined data from 139,681 postmenopausal women (median age 63 years) who reported at least 1 live birth upon enrolling in the Women's Health Initiative (WHI) observational study or controlled trials. Multivariable models were used to control for sociodemographic (age, parity, race, education, income, age at menopause), lifestyle, and family history variables when examining the impact of duration of lactation on risk factors for cardiovascular disease, including obesity (body mass index(BMI) at or above 30), hypertension, self-reported diabetes, hyperlipidemia, prevalent and incident cardiovascular disease.Results: Dose-response relationships were observed; in fully-adjusted models, women who reported a lifetime history of more than 12 months of lactation were less likely to have hypertension (OR=0.88, p<0.001), diabetes (OR= 0.80, p<0.001), hyperlipidemia (OR=0.81, p<0.001) or cardiovascular disease (OR= 0.91, p=0.008) than women who never breastfed, but they were not less likely to be obese. In models adjusted for all above variables and BMI, similar relationships were seen. Over an average of 7.9 years of postmenopausal participation in the WHI, women with a single live birth who breastfed for 7-12 months were significantly less likely to develop cardiovascular disease (HR 0.72 (0.53 to 0.97)) than women who never breastfed.

These data suggest that ongoing HIV replication and immune depletion significantly contribute to increased prevalence of elevated biomarkers of inflammation, altered coagulation, and monocyte activation. This contribution is independent of and in addition to the substantial contribution from comorbid conditions.