Background Limited attention has been paid to negative cardiovascular disease (CVD) risk markers despite their potential to improve medical decision-making. We compared thirteen negative risk markers using diagnostic likelihood ratios (DLR), which model the change in risk for an individual after the result of an additional test. Methods and Results We examined 6,814 participants from the Multi-Ethnic Study of Atherosclerosis. Coronary artery calcium (CAC) =0, carotid intima-media thickness (CIMT) <25th percentile, absence of carotid plaque, brachial flow-mediated dilation >5% change, ankle brachial index (ABI) >0.9 and <1.3, high sensitivity C-reactive protein (hsCRP) <2 mg/L, homocysteine <10 µmol/L, NTpro-BNP <100 pg/mL, no microalbuminuria, no family history of coronary heart disease (CHD) (any/premature), absence of metabolic syndrome, and healthy lifestyle were compared for all, hard CHD and all CVD events over 10-year follow-up. Models were adjusted for traditional CVD risk factors. Among all negative risk markers CAC=0 was the strongest, with adjusted mean DLR (SD) of 0.41 (0.12) for all CHD and 0.54 (0.12) for CVD, followed by CIMT <25th percentile (DLRs 0.65 [0.04] and 0.75 [0.04], respectively). HsCRP <2 mg/L and normal ABI had DLRs >0.80. Among clinical features, absence of any family history of CHD was the strongest (DLRs 0.76 [0.07] and 0.81 [0.06], respectively). Net Reclassification Improvement (NRI) analyses yielded similar findings, with CAC=0 resulting in the largest, most accurate downward risk reclassification. Conclusions Negative results of atherosclerosis-imaging tests, particularly CAC=0, resulted in the greatest downward shift in estimated CVD risk. These results may help guide discussions regarding identification of individuals less likely to receive net benefit from lifelong preventive pharmacotherapy.

The risk of nonalcoholic fatty liver disease (NAFLD) among obese individuals without obesity-related metabolic abnormalities, a condition referred to as metabolically healthy obese (MHO), is largely unexplored. Therefore, we examined the association between body mass index (BMI) categories and the development of NAFLD in a large cohort of metabolically healthy men and women. METHODS:A cohort study was conducted in 77,425 men and women free of NAFLD and metabolic abnormalities at baseline, who were followed-up annually or biennially for an average of 4.5 years. Being metabolically healthy was defi ned as not having any metabolic syndrome component and having a homeostasis model assessment of insulin resistance <2.5. The presence of fatty liver was determined using ultrasound. RESULTS:During 348,193.5 person-years of follow-up, 10,340 participants developed NAFLD (incidence rate, 29.7 per 1,000 person-years). The multivariable adjusted hazard ratios (95% confi dence intervals) for incident NAFLD comparing overweight and obese with normal-weight participants were 2.15 (2.06-2.26) and 3.55 (3.37-3.74), respectively. In detailed dose-response analyses, increasing baseline BMI showed a strong and approximately linear relationship with the incidence of NAFLD, with no threshold at no risk. This association was present in both men and women, although it was stronger in women ( P for interaction <0.001), and it was evident in all clinically relevant subgroups evaluated, including participants with low infl ammation status. CONCLUSIONS:In a large cohort of strictly defi ned metabolically healthy men and women, overweight and obesity were strongly and progressively associated with an increased incidence of NAFLD, suggesting that the obese phenotype per se , regardless of metabolic abnormalities, can increase the risk of NAFLD. Am J Gastroenterol 2016; 111:1133-1140 doi: 10.1038/ajg.2016 Specifi cally, it is unclear whether obesity is a risk factor for NALFD in subjects who do not have any of the metabolic abnormalities associated with excess adiposity, a group oft en described as metabolically healthy obese (MHO) ( 11,12 ). Th e health implications of . Only one study has evaluated the association of MHO with NAFLD ( 16 ). In this study, MHO subjects had an increased prevalence of NAFLD compared with metabolically healthy non-obese subjects, but the cross-sectional design of this study limited its ability to establish a temporal relation between obesity and NAFLD.No cohort study has evaluated the role of MHO as a determinant of incident NAFLD among subjects free of NAFLD at baseline. Th erefore, we examined the association between body mass index (BMI) categories and the development of NAFLD in a large cohort of metabolically healthy men and women who participated in a health screening examination program. METHODS Study populationTh e Kangbuk Samsung Health Study is a cohort study of men and women 18 years of age or older who underwent a comprehensive annual or biennial health examination at the clinics of the Kangbuk Samsu...

BackgroundHeart failure (HF) is frequent and its prevalence is increasing. We aimed to evaluate the epidemiologic features of HF patients, the 1-year follow-up outcomes and the independent predictors of those outcomes at a population level.Methods and resultsPopulation-based longitudinal study including all prevalent HF cases in Catalonia (Spain) on December 31st, 2012. Patients were divided in 3 groups: patients without a previous HF hospitalization, patients with a remote (>1 year) HF hospitalization and patients with a recent (<1 year) HF admission. We analyzed 1year all-cause and HF hospitalizations, and all-cause mortality. Logistic regression was used to identify the independent predictors of each of those outcomes. A total of 88,195 patients were included. Mean age was 77 years, 55% were women. Comorbidities were frequent. Fourteen percent of patients had never been hospitalized, 71% had a remote HF hospitalization and 15% a recent hospitalization. At 1-year follow-up, all-cause and HF hospitalization were 53% and 8.8%, respectively. One-year all-cause mortality rate was 14%, and was higher in patients with a recent HF hospitalization (24%). The presence of diabetes mellitus, atrial fibrillation or chronic kidney disease was independently associated with all-cause and HF hospitalization and all-cause mortality. Hospital admissions and emergency department visits the previous year were also found to be independently associated with the three study outcomes.ConclusionsOutcomes are different depending on the HF population studied. Some comorbidity, an all-cause hospitalization or emergency department visit the previous year were associated with a worse outcome.

Background: Recent American College of Cardiology/American Heart Association Primary Prevention Guidelines recommended considering low-dose aspirin therapy only among adults 40 to 70 years of age who are at higher atherosclerotic cardiovascular disease (ASCVD) risk but not at high risk of bleeding. However, it remains unclear how these patients are best identified. The present study aimed to assess the value of coronary artery calcium (CAC) for guiding aspirin allocation for primary prevention by using 2019 aspirin meta-analysis data on cardiovascular disease relative risk reduction and bleeding risk. Methods: The study included 6470 participants from the MESA Study (Multi-Ethnic Study of Atherosclerosis). ASCVD risk was estimated using the pooled cohort equations, and 3 strata were defined: <5%, 5% to 20%, and >20%. All participants underwent CAC scoring at baseline, and CAC scores were stratified as =0, 1 to 99, ≥100, and ≥400. A 12% relative risk reduction in cardiovascular disease events was used for the 5-year number needed to treat (NNT 5 ) calculations, and a 42% relative risk increase in major bleeding events was used for the 5-year number needed to harm (NNH 5 ) estimations. Results: Only 5% of MESA participants would qualify for aspirin consideration for primary prevention according to the American College of Cardiology/American Heart Association guidelines and using >20% estimated ASCVD risk to define higher risk. Benefit/harm calculations were restricted to aspirin-naive participants <70 years of age not at high risk of bleeding (n=3540). The overall NNT 5 with aspirin to prevent 1 cardiovascular disease event was 476 and the NNH 5 was 355. The NNT 5 was also greater than or similar to the NNH 5 among estimated ASCVD risk strata. Conversely, CAC≥100 and CAC≥400 identified subgroups in which NNT 5 was lower than NNH 5 . This was true both overall (for CAC≥100, NNT 5 =140 versus NNH 5 =518) and within ASCVD risk strata. Also, CAC=0 identified subgroups in which the NNT 5 was much higher than the NNH 5 (overall, NNT 5 =1190 versus NNH 5 =567). Conclusions: CAC may be superior to the pooled cohort equations to inform the allocation of aspirin in primary prevention. Implementation of current 2019 American College of Cardiology/American Heart Association guideline recommendations together with the use of CAC for further risk assessment may result in a more personalized, safer allocation of aspirin in primary prevention. Confirmation of these findings in experimental settings is needed.

Health care in the United States has seen many great innovations and successes in the past decades. However, to this day, the color of a person’s skin determines—to a considerable degree—his/her prospects of wellness; risk of disease, and death; and the quality of care received. Disparities in cardiovascular disease (CVD)—the leading cause of morbidity and mortality globally—are one of the starkest reminders of social injustices, and racial inequities, which continue to plague our society. People of color—including Black, Hispanic, American Indian, Asian, and others—experience varying degrees of social disadvantage that puts these groups at increased risk of CVD and poor disease outcomes, including mortality. Racial/ethnic disparities in CVD, while documented extensively, have not been examined from a broad, upstream, social determinants of health lens. In this review, we apply a comprehensive social determinants of health framework to better understand how structural racism increases individual and cumulative social determinants of health burden for historically underserved racial and ethnic groups, and increases their risk of CVD. We analyze the link between race, racism, and CVD, including major pathways and structural barriers to cardiovascular health, using 5 distinct social determinants of health domains: economic stability ; neighborhood and physical environment ; education ; community and social context ; and healthcare system . We conclude with a set of research and policy recommendations to inform future work in the field, and move a step closer to health equity.

In Catalonia, a large portion of the annual healthcare budget is devoted to HF patients. Unplanned hospitalization represents the main source of healthcare-related expenditure. The knowledge of how expenditure is distributed in a non-selected HF population might allow health providers to plan the distribution of resources in patients with HF.

Quantification of coronary artery calcium (CAC) has been shown to be reliable, reproducible, and predictive of cardiovascular risk. Formal CAC scoring was introduced in 1990, with early scoring algorithms notable for their simplicity and elegance. Yet, with little evidence available on how to best build a score, and without a conceptual model guiding score development, these scores were, to a large degree, arbitrary. In this review, we describe the traditional approaches for clinical CAC scoring, noting their strengths, weaknesses, and limitations. We then discuss a conceptual model for developing an improved CAC score, reviewing the evidence supporting approaches most likely to lead to meaningful score improvement (for example, accounting for CAC density and regional distribution). After discussing the potential implementation of an improved score in clinical practice, we follow with a discussion of the future of CAC scoring, asking the central question: do we really need a new CAC score?

Background: Substantial differences exist between United States counties with regards to premature (<65 years of age) cardiovascular disease (CVD) mortality. Whether underlying social vulnerabilities of counties influence premature CVD mortality is uncertain. Methods: In this cross-sectional study (2014–2018), we linked county-level CDC/ATSDR SVI (Centers for Disease Control and Prevention/Agency for Toxic Substances and Disease Registry Social Vulnerability Index) data with county-level CDC WONDER (Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiological Research) mortality data. We calculated scores for overall SVI and its 4 subcomponents (ie, socioeconomic status; household composition and disability; minority status and language; and housing type and transportation) using 15 social attributes. Scores were presented as percentile rankings by county, further classified as quartiles on the basis of their distribution among all US counties (1st [least vulnerable] = 0 to 0.25; 4th [most vulnerable = 0.75 to 1.00]). We grouped age-adjusted mortality rates per 100 000 person-years for overall CVD and its subtypes (ischemic heart disease, stroke, hypertension, and heart failure) for nonelderly (<65 years of age) adults across SVI quartiles. Results: Overall, the age-adjusted CVD mortality rate per 100 000 person-years was 47.0 (ischemic heart disease, 28.3; stroke, 7.9; hypertension, 8.4; and heart failure, 2.4). The largest concentration of counties with more social vulnerabilities and CVD mortality were clustered across the southwestern and southeastern parts of the United States. The age-adjusted CVD mortality rates increased in a stepwise manner from 1st to 4th SVI quartiles. Counties in the 4th SVI quartile had significantly higher mortality for CVD (rate ratio, 1.84 [95% CI, 1.43–2.36]), ischemic heart disease (1.52 [1.09–2.13]), stroke (2.03 [1.12–3.70]), hypertension (2.71 [1.54–4.75]), and heart failure (3.38 [1.32–8.61]) than those in the 1st SVI quartile. The relative risks varied considerably by demographic characteristics. For example, among all ethnicities/races, non-Hispanic Black adults in the 4th SVI quartile versus the 1st SVI quartile exclusively had significantly higher relative risks of stroke (1.65 [1.07–2.54]) and heart failure (2.42 [1.29–4.55]) mortality. Rural counties with more social vulnerabilities had 2- to 5-fold higher mortality attributable to CVD and subtypes. Conclusions: In this analysis, US counties with more social vulnerabilities had higher premature CVD mortality, varied by demographic characteristics and rurality. Focused public health interventions should address the socioeconomic disparities faced by underserved communities to curb the growing burden of premature CVD.