Food deserts (FD), low-income areas with low-access to healthful foods, are associated with higher burden of cardiovascular risk factors. Few studies have examined the impact of FD on clinical outcomes in heart failure (HF). FD status was assessed in 457 HF patients (mean age 55.9 ± 12.5 years; 50.3% Black) using the Food Desert Research Atlas. The Andersen-Gill extension of Cox model was used to examine the association of living in a FD with risk of repeat hospitalization (all-cause and HF-specific). Patients living in a FD were younger (P=0.01), more likely to be Black (P<0.0001), less educated (P=0.003), and less likely to have commercial insurance (P=0.003). During a median follow-up of 827 (506, 1379) days, death occurred in 60 (13.1%) subjects, and hospitalizations occurred in 262 (57.3%) subjects. There was no difference in the risk of death based on FD status. The overall frequency of all-cause (94.1 vs. 63.6 per 100 patient-years) and HF-specific (59.6 vs. 30.5 per 100 patient-years) hospitalizations was higher in subjects who lived in a FD. After adjustment for covariates, living in a FD was associated with an increased risk of repeat all-cause (hazard ratio [HR] 1.39, 95% confidence interval [Cl] 1.19-1.63; P=0.03) and HF-specific (HR 1.30, 95% Cl 1.02-1.65; P=0.03) hospitalizations. In conclusion, patients living in a FD have a higher risk of repeat all-cause and HF-specific hospitalization.

Background and objectivesMitochondrial DNA copy number is a biomarker of mitochondrial function, which has been hypothesized to contribute to pathogenesis of CKD through podocyte injury, tubular epithelial cell damage, and endothelial dysfunction. The prospective association of mitochondrial DNA copy number with CKD progression has not been previously evaluated.Design, setting, participants, & measurementsChronic Renal Insufficiency Cohort study participants had serum levels of mitochondrial DNA copy number calculated from probe intensities of mitochondrial single nucleotide polymorphisms genotyped on the Illumina HumanOmni 1-Quad Array. CKD progression was defined as kidney failure or halving of eGFR from baseline. Cox proportional hazards models were used to calculate hazard ratios for mitochondrial DNA copy number and risk of CKD progression.ResultsAmong 2943 participants, mean age was 58 years, 45% were women, and 48% self-identified as Black. There were 1077 patients who experienced CKD progression over a median follow-up of 6.5 years. The incidence rate of CKD progression was highest for those in the lowest tertile of mitochondrial DNA copy number (tertile 1, 58.1; tertile 2, 50.8; tertile 3, 46.3 per 1000 person-years). Risk for CKD progression was higher for participants with lower levels of mitochondrial DNA copy number after adjustment for established risk factors (for tertile 1 versus 3, hazard ratio, 1.28 [95% confidence interval, 1.10 to 1.50]; for tertile 2 versus 3, hazard ratio, 0.99 [95% confidence interval, 0.85 to 1.16]; trend P=0.002). Similar results were seen among those with albuminuria (for tertile 1 versus 3, hazard ratio, 1.24; 95% confidence interval, 1.05 to 1.47), but there were no statistically significant associations among individuals without albuminuria (for tertile 1 versus 3, hazard ratio, 1.04; 95% confidence interval, 0.70 to 1.53; interaction P<0.001).ConclusionsThese findings suggest lower mitochondrial DNA copy number is associated with higher risk of CKD progression, independent of established risk factors among patients with CKD.

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Burkitt’s Lymphoma is a highly malignant B-cell non-Hodgkin’s lymphoma that is extremely sensitive to intensified chemotherapy and its occurrence is closely associated with Epstein-Barr virus. Extranodal lymphoma often involves the gastrointestinal tract, but primary gastrointestinal lymphoma is rare, and primary gastric Burkitt’s Lymphoma is even rarer. We report a case of upper abdominal distension, eventually diagnosed as primary Burkitt’s Lymphoma of the stomach, including clinical manifestations, diagnosis and treatment. The patient showed favorable treatment response to intensified combination chemotherapy. We evaluate treatment response through endoscopy and radiological tests. This report suggested that primary gastric Burkitt’s Lymphoma is a rare yet treatable disease. The etiology and prognosis of Burkitt’s Lymphoma need to be explored in the future.

Background: Traditional cardiovascular disease (CVD) risk factors contribute to racial disparities in CVD mortality. However, there are scarce data on the role of social determinants in these disparities. Methods: A nationally representative sample of 50,808 individuals aged ≥20 years from NHANES 1999-2018 were included in the analysis. Data on social, behavioral, and metabolic factors were collected in each NHANES survey. CVD deaths were ascertained from linkage to the National Death Index with follow-up through 2019. Multiple mediation analysis was used to simultaneously investigate the contribution of each risk factor to racial differences in CVD mortality. Results: Over an average 9.4 years of follow-up, 2,589 CVD deaths were confirmed. Age- and sex-adjusted CVD mortality rates (95% CI) per 100,000 were 380.1 (334.0, 437.3) in White, 479.6 (393.3, 592.5) in Black, 288.2 (214.1, 397.8) in Hispanic, and 251.2 (140.9, 502.8) in other racial/ethnic populations. After adjusting for all risk factors in the table, individuals who were unemployed, had a low family income, did not own a home, were not married or living with a partner, were a current smoker, reported no leisure time physical activity, slept <6 hours or >8 hours per day, had obesity, hypertension, diabetes, or hypercholesterolemia, or had an albumin-to-creatinine ratio ≥30 mg/g or estimated glomerular filtration rate <60 ml/min/1.73 m 2 were at significantly higher risk for CVD mortality. After adjusting for the above risk factors, the hazard ratio (95% CI) for the Black-White difference in CVD mortality decreased from 1.54 (1.34, 1.77) to 0.86 (0.75, 1.00). Family income, not being married or living with a partner, not owning a home, and unemployment explained 24.8%, 20.8%, 14.5%, and 12.8% of Black-White differences in CVD mortality, respectively. Conclusion: Social determinants of health play an important role in racial disparities in CVD mortality. These findings call for public health interventions beyond lifestyle changes and medical treatment.

Background: Previous studies suggest that prevalence and associations of metabolic risk factors with cardiovascular disease (CVD) differ between women and men. However, few studies have investigated the simultaneous contributions of social, behavioral, and metabolic risk factors to CVD mortality for women and men in a US nationally representative sample. Results of this study could aid researchers, clinicians, and policymakers in developing precision strategies to reduce the burden of CVD. Hypothesis: Metabolic risk factors contribute to CVD mortality more in men than women, and social determinants of health (SDOH) and behavioral risk factors contribute to CVD mortality more in women than men. Methods: We included 50,808 participants aged ≥20 years from the National Health and Nutrition Examination Survey 1999-2018, linked to the National Death Index for cause-specific mortality follow-up through December 31, 2019. Social determinants of health and behavioral and metabolic risk factors were collected in each survey cycle. CVD mortality was ascertained by ICD-10 codes I00-I09, I11, I13, I20-I51, and I60-I69. We estimated the simultaneous impact of social, behavioral, and metabolic risk factors on CVD mortality in women and men using average population attributable fractions, which consider both the prevalence and strength of association of all risk factors in one model. Results: During a median 9.0-year follow-up, 2,589 CVD deaths were recorded (1,140 in women; 1,449 in men). Current smoking, hypertension, diabetes, and albuminuria contributed to CVD mortality significantly among both women and men. SDOH, behavioral and metabolic risk factors contributed 11.2%, 9.0%, and 30.2% to CVD mortality among women, but 9.6%, 7.4%, and 33.9% among men (Table). Conclusions: Social and behavioral risk factors have a larger role in population-level CVD mortality among women, while metabolic factors play a larger role in men. However, overall population attributable fractions of CVD mortality were similar in women and men.

Background: Food deserts (FD) are low-income areas with low access to healthful foods. Prior studies have shown that a diet rich in fruits, vegetables and dairy products substantially lowers homocysteine (Hcy) levels by supplementing folate, vitamin B 12 , B 6 and choline intake. Since Hcy is an independent risk factor for cardiovascular disease, and may be abnormal in subjects living in a FD, we examined the impact of living in a FD on serum Hcy levels and the risk of recurrent heart failure hospitalizations (HFH). Methods: FD status was assessed using the USDA FD Research Atlas in 173 HF patients (mean age 57 ± 12 yrs, 63% male, 38% black), prospectively enrolled in the Atlanta Cardiomyopathy Consortium from 2007 to 2011. Hcy values were log-transformed (log 2 Hcy) for analysis. Linear regression was used to determine the association of FD with log 2 Hcy, and Poisson regression to examine the association of FD with risk of repeat HFH. Models were adjusted for age, gender, race, HF etiology, NYHA class, smoking status, EF, DM, hyperlipidemia, mean arterial pressure, BMI and serum creatinine. Results: Patients who lived in a FD (n=29) were younger (p=0.08) and more likely to be black (p<0.001). After adjusting for covariates, FD status was associated with higher log 2 Hcy levels (adjusted β estimate: 0.32, 95% CI: 0.11- 0.52, p=0.003). During a median follow-up of 827 (IQR 506, 1379) days, 60 (34.7%) subjects had at least 1 HFH. The overall frequency of HFH (40.9 vs. 29.2 per 100 patient-years) was higher in patients who lived in a FD. In a fully adjusted model, for each unit increase in log 2 Hcy, there were 1.98 (adjusted, 95% CI: 1.38-2.82, p<0.001) times more HFH. Living in a FD was associated with 1.46 (adjusted, 95% CI: 1.1-1.94, p=0.009) times more HFH. Addition of log 2 Hcy to the Poisson model eliminated the association of FD with recurrent HFH (adjusted HR: 1.14, 95% CI: 0.74- 1.76, p=0.54). Conclusions: Living in a FD is associated with higher serum Hcy. These results provide insights into the mechanisms by which FD status influences the risk of recurrent HFH.