Last data update: May 13, 2024. (Total: 46773 publications since 2009)
Records 1-3 (of 3 Records) |
Query Trace: Sells M[original query] |
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Excess burden of poverty and hypertension, by race and ethnicity, on the prevalence of cardiovascular disease
Sells ML , Blum E , Perry GS , Eke P , Presley-Cantrell L . Prev Chronic Dis 2023 20 E109 INTRODUCTION: Cardiovascular disease (CVD) is the leading cause of death in the United States. Certain demographic characteristics are associated with disparities in CVD and its risk factors, which may interact with specific social determinants of health (SDOH). We examined the association of a single SDOH (ie, poverty level) with diagnosed CVD morbidity and the joint influence of poverty and hypertension on the prevalence of CVD morbidity among non-Hispanic Black, non-Hispanic White, and Hispanic people aged 30 years or older. METHODS: We used data from the National Health and Nutrition Examination Survey collected during 1999 to 2018. We assessed the prevalence of diagnosed CVD morbidity (eg, self-reported coronary heart disease, angina, myocardial infarction, or stroke) by using a Poisson family with a log link regression model. We calculated the additive interaction of poverty level with hypertension on diagnosed CVD morbidity for each race and ethnicity. RESULTS: We found excess CVD morbidity among non-Hispanic Black and Hispanic people experiencing poverty and diagnosed with hypertension compared with their non-Hispanic White counterparts. Multivariate analysis found a higher prevalence of CVD among participants of all races and ethnicities who were experiencing poverty and among non-Hispanic White people who had less than a college education. In addition, age, hypertension, poverty, smoking, and weight were significant predictors of the prevalence of CVD morbidity among all racial and ethnic groups. CONCLUSION: Changes to interventions, policies, and research may be needed to address the effect of key indicators of health disparities and specific SDOH, such as poverty level, that intersect with hypertension and contribute to excess CVD morbidity among people of some racial and ethnic groups, particularly non-Hispanic Black and Hispanic populations. |
A public health framework to improve population health through health care and community clinical linkages: The ASTHO/CDC Heart Disease and Stroke Prevention Learning Collaborative
Felipe RA , Plescia M , Peterman E , Tomlin H , Sells M , Easley C , Ahmed K , Presley-Cantrell L . Prev Chronic Dis 2019 16 E124 Thirty-one state and territorial public health agencies participated in a learning collaborative to improve diagnosis and management of hypertension in clinical and community settings. These health agencies implemented public health and clinical interventions in medical settings and health organizations using a logic model and rapid quality improvement process focused on a framework of 4 systems-change levers: 1) data-driven action, 2) clinical practice standardization, 3) clinical-community linkages, and 4) financing and policy. We provide examples of how public health agencies applied the systems-change framework in all 4 areas to assess and modify population-based interventions to improve control of hypertension. This learning collaborative approach illustrates the importance of public health in the prevention and control of chronic disease by supporting interventions that address community and clinical linkages to address medical risk factors associated with cardiovascular disease. |
Persistence of endothelial thrombomodulin in a patient with infectious purpura fulminans treated with protein C concentrate
Bendapudi PK , Robbins A , LeBoeuf N , Pozdnyakova O , Bhatt A , Duke F , Sells R , McQuiston J , Humrighouse B , Rouaisnel B , Colling M , Stephenson KE , Saavedra A , Losman JA . Blood Adv 2018 2 (21) 2917-2921 Purpura fulminans (PF) is a rare life-threatening complication of bacterial sepsis that is characterized by a highly thrombotic subtype of disseminated intravascular coagulation (DIC) and mortality of up to 80%.1 Patients with PF develop a severe deficiency in protein C (PC), a serine protease that is a key endogenous anticoagulant.2 PC is activated at the endothelial surface by thrombin in the presence of the cofactor thrombomodulin (TM). Activated PC (APC) is cytoprotective3 and inhibits thrombin generation by cleaving coagulation factors Va and VIIIa.4 Therefore, TM is a crucial regulatory “switch” governing negative feedback of coagulation. The initiating event in PF is hypothesized to be loss of TM from the endothelial surface in response to infection.5 As a result, conversion of PC to APC is impaired, and coagulation proceeds unchecked.3 Although therapy with PC concentrate has been proposed as a strategy to target the underlying pathophysiologic lesion in PF,6 the belief that endothelial TM loss is an early event in PF that renders infused PC ineffective has limited its widespread adoption.2,5 We report herein data on the kinetics of TM loss in a patient with PF that support the use of supplemental PC in upfront treatment of severe cases. |
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