BackgroundFew qualitative studies have explored factors influencing medication adherence among people with coronary heart disease (CHD) or CHD risk factors. We explored how factors related to the patient (e.g. self-efficacy), social/economic conditions (e.g. social support and cost of medications), therapy (e.g. side effects), health condition (e.g. comorbidities), and the healthcare system/healthcare team (e.g. support from healthcare providers and pharmacy access) influence medication adherence, based on the World Health Organization Multidimensional Adherence Model (WHO-MAM).MethodsWe conducted 18 in-depth qualitative interviews from April to July 2018 with ambulatory care patients aged ≥45 years (8 black men, 5 black women, 2 white men, and 3 white women) who were using medications for diabetes, hypertension, dyslipidemia and/or CHD. We used thematic analysis to analyze the data, and sub-themes emerged within each WHO-MAM dimension.FindingsPatient-related factors included beliefs about medications as important for self and faith; the desire to follow the advice of family, friends, and influential others; and self-efficacy. Social/economic factors included observations of social network members and information received from them; social support for medication adherence and pharmacy utilization; and economic influences. Therapy-related barriers included side effects and medicine schedules. Only a few participants mentioned condition-related factors. Healthcare system/healthcare team-related factors included support from doctors and pharmacists; and ease of pharmacy access and utilization.ConclusionThese results underscore the need for multidimensional interventions aimed at improving medication adherence and overall health of patients with CHD and CHD risk factors.
Aims We sought to compare the generalizability and prognostic implications of heart failure with preserved ejection fraction (HFpEF) scores (HFA-PEFF and H 2 FPEF score) in Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist (TOPCAT) and Phosphodiesterase-5 Inhibition to Improve Clinical Status and Exercise Capacity in Heart Failure with Preserved Ejection Fraction (RELAX) trial participants and matched controls from the Atherosclerosis Risk in Community (ARIC) study. Methods and results Based on the respective scores, the study participants from the TOPCAT (N = 356), RELAX (N = 216), and ARIC (N = 379) studies were categorized as having a low, intermediate, or high likelihood of HFpEF. Age, sex, and race matched controls free of cardiovascular disease who had unexplained dyspnoea were used to evaluate the diagnostic performance. The prognostic value of scores was assessed using multivariable-adjusted Cox regression analyses. The median HFA-PEFF scores in the TOPCAT, RELAX, and ARIC studies were 5.0 [interquartile range (IQR): 5.0-6.0], 4.0 (IQR: 2.0-4.0), and 3.0 (IQR: 2.0-4.0), respectively. The median H 2 FPEF scores in the three studies were 5.5 (IQR: 4.0-7.0), 6.0 (IQR: 4.0-7.0), and 3.0 (IQR: 2.0-5.0), respectively. A low HFA-PEFF and H 2 FPEF score can rule out HFpEF with high sensitivity (99.5% and 99.6%, respectively) and negative predictive value (95.7% and 98.3%, respectively). A high HFA-PEFF and H 2 FPEF score can rule-in HFpEF with good specificity (82.8% and 95.6%, respectively) and positive predictive value (79.9% and 90.4%, respectively). Among TOPCAT participants, the hazard for adverse cardiovascular events per point increase in HFA-PEFF and H 2 FPEF score was 1.26 (95% confidence interval: 0.98-1.63) and 1.01 (95% confidence interval: 0.88-1.15), respectively. A higher H 2 FPEF score was associated with lower peak oxygen intake in RELAX trial participants (adjusted P = 0.01). Conclusions The HFA-PEFF and the H 2 FPEF scores are reliable diagnostic tools for HFpEF. The prognostic utility of HFpEF scores requires further validation in larger rigorously phenotyped populations.
Key PointsQuestionsWhat is the association between amyloidogenic TTR gene variation (Val122Ile) and the risk of heart failure?FindingsIn this retrospective cohort study that included 7514 Black participants in the US with a median 11.1 years of follow-up, the incidence of heart failure was 15.6 per 1000 person-years among Val122Ile variant carriers compared with 7.2 per 1000 person-years among noncarriers, with an adjusted hazard ratio of 2.43.MeaningBeing a carrier of the Val122Ile variant was significantly associated with an increased risk of heart failure among Black individuals living in the US.
Objective To evaluate the race-stratified state-level prevalence of health determinants and the racial disparities in coronavirus disease-2019 (COVID-19) cumulative incidence and mortality in the United States. Patients and Methods Age-adjusted race-stratified prevalence of comorbidities (hypertension, diabetes, dyslipidemia, obesity), preexisting medical conditions (pulmonary disease, heart disease, stroke, kidney disease, malignancy), poor health behaviors (smoking, alcohol abuse, physical inactivity), and adverse socioeconomic factors (education, household income, health insurance) was computed in 435,139 American adult participants from 2017 Behavioral Risk Factor Surveillance System survey (BRFSS). Correlation was assessed between health determinants and the race-stratified COVID-19 crude mortality and infection-fatality-ratio computed from respective state public health departments in 47 states. Results Blacks had a higher prevalence of comorbidities (63.3% [95%CI:62.4-64.2%] vs. 55.1% [95%CI:54.7-55.5]) and adverse socioeconomic factors (47.0% [95%CI:46.0-47.9%] vs. 30.9% [95%CI:30.6-31.3]) than Whites. The prevalence of preexisting medical conditions was similar among Blacks (30.4% [95%CI:28.8-32.1%]) and Whites (30.8% [95%CI:30.2-31.4%]). The prevalence of poor health behaviors was higher in Whites (57.2% [95%CI:56.3-58.0%]) than Blacks (50.2% [95%CI:46.2-54.2%]). The comorbidities and adverse socioeconomic factors were highest in the Southern region, and poor health behaviors were highest in the Western region. Cumulative incidence rate (per 100,000 persons) was three-fold higher in Blacks (1546.4) compared withwith Whites (540.4). The crude mortality (per 100,000 persons) was two-fold higher in Blacks (83.2) than Whites (33.2). However, the infection-fatality-ratio (per 100-cases) was similar between Whites (6.2) and Blacks (5.4). Within racial groups, the geographic distribution of health determinants did not correlate with state-level COVID-19 mortality and infection-fatality ratio (p>0.05 for all). Conclusions Racial disparities in COVID-19 are largely driven by the higher cumulative incidence of infection in Blacks. There is a discordance between the geographic dispersion of COVID-19 mortality and the regional distribution of health determinants.
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