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BACKGROUND: Digital health tools may improve quality of life (QoL) in patients with heart failure (HF) by promoting self-care, knowledge, and engagement. OBJECTIVES: This study evaluates the effect of 3 digital technologies on QoL in patients with HF. METHODS: A total of 182 patients were randomized to usual care or one of the technologies promoting self-care: Bodyport (cardiac scale), Conversa (conversational platform), or Noom (smartphone application). The primary outcome was 90-day change in QoL, as assessed by the Kansas City Cardiomyopathy Questionnaire (KCCQ) Overall Summary Score (OSS). RESULTS: A total of 151 participants (83%) completed their 90-day surveys. The median age of enrolled participants was 61 years (IQR: 53-69 years), and 37.9% were women. No group had any significant change in KCCQ OSS or improvement relative to usual care. However, symptoms and physical function at 90 days, as assessed by the Total Symptom Score (TSS) and Clinical Summary Score (CSS), were significantly improved in the Noom group relative to usual care: TSS median change of +4.2 points (IQR -1 to +16.7) vs -1 points (IQR: -13.5 to +7.8; P = 0.006); CSS median change of +2.8 points (IQR: -1 to +14.6) vs -3.1 points (IQR: -10.2 to +3; P = 0.002). CONCLUSIONS: Three digital interventions showed no independent effect on QoL as assessed by the KCCQ OSS. However, participants randomized to the Noom technology demonstrated improved KCCQ TSS and CSS relative to usual care. Although digital tools may be an important component of longitudinal care for patients with HF, larger studies are needed to better understand their effectiveness and optimal deployment. (Evaluating Efficacy of Digital Health Technology in the Treatment of Congestive Heart Failure; NCT04394754).
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Insuficiencia Cardíaca , Calidad de Vida , Humanos , Femenino , Persona de Mediana Edad , Anciano , Masculino , Insuficiencia Cardíaca/tratamiento farmacológico , Salud DigitalRESUMEN
BACKGROUND: Surveillance mammography is recommended for all women with a history of breast cancer. Risk-guided surveillance incorporating advanced imaging modalities based on individual risk of a second cancer could improve cancer detection. However, personalized surveillance may also amplify disparities. METHODS: In simulated populations using inputs from the Breast Cancer Surveillance Consortium (BCSC), we investigated race- and ethnicity-based disparities. Disparities were decomposed into those due to primary breast cancer and treatment characteristics, social determinants of health (SDOH) and differential error in second cancer ascertainment by modeling populations with or without variation across race and ethnicity in the distribution of these characteristics. We estimated effects of disparities on mammography performance and supplemental imaging recommendations stratified by race and ethnicity. RESULTS: In simulated cohorts based on 65,446 BCSC surveillance mammograms, when only cancer characteristics varied by race and ethnicity, mammograms for Black women had lower sensitivity compared with the overall population (64.1% vs. 71.1%). Differences between Black women and the overall population were larger when both cancer characteristics and SDOH varied by race and ethnicity (53.8% vs. 71.1%). Basing supplemental imaging recommendations on high predicted second cancer risk resulted in less frequent recommendations for Hispanic (6.7%) and Asian/Pacific Islander women (6.4%) compared with the overall population (10.0%). CONCLUSIONS: Variation in cancer characteristics and SDOH led to disparities in surveillance mammography performance and recommendations for supplemental imaging. IMPACT: Risk-guided surveillance imaging may exacerbate disparities. Decision-makers should consider implications for equity in cancer outcomes resulting from implementing risk-guided screening programs. See related In the Spotlight, p. 1479.
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Neoplasias de la Mama , Neoplasias Primarias Secundarias , Femenino , Humanos , Mamografía , Mama , Neoplasias de la Mama/diagnóstico por imagen , Neoplasias de la Mama/epidemiología , EtnicidadRESUMEN
Importance: Multiple sclerosis (MS) is an immune-mediated neurological disorder that affects nearly one million people in the United States. Up to 50% of patients with MS experience depression. Objective: To investigate how white matter network disruption is related to depression in MS. Design: Retrospective case-control study of participants who received research-quality 3-tesla neuroimaging as part of MS clinical care from 2010-2018. Analyses were performed from May 1 to September 30, 2022. Setting: Single-center academic medical specialty MS clinic. Participants: Participants with MS were identified via the electronic health record (EHR). All participants were diagnosed by an MS specialist and completed research-quality MRI at 3T. After excluding participants with poor image quality, 783 were included. Inclusion in the depression group (MS+Depression) required either: 1) ICD-10 depression diagnosis (F32-F34.*); 2) prescription of antidepressant medication; or 3) screening positive via Patient Health Questionnaire-2 (PHQ-2) or -9 (PHQ-9). Age- and sex-matched nondepressed comparators (MS-Depression) included persons with no depression diagnosis, no psychiatric medications, and were asymptomatic on PHQ-2/9. Exposure: Depression diagnosis. Main Outcomes and Measures: We first evaluated if lesions were preferentially located within the depression network compared to other brain regions. Next, we examined if MS+Depression patients had greater lesion burden, and if this was driven by lesions specifically in the depression network. Outcome measures were the burden of lesions (e.g., impacted fascicles) within a network and across the brain. Secondary measures included between-diagnosis lesion burden, stratified by brain network. Linear mixed-effects models were employed. Results: Three hundred-eighty participants met inclusion criteria, (232 MS+Depression: age[SD]=49[12], %females=86; 148 MS-Depression: age[SD]=47[13], %females=79). MS lesions preferentially affected fascicles within versus outside the depression network (ß=0.09, 95% CI=0.08-0.10, P<0.001). MS+Depression had more white matter lesion burden (ß=0.06, 95% CI=0.01-0.10, P=0.015); this was driven by lesions within the depression network (ß=0.02, 95% CI 0.003-0.040, P=0.020). Conclusions and Relevance: We provide new evidence supporting a relationship between white matter lesions and depression in MS. MS lesions disproportionately impacted fascicles in the depression network. MS+Depression had more disease than MS-Depression, which was driven by disease within the depression network. Future studies relating lesion location to personalized depression interventions are warranted.
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BACKGROUND: Multiple sclerosis (MS) is an immune-mediated neurological disorder, and up to 50% of patients experience depression. We investigated how white matter network disruption is related to depression in MS. METHODS: Using electronic health records, 380 participants with MS were identified. Depressed individuals (MS+Depression group; n = 232) included persons who had an ICD-10 depression diagnosis, had a prescription for antidepressant medication, or screened positive via Patient Health Questionnaire (PHQ)-2 or PHQ-9. Age- and sex-matched nondepressed individuals with MS (MS-Depression group; n = 148) included persons who had no prior depression diagnosis, had no psychiatric medication prescriptions, and were asymptomatic on PHQ-2 or PHQ-9. Research-quality 3T structural magnetic resonance imaging was obtained as part of routine care. We first evaluated whether lesions were preferentially located within the depression network compared with other brain regions. Next, we examined if MS+Depression patients had greater lesion burden and if this was driven by lesions in the depression network. Primary outcome measures were the burden of lesions (e.g., impacted fascicles) within a network and across the brain. RESULTS: MS lesions preferentially affected fascicles within versus outside the depression network (ß = 0.09, 95% CI = 0.08 to 0.10, p < .001). MS+Depression patients had more lesion burden (ß = 0.06, 95% CI = 0.01 to 0.10, p = .015); this was driven by lesions within the depression network (ß = 0.02, 95% CI = 0.003 to 0.040, p = .020). CONCLUSIONS: We demonstrated that lesion location and burden may contribute to depression comorbidity in MS. MS lesions disproportionately impacted fascicles in the depression network. MS+Depression patients had more disease than MS-Depression patients, which was driven by disease within the depression network. Future studies relating lesion location to personalized depression interventions are warranted.
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PURPOSE: To report the effects of photodynamic therapy using verteporfin in the treatment of patients with subfoveal idiopathic choroidal vascularization (CNV). DESIGN: Interventional case series. METHODS: In a retrospective study, eight eyes of eight consecutive patients aged 55 years or younger with subfoveal idiopathic CNV treated with photodynamic therapy using verteporfin were evaluated. Visual acuity was considered to be improved if the visual angle was halved, while acuity was thought to be worse if the visual angle doubled. RESULTS: The eight patients included three men and five women with a mean (+/- SD) age of 34.6 (+/- 9.7) years (range 25-53 years). The mean follow-up time was 13.5 months. At the end of the follow-up period the visual acuity improved in five eyes (62.5%), remained unchanged in one (12.5%), and decreased in two (25%). The mean acuity improvement was 3.6 lines of Snellen acuity by the end of the follow-up period, a change that was statistically significant (P =.027, Wilcoxon signed-rank test). No patient had any complication from the treatment. CONCLUSIONS: There is no widely accepted method for treating subfoveal idiopathic CNV and all previously investigated methods have had a significant number of serious side effects. Although the follow-up time and the number of patients in this pilot study were limited, the encouraging results and lack of complications suggest that further study is indicated.
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Neovascularización Coroidal/tratamiento farmacológico , Fotoquimioterapia , Fármacos Fotosensibilizantes/uso terapéutico , Porfirinas/uso terapéutico , Adulto , Neovascularización Coroidal/diagnóstico , Femenino , Angiografía con Fluoresceína , Estudios de Seguimiento , Fóvea Central , Humanos , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Resultado del Tratamiento , Verteporfina , Agudeza VisualRESUMEN
The cardiac fibroblast (CF) has historically been thought of as a quiescent cell of the heart, passively maintaining the extracellular environment for the cardiomyocytes (CM), the functional cardiac cell type. The increasingly appreciated role of the CF, however, extends well beyond matrix production, governing many aspects of cardiac function including cardiac electrophysiology and contractility. Importantly, its contributions to cardiac pathophysiology and pathologic remodeling have created a shift in the field's focus from the CM to the CF as a therapeutic target in the treatment of cardiac diseases. In response to cardiac injury, the CF undergoes a pathologic phenotypic transition into a myofibroblast, characterized by contractile smooth muscle proteins and upregulation of collagens, matrix proteins, and adhesion molecules. Further, the myofibroblast upregulates expression and secretion of a variety of pro-inflammatory, profibrotic mediators, including cytokines, chemokines, and growth factors. These mediators act in both an autocrine fashion to further activate CFs, as well as in a paracrine manner on both CMs and circulating inflammatory cells to induce myocyte dysfunction and chronic inflammation, respectively. Together, cell-specific cytokine-induced effects exacerbate pathologic remodeling and progression to HF. A better understanding of this dynamic intercellular communication will lead to novel targets for the attenuation of cardiac remodeling. Current strategies aimed at targeting cytokines have been largely unsuccessful in clinical trials, lending insights into ways that such intercellular cross talk can be more effectively attenuated. This review will summarize the current knowledge regarding CF functions in the heart and will discuss the regulation and signaling behind CF-mediated cytokine production and function. We will then highlight clinical trials that have exploited cytokine cross talk in the treatment of heart failure and provide novel strategies currently under investigation that may more effectively target pathologic CF-CM communication for the treatment of cardiac disease. This review explores novel mechanisms to directly attenuate heart failure progression through inhibition of signaling downstream of pro-inflammatory cytokines that are elevated after cardiac injury.