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1.
J Gen Intern Med ; 2023 Nov 08.
Artigo em Inglês | MEDLINE | ID: mdl-37940753

RESUMO

BACKGROUND: Rectal bleeding is the most common presenting symptom of colorectal cancer, and guidelines recommend timely follow-up, usually with colonoscopy to ensure timely diagnoses of colorectal cancer. OBJECTIVE: Identify loop closure rates and vulnerable process points for patients with rectal bleeding. DESIGN: Retrospective cohort study, using medical record review of patients aged ≥ 40 with index diagnosis of rectal bleeding at 2 primary practices-an urban academic practice and affiliated community health center, between January 1, 2018, and December 31, 2020. Patients were classified as having completed recommended follow-up workup ("closed loop") vs. not ("open loop"). Open loop patient cases were categorized into six types of process failures. PARTICIPANTS: A total of 837 patients had coded diagnoses of rectal bleeding within study window. Sixty-seven were excluded based on prior colectomy, clinical presentation more consistent with upper GI bleed, no rectal bleeding documented on chart review, or expired during the follow-up period, leaving 770 patients included. MAIN MEASURES: Primary outcomes were percentages of patient cases classified as "open loops" and distribution of these cases into six categories of process failure that were identified. KEY RESULTS: 22.3% of patients (N = 172) failed to undergo timely recommended workup for rectal bleeding. Largest failure categories were patients for whom no procedure was ordered (N = 62, 36%), followed by patients with procedures ordered but never scheduled (N = 44, 26%) or scheduled but subsequently cancelled or not kept (N = 31, 18%). While open loops increased after the onset of the COVID-19 pandemic, this difference was not significant within our study period. CONCLUSIONS: Significant numbers of patients presenting to primary care with rectal bleeding fail to undergo recommended workup. The majority either have no procedure ordered, or procedure ordered but never scheduled or cancelled and not kept, suggesting these are important failure modes to target in future interventions. Ensuring reliable ordering and processes for timely scheduling and completion of procedures represent critical areas for improving the diagnostic process for patients with rectal bleeding in primary care.

2.
World J Cardiol ; 9(5): 396-406, 2017 May 26.
Artigo em Inglês | MEDLINE | ID: mdl-28603586

RESUMO

Numerous health behaviors, including physical activity, diet, smoking, and sleep, play a major role in preventing the development and progression of cardiovascular disease (CVD). Among these behaviors, sleep may play a pivotal role, yet it has been studied somewhat less than other behaviors and there have been few well-designed sleep intervention studies targeting CVD. Furthermore, despite the fact that these behaviors are often interrelated, interventions tend to focus on changing one health behavior rather than concurrently intervening on multiple behaviors. Psychological constructs from depression to positive affect may also have a major effect on these health behaviors and ultimately on CVD. In this review, we summarize the existing literature on the impact of sleep and other cardiac health behaviors on CVD onset and prognosis. We also describe interventions that may promote these behaviors, from established interventions such as motivational interviewing and cognitive behavioral therapy, to more novel approaches focused on mindfulness and other positive psychological constructs. Finally, we outline population-health-level care management approaches for patients with psychiatric conditions (e.g., depression) that may impact cardiac health, and discuss their potential utility in improving mental health, promoting health behaviors, and reducing CVD-related risk. Much work is still needed to better understand how sleep and other health behaviors may uniquely contribute to CVD risk, and additional high-quality studies of interventions designed to modify cardiac health behaviors are required to improve cardiovascular health in individuals and the population at large.

3.
Arterioscler Thromb Vasc Biol ; 32(12): 2855-61, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-23042815

RESUMO

OBJECTIVE: Inhibitor of differention-3 (Id3) promotes B cells homing to the aorta and atheroprotection in Apoe(-/-) mice. We sought to determine the impact of loss of Id3 in the Ldlr((-/-)) mouse model of diet-induced atherosclerosis and identify novel Id3 targets in the vessel wall. METHODS AND RESULTS: Ex vivo optical imaging confirmed that Id3((-/-)) Ldlr((-/-)) mice have significantly fewer aortic B cells than Id3((+/+)) Ldlr(-/-) mice. After 8 and 16 weeks of Western diet, Id3((-/-)) Ldlr((-/-)) mice developed significantly more atherosclerosis than Id3((+/+)) Ldlr((-/-)) mice, with Id3(+/-) Ldlr(-/-) mice demonstrating an intermediate phenotype. There were no differences in serum lipid levels between genotypes. Immunostaining demonstrated that aortas from Id3((-/-)) Ldlr((-/-)) mice had greater intimal macrophage density and C-C chemokine ligand 20 and vascular cell adhesion molecule 1 (VCAM-1) expression compared with Id3((+/+)) Ldlr(-/-) mice. Real-time polymerase chain reaction demonstrated increased VCAM-1 mRNA levels in the aortas of Id3(-/-) Ldlr(-/-) mice. Primary vascular smooth muscle cells from Id3((-/-)) mice expressed greater amounts of VCAM-1 protein compared with control. Gain and loss of function studies in primary vascular smooth muscle cells identified a role for Id3 in repressing VCAM-1 promoter activation. Chromatin immunoprecipitation demonstrated interaction of E12 with the VCAM-1 promoter, which is inhibited by Id3. CONCLUSIONS: Id3 is an atheroprotective transcription regulator with targets in both B cells and vessel wall cells leading to reduced macrophage accumulation and reduced atherosclerosis formation.


Assuntos
Aterosclerose/fisiopatologia , Movimento Celular/fisiologia , Proliferação de Células , Proteínas Inibidoras de Diferenciação/deficiência , Macrófagos/patologia , Receptores de LDL/deficiência , Molécula 1 de Adesão de Célula Vascular/metabolismo , Animais , Aorta/metabolismo , Aorta/patologia , Aterosclerose/epidemiologia , Aterosclerose/metabolismo , Aterosclerose/patologia , Linfócitos B/metabolismo , Linfócitos B/patologia , Quimiocina CCL20/metabolismo , Modelos Animais de Doenças , Proteínas Inibidoras de Diferenciação/genética , Proteínas Inibidoras de Diferenciação/metabolismo , Macrófagos/metabolismo , Camundongos , Camundongos Knockout , Prevalência , Receptores de LDL/genética , Receptores de LDL/metabolismo , Fatores de Risco
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