Citations

This executive summary highlights evidence-based recommendations for using lifestyle interventions in the treatment and remission of type 2 diabetes (T2D) and prediabetes in adults. The summary and guideline are intended for any clinician or healthcare professional in a community or non-inpatient healthcare setting involved in managing non-pregnant adults with T2D, prediabetes or a history of gestational diabetes mellitus (GDM). The purpose of this executive summary is to provide a succinct overview of the key action statements (recommendations) from Lifestyle Interventions for Treatment and Remission of Type 2 Diabetes and Prediabetes in Adults: A Clinical Practice Guideline from the American College of Lifestyle Medicine. This is the first diabetes guideline to emphasize lifestyle interventions as the foundation of management and is also the first to focus on all six pillars of lifestyle medicine (plant-predomination nutrition, regular physical activity, restorative sleep, stress reduction, social connectedness, and avoiding risky substances), including behavior change strategies. This summary is not intended to substitute for the full guideline, which should be read before taking the recommended actions. The guideline on which this summary is based was developed with a priori methodology that has been previously published, refined, and used in over 20 multidisciplinary, trustworthy, and evidence-based national guidelines. The guideline development group included 20 members representing consumers, advanced practice nursing, cardiology, clinical pharmacology, behavioral medicine, endocrinology, family medicine, lifestyle medicine, nutrition and dietetics, health education, health and wellness coaching, sleep medicine, sports medicine, and obesity medicine. We developed 14 key action statements and associated evidence profiles, each with a distinct quality improvement goal in the context of lifestyle interventions for T2D. Strong recommendations were made regarding advocacy for lifestyle interventions; assessing baseline lifestyle habits; establishing priorities for lifestyle change; prescribing aerobic and muscle strength physical activity; reducing sedentary time; identifying sleep disorders; prescribing nutrition plans for prevention and treatment; promoting peer/familial support and social connections; counseling regarding tobacco, alcohol, and recreational drugs, and establishing a plan for continuity of care. Recommendations were made regarding identifying the need for psychological interventions and for adjusting (deprescribing) pharmacologic therapy. We include numerous tables and figures to facilitate implementation, a plain-language summary for consumers, and an executive summary for clinicians as separate publications. Although not a substitute for the full clinical practice guideline, this executive summary can provide insight into the key guideline recommendations, to whom they apply, and to how they might alter care. These recommendations offer detailed, explicit, and evidence-based strategies for successful lifestyle behavior change, making them relevant not only to our guideline but to other guidelines and standards that advocate for lifestyle change in managing adults with T2D.

Cerebrospinal fluid venous fistulas (CSFVF) can lead to spontaneous intracranial hypotension, causing debilitating symptoms in patients. The transvenous embolization technique has been developed to occlude leakage sites via an endovascular approach. However, the spinal venous anatomy remains relatively unfamiliar to many neurointerventionalists. This technical video presents a swine model designed to train physicians in navigating the spinal venous system, performing embolization injections, observing their spread, and testing new embolization systems for treating CSFVF. Although there are slight anatomical differences, the spinal venous system in swine closely resembles that of humans, including its navigability and employing liquid embolic agents. We successfully embolized multilevel spinal vasculature that can potentially drain into a fistula formation, without any complications.

Prosthetic heart valve (PHV) dysfunction is increasingly seen due to the increase in the number of PHV that are being implanted worldwide. Cardiac CT imaging has emerged as a valuable tool to assess PHVs and determine the cause of dysfunction. This consensus document first summarizes the available techniques for PHV assessment. Then the use of CT in PHV (dys)function assessment is discussed in detail including consensus statements for correct indications and patient selection for CT assessment of PHVs, image acquisition, reconstruction and measurement protocols and how to interpret and report the CT findings for specific types of PHV dysfunction. This article was published in Journal of Cardiovascular Computed Tomography, Budde RPJ et al, Cardiac computed tomography for prosthetic heart valve assessment: An expert consensus document of the Society of Cardiovascular Computed Tomography (SCCT), the American College of Cardiology (ACC), the European Society of Cardiovascular Radiology (ESCR), the North American Society for Cardiovascular Imaging (NASCI), the Radiological Society of North America (RSNA), the Society for Cardiovascular Angiography & Interventions (SCAI), and the Society of Thoracic Surgeons (STS). The articles are identical except for minor stylistic and spelling differences in keeping with each journal’s style. Either citation may be used when referencing this document. © 2025 Society of Cardiovascular Computed Tomography. Published by Elsevier Inc. on behalf of the Society of Cardiovascular Computed Tomography. This is an open access article under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ). Keywords: Computed Tomography, Valve, Cardiac, Imaging, Dysfunction, Prosthetic

Abstract Purpose Clozapine is primarily metabolized by cytochrome P450 (CYP) 1A2 and to a lesser extent by CYP2C19, CYP2D6, and CYP3A4. The global pandemic of coronavirus disease 2019 (COVID-19) and use of nirmatrelvir/ritonavir brought forth new challenges for those caring for patients prescribed clozapine. Prescribing information describes a consideration for a clozapine dose reduction while monitoring for adverse reactions when clozapine is used with nirmatrelvir/ritonavir. Other drug information resources consider the combination a contraindication. A case is reported in which therapeutic drug monitoring demonstrated a lack of interaction between clozapine and nirmatrelvir/ritonavir. The complexities of infection-associated clozapine toxicity are discussed and a review is provided of CYP3A4 drug and gene interactions with clozapine. Summary A 75-year-old woman with schizophrenia, prescribed clozapine 200 mg by mouth at bedtime, was initiated on nirmatrelvir/ritonavir after developing a mild COVID-19 infection. Two days later, the patient was brought to the emergency department after an unwitnessed fall. Clozapine toxicity was included in the differential diagnosis, although no other signs or symptoms of elevated clozapine levels were present. Nirmatrelvir/ritonavir was discontinued. Clozapine was withheld for 1 day while a clozapine level was pending, but this measurement revealed no interaction when compared to a baseline level of clozapine. Conclusion Although there are hypothetical concerns when initiating a CYP3A4 inhibitor with concomitant clozapine, the information derived from this case does not clearly support an interaction with the addition of nirmatrelvir/ritonavir during mild COVID-19 infection. It is important to understand the risks of withholding clozapine, although fortunately no psychiatric concerns developed. In reviewing the literature, CYP3A4 inhibitors or genetic polymorphisms seem to have a minimal impact on clozapine levels, although clinical monitoring is warranted.

Importance Tau positron emission tomography (PET) allows in vivo detection of neurofibrillary tangles, a core neuropathologic feature of Alzheimer disease (AD). Objective To provide estimates of the frequency of tau PET positivity and its associated risk of clinical outcomes. Design, Setting, and Participants Longitudinal study using data pooled from 21 cohorts, comprising a convenience sample of 6514 participants from 13 countries, collected between January 2013 and June 2024. Cognitively unimpaired individuals and patients with a clinical diagnosis of mild cognitive impairment (MCI), AD dementia, or other neurodegenerative disorders were included. Exposures Tau PET with flortaucipir F 18, amyloid-β (Aβ) PET, and clinical examinations. Tau PET scans were visually rated as positive according to a US Food and Drug Administration– and European Medicines Agency–approved method, designed to indicate the presence of advanced neurofibrillary tangle pathology (Braak stages V-VI). Main Outcomes and Measures Frequency of tau PET positivity and absolute risk of clinical progression (eg, progression to MCI or dementia). Results Among the 6514 participants (mean age, 69.5 years; 50.5% female), median follow-up time ranged from 1.5 to 4.0 years. Of 3487 cognitively unimpaired participants, 349 (9.8%) were tau PET positive; the estimated frequency of tau PET positivity was less than 1% in those aged younger than 50 years, and increased from 3% (95% CI, 2%-4%) at 60 years to 19% (95% CI, 16%-24%) at 90 years. Tau PET positivity frequency estimates increased across MCI and AD dementia clinical diagnoses (43% [95% CI, 41%-46%] and 79% [95% CI, 77%-82%] at 75 years, respectively). Most tau PET–positive individuals (92%) were also Aβ PET positive. Cognitively unimpaired participants who were positive for both Aβ PET and tau PET had a higher absolute risk of progression to MCI or dementia over the following 5 years (57% [95% CI, 45%-71%]) compared with both Aβ PET–positive/tau PET–negative (17% [95% CI, 13%-22%]) and Aβ PET–negative/tau PET–negative (6% [95% CI, 5%-8%]) individuals. Among participants with MCI at the time of the tau PET scan, an Aβ PET–positive/tau PET–positive profile was associated with a 5-year absolute risk of progression to dementia of 70% (95% CI, 59%-81%). Conclusions and Relevance In a large convenience sample, a positive tau PET scan occurred at a nonnegligible rate among cognitively unimpaired individuals, and the combination of Aβ PET positivity and tau PET positivity was associated with a high risk of clinical progression in both preclinical and symptomatic stages of AD. These findings underscore the potential of tau PET as a biomarker for staging AD pathology.

This international multicenter study seeks to determine the frequency and characteristics of meningitis in myelin oligodendrocyte glycoprotein antibody (MOGAD)–associated disease and highlight its pathology.