Review Article Transforming clinical documentation with ambient artificial intelligence (AI) scribes: a narrative review of technology, impact, and implementation Mahshad Razaghi, Abdelrahman Hafez, Juan M. Farina, Isabel G. Scalia, Milagros Pereyra, Fatmaelzahraa E. Abdelfattah, Hesham Sheashaa, Kamal Awad, Steven J. Lester, Chadi Ayoub, Reza Arsanjani

Crohn's disease (CD) is a chronic disorder that often starts at a young age and involves periods of remission and relapse. Prompt diagnosis of relapses through screening is crucial due to the potential morbid complications of untreated active inflammation. Magnetic resonance enterography (MRE) is a noninvasive technique to screen for active inflammation. The standard protocol involves intravenous injection of contrast agents with potential side effects. Some abbreviated non-contrast-enhanced MRE protocols are proposed as alternatives for conventional MRE to identify active inflammation. Currently, there is controversy regarding the applicability and accuracy of these protocols. This study aims to describe and compare these protocols and evaluate their accuracy in detecting active inflammation and CD complications. Results from a systematic search of three databases in August 2022 were queried and screened by abstract and full text. Eligible studies were qualitatively and quantitatively analyzed by diagnostic test accuracy meta-analysis. 59 studies entered the systematic review, and 37 were eligible for meta-analysis. Diffusion-weighted imaging (DWI) and fast T2-weighted (T2w) sequences were most frequently used in abbreviated protocols and showed non-inferior accuracy compared to the full protocol in detecting active inflammation. ADC and qualitative DWI had pooled sensitivity of 90% (CI: 82–95%) and 89% (CI:82–93%) and pooled specificity of 94% (CI: 88–97%) and 89% (CI: 79–94%), respectively for detecting active inflammation. Moreover, T2w and combined T2w+DWI sequences had pooled sensitivity of 80% (CI: 64–90%) and 76% (CI: 61–86%) and pooled specificity of 90% (CI: 80–95%) and 87% (CI: 74 – 94%), respectively. Unenhanced protocols show relatively poor diagnostic accuracy in detecting penetrating complications of CD. Magnetization transfer imaging (MTI) has demonstrated excellent accuracy in detecting fibrosis. High heterogeneity was observed in all subgroups, and accuracy was reported to be highly operator dependent in most studies. An abbreviated protocol consisting of DWI and fast T2w imaging can potentially replace the full protocol MRE. Full protocol MRE will still have its role in identifying penetrating complications. MTI should be indicated in case of suspected fibrostenotic disease.

Coronary microvascular dysfunction (CMD) has emerged as a crucial contributor to cardiovascular morbidity and mortality, particularly in patients with ischemia and non-obstructive coronary arteries (INOCA). The condition arises from a complex interplay of structural and functional abnormalities within the small coronary vessels, driven by underlying molecular mechanisms including endothelial nitric oxide synthase (eNOS) uncoupling, oxidative stress, and chronic inflammation. Lipid metabolism plays a central role in this pathology, especially in the setting of elevated low-density lipoprotein cholesterol (LDL-C). Furthermore, the protective capacity of high-density lipoprotein (HDL) is increasingly understood to depend on its functionality rather than absolute levels, as it can become dysfunctional and pro-inflammatory in pathological states. Emerging evidence has identified lipoprotein(a) [Lp(a)] and triglyceride-rich lipoproteins as significant, independent contributors to microvascular injury. Comprehensive clinical assessment of microvascular dysfunction therefore requires integration of advanced lipid profiling, including apolipoprotein B (ApoB), [Lp(a)], and the triglyceride-glucose (TyG) index with invasive and non-invasive measures of coronary flow reserve to more precisely stratify risk. In this narrative review, we synthesize current observational, mechanistic, and early interventional data linking diverse lipid phenotypes to coronary microvascular dysfunction. We propose a concept of lipid-driven CMD endotypes, such as ApoB-/particle overload, dysfunctional HDL, Lp(a)-mediated risk, and metabolic/TyG-high states, and map these to a practical, mechanism-informed management framework. While intensive LDL-C lowering with high-intensity statins and combination therapy remains guideline-directed care for high-risk patients, evidence for dedicated microvascular benefit from newer lipid and cardiometabolic agents is still largely hypothesis-generating. A personalized approach that aligns lipid phenotyping, CMD endotyping, and existing guideline-based therapies may help refine risk assessment and inform future trials.

Aims: The aims of this study were to evaluate the association between the red cell distribution width (RDW)–albumin ratio (RAR) and subclinical myocardial impairment, as assessed by left ventricular global longitudinal strain (LVGLS), and to examine the relationships between the RAR, heart failure (HF) hospitalization, and all-cause mortality. Methods: We conducted a retrospective cohort study on adults who underwent transthoracic echocardiography (TTE) with LVGLS assessment across three Mayo Clinic centers (2017–2024) and who had RDW and serum albumin measured on the same day or within seven days. The RAR was calculated as RDW/albumin and categorized into the following tertiles: 3.48. Impaired LVGLS was defined as >−18%. Associations between the RAR and outcomes were assessed using multivariable logistic regression (LVGLS) and Cox models (HF and mortality), adjusting for demographics and comorbidities. Results: Among 5069 patients, 39.7% had impaired LVGLS, and its prevalence increased across RAR tertiles (26.8%, 41.9%, and 51.1%). Adjusted odds ratios for impaired LVGLS were 1.74 and 2.30 for tertiles 2 and 3, respectively. A higher RAR was associated with increased risk of HF hospitalization (aHR 2.54 and 4.48) and all-cause mortality (aHR 2.39 and 7.30). These associations persisted after adjusting for LVGLS. The effect of the RAR on mortality was stronger in patients with normal LVGLS compared to those with impaired LVGLS (p for interaction = 0.0004). Conclusions: A higher RAR was associated with abnormal LVGLS, HF hospitalization, and all-cause mortality after adjustment for clinical risk factors. However, the RAR did not provide discriminative value beyond its individual components.