VanDolah, Hunter

Abstract Aims Nutritional counselling is a core component of cardiac rehabilitation (CR), yet the evidence base for specific dietary interventions within CR remains fragmented. This scoping review aimed to map the range of nutritional interventions evaluated in adult CR programmes, characterize their reported outcomes, and identify key gaps in current evidence and practice. Methods and results Following the Arksey and O’Malley framework and reporting according to PRISMA-ScR, a systematic search of PubMed, Embase, Web of Science, and Cochrane Library was conducted from inception to June 2026. Eligible studies included randomized controlled trials, non-randomized trials, and observational studies evaluating an explicitly described nutritional intervention within a structured CR programme in adults with established cardiovascular disease. Of 2765 identified records, 35 studies met eligibility criteria. Interventions spanned Mediterranean and heart-healthy dietary patterns, calorie-restriction and weight-loss programmes, comprehensive lifestyle interventions, structured nutrition education and counselling, supplementation, functional foods, and individualized diet prescriptions. Across categories, improvements in body weight, central adiposity, and adherence to cardioprotective dietary recommendations were commonly reported, particularly when nutrition was delivered with repeated contact and individualized support. Effects on lipid profiles, inflammatory markers, blood pressure, functional capacity, and clinical outcomes were more variable. Conclusion Nutritional interventions within CR were most consistently associated with improvements in intermediate behavioural, anthropometric, and cardiometabolic outcomes, particularly when structured and reinforced over time. However, heterogeneity in study design, intervention delivery, comparator groups, outcome reporting, and follow-up duration precludes definitive conclusions about comparative efficacy, optimal intervention format, or the magnitude of benefit. Greater standardization, longer follow-up, and further evaluation of personalized nutritional strategies are needed to strengthen the nutritional component of CR.

Abstract Background Legionella pneumonia is an important cause of severe pneumonia, yet contemporary data describing its clinical phenotype, diagnostic patterns, and outcomes in the modern era are limited. Methods We conducted a retrospective multicenter cohort study of adults with laboratory-confirmed Legionella pneumonia across an integrated health system between January 2019 and September 2025. The primary outcome was 30-day mortality. Severe disease was defined as having a requirement for high-flow nasal cannula, noninvasive ventilation, mechanical ventilation, or extracorporeal membrane oxygenation (ECMO). Univariate and multivariable logistic regression were used to identify predictors of mortality and severe disease. Results There were 344 patients with laboratory-confirmed Legionella pneumonia during the study period. The median age was 66.6 years, and 45.1% were immunocompromised. Most patients required hospital admission (94.2%), with 36.1% admitted to the intensive care unit; 22.7% required mechanical ventilation and 1.5% ECMO. Thirty- and 90-day mortality were 11.9% and 16.6%, respectively. In multivariable analysis, cirrhosis (OR 10.2, 95% CI 2.15–48.3, P = .003), immunocompromised status (odds ratio [OR] 2.24, 95% CI 1.05–4.77, P = .036), age (OR 1.03, 95% CI 1.00–1.06, P = .031), and lymphopenia at presentation (OR 2.09, 95% CI 1.02–4.24, P = .043) were independently associated with increased 30-day mortality. Among patients who were polymerase chain reaction (PCR) or culture positive, urinary antigen testing was positive in only 25.6%. Conclusions Legionella pneumonia was associated with substantial short-term mortality. Cirrhosis, age, immunocompromised status, and lymphopenia at presentation emerged as independent predictors of 30-day mortality, underscoring the importance of host vulnerability in determining outcomes.

Thoracic aortic aneurysm and dissection (TAAD) encompasses a clinically heterogeneous group of diseases characterized by high morbidity and mortality. Genetic studies over the past two decades have significantly expanded our understanding of the molecular landscape underlying heritable TAAD, revealing contributions from multiple interconnected biological pathways. This review systematically summarizes more than 75 genes implicated in TAAD pathogenesis, categorizing them according to major mechanistic roles including TGF-β signaling, extracellular matrix remodeling, smooth muscle cell contractility and cytoskeletal regulation, cell–matrix and cell–cell adhesion, metabolic processes, ion transport, and transcriptional regulation. Special emphasis is placed on emerging genes with variable or overlapping clinical phenotypes, dual-mechanism candidates, and their implications for personalized clinical management, including surveillance and surgical intervention thresholds. The integration of molecular insights into clinical practice, along with cautious consideration of genes of uncertain significance, promises to enhance diagnostic precision and risk stratification in individuals and families affected by heritable aortic disease.

Abstract Introduction Hypertrophic cardiomyopathy (HCM) is an autosomal dominant disorder with a pathogenic mutation identified in approximately 50% of cases. The MYH7 and MYBPC3 genes account for over half of these cases, while dozens of other genes can be pathogenic(1). Genetic test results are not independently used to determine which people with HCM benefit from implanted cardiac defibrillators (ICDs)(2, 3). Little is known about the additive role of genetic testing results to existing indications for ICD insertion. Purpose This study aims to examine the interaction between genetic testing results and existing ICD indications and imaging results on defibrillator discharge rates in HCM. Methods Patients who underwent an ICD for HCM, who underwent a cardiac magnetic resonance (CMR) study and who underwent genetic testing were included across 3 sites. The outcome was the incidence rate of appropriate ICD discharges, calculated using cox regression controlling for current age and primary vs secondary prevention. Interaction analysis between genetic risk factors and existing ICD indications, and with CMR quantification of LGE and septal thickness, was performed, and stratum specific estimates calculated using linear computation. Results 177 patients were included in the study, of whom 70 (39.55%) had a pathogenic mutation, 5 (2.82%) had a variant likely pathogenic (VLP), 44 (24.86%) had a variant of undetermined significance (VUS) and 58 (39.55%) had no identifiable mutation. The event rate was 3.32 {2.28 to 4.84) per 100 person years. There was no association between genetic variables and ICD discharge rate. There was an 80% reduction in ICD discharge rate in people who underwent ICD insertion exclusively for family history of sudden cardiac death or for syncope who had no pathogenic or likely pathogenic mutation, however this change was not statistically significant (table 2). Conclusion There is no strong association between genetic characteristics and ICD discharge rates among people with hypertrophic cardiomyopathy with an existing ICD indication. There is a nonsignificant trend towards fewer ICD discharges among people who underwent ICD insertion for family history alone or for a history of syncope and did not have a pathologic variant.Table 1 Table 2