Monsanto, Michael Acevedo

Background Studies suggest that hypoperfusion from heart failure (HF) may contribute to cognitive decline. However, the relationship between the HF subtypes and cognition remains poorly described in real‐world populations. Methods We conducted a cross‐sectional study of patients aged ≥18 years seen at the Mayo Clinic in 2022 who underwent echocardiogram and cognitive assessment within 1 year. HF was classified per the 2022 American Heart Association as no HF, HF with preserved ejection fraction (EF), HF with mildly reduced EF, and HF with reduced EF. Cognitive impairment was categorized using the Montreal Cognitive Assessment score as normal (≥26), mild (18–25), and moderate to severe (<18). Linear regression assessed EF–Montreal Cognitive Assessment correlation and logistic regression the association between HF subtypes and cognitive dysfunction, adjusting for age, sex, race, and vascular risk factors. Results A total of 1592 patients met inclusion criteria (mean age, 75.7±13.8 years; 48.5% women). Lower EF was associated with worse cognitive performance (postadjustment β=0.033, P =0.013). Patients with HF with reduced EF and patients with HF with preserved EF had significantly lower Montreal Cognitive Assessment scores than those without HF (17.6±6.2 and 18.9±5.8 versus 19.9±6.0, P <0.001). The prevalence of moderate to severe cognitive impairment was highest in HF with reduced EF (43.3%), followed by HF with preserved EF (34.4%), no heart failure (28.6%), and HF with mildly reduced EF (23.4%) (adjusted trend P =0.032). Conclusions HF, independent of ejection fraction alone, is associated with cognitive impairment. Further studies should confirm these findings and evaluate the impact of interventions targeting EF and HF subtypes on cognitive outcomes.

Abstract Background Immune checkpoint inhibitors (ICIs) improve outcomes across malignancies but can cause immune-related adverse events (irAEs), notably myocarditis, with case-fatality up to 50% Methods We retrospectively reviewed five patients with potential ICI-associated myocarditis treated at Mayo Clinic Florida (2019–2024) and summarize the existing literature. Cases were retrospectively categorized as definite, probable, or possible myocarditis according to cardiac magnetic resonance (CMR) findings and histopathology when available. Results The median age was 74 years, and four of the five patients were male. Myocarditis developed between 5 and 30 days after initiation of anti–PD-1 therapy. Presentations included dyspnea (three patients), chest pain (one patient), and asymptomatic troponin elevation detected on routine monitoring (one patient). Troponin T elevation above the 99th percentile was seen in all five cases (normal <= 15 ng/L). Electrocardiograms (ECG) demonstrated conduction abnormalities or ventricular ectopy in each patient. Left ventricular ejection fraction was preserved in four patients and severely reduced in one. CMR provided findings supportive of myocarditis in two of the five cases, while one endomyocardial biopsy (EMB) was performed and did not demonstrate active inflammation. Based on predefined criteria, one case was classified as definite myocarditis, one as probable, and three as possible ICI-associated myocarditis. All five patients received corticosteroid therapy. Two required escalation of immunosuppression. One patient developed concurrent myasthenia gravis, consistent with myocarditis–myositis–myasthenia (MMM) overlap, and underwent plasmapheresis for the neuromuscular component. Three patients recovered. Two patients died during follow-up; in both cases, myocarditis was considered a contributing factor, although direct causality could not be definitively established.