Citations

Background and Clinical Significance: Nonbacterial thrombotic endocarditis (NBTE) is a sterile fibrin-platelet valvular condition associated with malignancy and hypercoagulable states. It produces friable vegetations prone to systemic embolization, often presenting as multifocal ischemic stroke. While modestly linked to advanced adenocarcinomas, its association with melanoma is exceedingly rare; Case Presentation: We present a 43-year-old man with recently diagnosed metastatic melanoma who presented with fever, confusion and abdominal pain. Brain magnetic resonance imaging (MRI) revealed multifocal bilateral acute infarcts. Additional imaging demonstrated splenic and bilateral renal infarcts. Transesophageal echocardiography (TEE) revealed an 8 mm × 7 mm multilobar lesion on the posterior mitral valve leaflet. Blood cultures remained persistently negative; autoimmune and infectious workup were unrevealing, and positron emission tomography-computed tomography (PET-CT) showed no cardiac hypermetabolism. Despite empiric antibiotics for suspected infective endocarditis (IE), progressive embolic infarcts occurred. After exclusion of infection, NBTE was considered, and therapeutic enoxaparin was initiated, resulting in clinical stabilization without hemorrhagic conversion; Conclusions: Distinguishing NBTE from IE remains challenging due to overlapping and nonspecific imaging findings. TEE is the preferred diagnostic modality because of its high sensitivity for detecting small valvular vegetations. Adjunctive imaging modalities such as brain MRI and PET-CT may support the diagnosis by demonstrating embolic patterns or excluding metabolically active infectious vegetations. Management primarily relies on systemic anticoagulation, while percutaneous vegetation aspiration may represent a potential diagnostic and therapeutic strategy. Clinicians should maintain high suspicion of this condition in patients with advanced melanoma and other malignancies presenting with multifocal embolic phenomena and negative cultures to enable timely anticoagulation.

Abstract Aims Routine aspirin use for primary prevention yields modest cardiovascular benefit but increases bleeding risk in average-risk adults. Whether individuals with elevated lipoprotein(a) [Lp(a)] levels or high-risk LPA variants derive greater benefit remains uncertain. Methods and results Following Cochrane and PRISMA guidelines, we systematically searched PubMed/MEDLINE, Embase, and Cochrane Central for studies of adults without ASCVD, elevated Lp(a) (≥50 mg/dL), high-risk LPA genotypes, or elevated genetic risk scores, comparing aspirin vs. no aspirin use. Random-effects meta-analyses using restricted maximum-likelihood (REML) estimation with Hartung–Knapp–Sidik–Jonkman (HKSJ) adjustment were used to pool hazard ratios (HR) and 95% confidence intervals (CI). In six studies, 6628 participants were included. Pooled random effects showed no significant reduction in major adverse cardiovascular events (MACE) with aspirin (HR = 0.60; 95% CI 0.31–1.17; P = 0.1) or clinical bleeding events (HR = 1.24; 95% CI 0.83–1.87; P = 0.18). Subgroup analyses showed a nonsignificant reduction MACE among elevated Lp(a) (HR = 0.63; 95% CI 0.16 to 2.49; P = 0.284) and statistically significant reduction among LPA rs3798220 carriers (HR = 0.37; 95% CI 0.19 to 0.71; P = 0.003), though this finding was not consistent in the sensitivity analyses. Conclusion Among adults without ASCVD but with elevated Lp(a) or high-risk LPA genotypes, aspirin use did not confer a statistically significant cardiovascular benefit and was associated with numerically higher bleeding risk. The apparent reduction seen in rs3798220 carriers was inconsistent and likely reflects small-sample bias.

Introduction: Apolipoprotein B (ApoB) and coronary artery calcium score (CAC) are well-established risk factors for coronary heart disease (CHD). However, the interaction between these risk factors on CHD risk has not been well-studied. We investigated the association between ApoB levels and CAC with CHD risk. Methods: We analyzed 4,649 participants from the Multiethnic Study of Atherosclerosis cohort (median follow-up 13.9 years) without baseline CHD or statin use. High ApoB was defined as ≥120 mg/dL. Participants were divided into 6 groups; group 1: CAC = 0 with normal ApoB, group 2: CAC = 0 with high ApoB, group 3: CAC 1-99 with normal ApoB, group 4: CAC 1-99 with high ApoB, group 5: CAC ≥100 with normal ApoB, group 6: CAC ≥100 with high ApoB. CHD was defined as myocardial infarction, resuscitated cardiac arrest, or CHD death. Survival analysis using Kaplan-Meier and multivariable Cox proportional hazard models were performed to assess the relationship between ApoB, CAC, and time to first CHD event. Results: In an adjusted model, high ApoB, CAC (1-99), and CAC (≥100) were independently associated with CHD (HR: 1.48; 95% CI: 1.04, 2.11; HR: 2.54; 95% CI: 1.78, 3.64; and HR: 4.41; 95% CI: 3.08, 6.31, respectively). Compared to group 1 (CAC 0 with normal ApoB), CAC 0 and high ApoB (group 2) was not associated with increased risk of CHD (HR: 1.15; 95% CI: 0.59, 2.23). However, a statistically significant greater risk of CHD was observed in those with CAC 1-99 and normal ApoB (group 3) (HR: 2.12; 95% CI: 1.37, 3.28), CAC 1-99 and high ApoB (group 4) (HR: 4.12; 95% CI: 2.42, 7.00), CAC ≥100 and normal ApoB (group 5) (HR: 4.20; 95% CI: 2.78, 6.34), CAC ≥100 and high ApoB (group 6) (HR: 5.72; 95% CI: 3.40, 9.63). Conclusions: In this analysis, ApoB and CAC are independently associated with CHD risk. Individuals with high ApoB and CAC ≥100 had the highest risk of CHD. In contrast, individuals with CAC = 0 and high ApoB had no significant increase in CHD risk compared to individuals with normal ApoB levels. These findings suggest that ApoB and CAC may be complementary tools for CHD risk stratification in the context of primary prevention.

Backround: Atrial fibrillation (AF) is a common complication following veno-venous extracorporeal membrane oxygenation (VV-ECMO), leading to further complications from anticoagulation or stroke. The Artificial Intelligence AF Prediction Dashboard developed at Mayo Clinic generates two predictive outputs: (1) a continuous probability score and (2) a binary threshold-based signal to predict the likelihood of AF at an individual level after 12-lead electrocardiogram (ECG) is obtained. Using both continuous risk (%) and binary (yes/no) likelihood, we present a novel method to understand AF risk after VV-ECMO cannulation based on pre-ECMO 12-lead ECG. Methods: We reviewed a total of 147 patients on ECMO between 2018 and 2024, from which 85 VV-ECMO patients with complete data were included. AI Dashboard outputs were quantified as binary (1/0) or percent likelihood for AF. R was utilized for statistical analysis. Results: 85 patients met our inclusion criteria from which AF after cannulation occurred in 31 (36%). 17 patients had a history of AF prior to VV-ECMO initiation. The mean age of our cohort was 49 years with a mean BMI of 29.3. Baseline AI Dashboard continuous assessment identified 39 patients (46%) compared to the binary assessment identifying 31 patients (36%). Logistic regression in the binary assessment demonstrated an odds ratio of 1.08 (95% CI 1.04 – 1.12) with a p value of <0.001. The binary AF Prediction yielded a 58% sensitivity, 76% specificity, 58% PPV, and 76% NPV, with an accuracy of 67%. The continuous AF Probability score achieved 72% balanced accuracy with sensitivity 74%, specificity 70%, PPV 59% and NPV 83%, indicating fair overall performance and suggesting good utility for ruling out AF in low-risk patients. Although both outputs provided moderate predictive accuracy, the continuous score reported before ECMO cannulation demonstrated stronger overall performance with fewer false negatives and higher rule-out value. Conclusions: We demonstrate the novel use of an AI predictive model in the VV-ECMO population for the prediction of AF risk with both continuous and binary risk cutoffs from baseline ECG. This data highlights the need for further development in ECMO-specific AI models to help mitigate risk after the onset of atrial arrhythmias. As AI-driven tools become increasingly integrated into care, their performance must be continuously validated and recalibrated for specific populations to ensure their safe and effective use.

Background: Lipoprotein(a) [Lp(a)] and metabolic syndrome (MetS) are well-established risk factors for cardiovascular disease. Recent evidence suggests that high Lp(a) levels may increase the risk of coronary heart disease (CHD) in patients with diabetes, raising the question of whether similar interactions exist between Lp(a) and metabolic syndrome. We aimed to evaluate the joint association of Lp(a) and MetS with incident CHD risk in a large, multi-ethnic, prospective cohort. Methods: We analyzed 6,664 participants from the MESA (Multiethnic Study of Atherosclerosis) cohort (median follow-up 14.0 years) without baseline CHD. MetS was defined as ≥3 of the following criteria: waist circumference ≥102 cm (men), or ≥88 cm (women), triglycerides ≥150 mg/dL or use of a fibrate medication, HDL-C <40 (men) or <50 (women) or use of a fibrate medication, SBP ≥130 mm Hg and/or DBP ≥85 mm Hg or use of antihypertensive medication, fasting glucose ≥100 mg/dL or use of antidiabetic medication (4). Elevated Lp(a) was defined as a level ≥50 mg/dL. CHD was defined as myocardial infarction, resuscitated cardiac arrest, or CHD death. Participants were divided into four groups: group 1: Normal Lp(a) without MetS, group 2: elevated Lp(a) without MetS, group 3: normal Lp(a) with MetS, group 4: elevated Lp(a) with MetS. Survival analysis using Kaplan-Meier and multivariable Cox proportional hazard models were performed to assess the relationship between Lp(a), MetS, and time to CHD. Results: In an adjusted model, log [Lp(a)] and MetS were both independently associated with CHD (HR: 1.14; 95% CI: 1.03, 1.25) and (HR: 1.75; 95% CI: 1.35, 2.27). Compared to the reference group (normal Lp(a) without MetS), those with elevated Lp(a) without MetS (group 2) did not have increased risk of CHD (HR: 1.30; 95% CI: 0.94, 1.80). However, those with normal Lp(a) with MetS (group 3) had greater risk of CHD (HR: 1.56; 95% CI: 1.18, 2.05). The highest risk for CHD were in those with elevated Lp(a) with MetS (group 4) (HR: 2.37; 95% CI: 1.66, 3.37). Conclusions: In this analysis. elevated Lp(a) and MetS independently increase CHD risk. MetS alone significantly increases risk, whereas elevated Lp(a) without MetS does not demonstrate a significant effect. However, their combination confers the highest risk, suggesting a synergistic interaction. These results emphasize the value of assessing Lp(a) in individuals with MetS to improve cardiovascular risk stratification and guide targeted prevention.

Background: The comparable long-term benefits of coronary artery bypass grafting (CABG) versus percutaneous coronary intervention (PCI) in patients with multivessel disease remains limited in underrepresented populations, particularly in patients with multivessel coronary artery disease and heart failure with severely reduced left ventricular ejection fraction (LVEF <35%). Research Question: Among patients with HF and LVEF < 35% which revascularization strategy (CABG or PCI) provides superior long-term clinical outcomes? Methods: We conducted a systematic review and meta-analysis of observational studies involving patients with ischemic heart disease (IHD), HF and LVEF < 35% undergoing PCI or CABG with a minimum follow-up duration of five years. PubMed, Embase, and Cochrane databases were searched for studies published up to April 15, 2025. We computed hazard ratios (HR) from propensity score matched results. We used Cochrane Review Manager version 9.2.1 for statistical analysis. The primary endpoints of interest included all-cause mortality at 5 to 10 years, repeat revascularization, and all-cause mortality at 10 or more years. Results: We included 8 studies with 12,697 patients (6,187 PCI vs 6,510 CABG). Median follow-up duration ranged from 3.8 to 5.2 years, with the longest reported follow-up up to 13 years. The cumulative, propensity adjusted, incidence of all-cause mortality was significantly lower in the CABG group compared to PCI in 5 to 10 years of follow-up (HR 0.61; 95% CI 0.54-0.69; p<0.001) and ≥ 10 years (HR 0.63; 95% CI 0.53-0.74; p<0.001). Additionally, CABG was associated with a reduced need for repeat revascularization in the 5 to 10 year time frame, with a HR of 0.42 (95% CI 0.22-0.81; p=0.01). Conclusion: In this systematic review and meta-analysis of patients with IHD and an ejection fraction ≤ 35% undergoing revascularization, CABG was associated with a reduction in all-cause mortality at ≥ 5 and ≥ 10 years of follow-up, as compared to PCI.

Problem Statement: The prognostic value of troponin elevation in septic ICU patients without known history of cardiac disease remains unclear, particularly after accounting for overall illness severity. Background: Minor troponin rises are frequent during sepsis, yet clinicians still lack a clear cut-point that signals danger once cardiac disease is ruled out. We asked whether a modest increase in troponin-T predicts in-hospital death beyond global illness severity. Methods: We studied 1 221 adult first ICU stays labelled “sepsis” in the eICU Collaborative Research Database and removed any case with a cardiac admission diagnosis. Implausible or missing laboratory values were imputed by multiple imputation. Hospital mortality was modelled with logistic regression that included troponin (a continuous and a binary model with threshold > 0.04 ng/mL) together with age, sex, lactate, albumin, BUN, creatinine, intubation status, vasopressor use, dialysis requirement and APACHE-IV predicted mortality. A natural-spline model explored non-linear behavior. Findings were checked in a 1:1 propensity-matched cohort. Results: Overall mortality was 11.7%. Troponin exceeded 0.04 ng/mL in 38% of patients. After adjustment for APACHE-IV probability and other covariates, a troponin level > 0.04 ng/mL was associated with almost twice the odds of death (OR ≈ 1.9), whereas the continuous model suggested only a modest trend (OR ≈ 1.1 per ng/mL). The spline curve rose steeply between 0 and 0.10 ng/mL and flattened thereafter, pinpointing an inflection near 0.05 ng/mL. Matching on all measured confounders confirmed that high-troponin patients had about three-fold greater mortality (OR ≈ 2.8, 1.55-5.05; p<0.001), highlighting that even modest troponin elevation is an independent risk marker for death in septic ICU patients. A bedside heat-map combining troponin, albumin and need for intubation illustrated a simple gradient: risk climbs from 2 % in low-troponin, well-albuminised, non-intubated patients to nearly 7 % when troponin exceeds 0.10 ng/mL in intubated, hypo-albuminemic patients. Conclusions: Even modest troponin elevations (> 0.04 ng/mL) independently predict mortality in sepsis after rigorous adjustment and matching on APACHE-IV physiology, lactate, and organ-support variables. This biologic threshold supports incorporating troponin into bedside triage and future septic cardiomyopathy trials.

Septal Myectomy (SM) and Alcohol Septal Ablation (ASA) improve symptoms in patients with Hypertrophic Cardiomyopathy with outflow tract obstruction (oHCM). However, outcomes data in this population is predominantly from specialized centers. The National Inpatient Database was queried from 2011 to 2019 for relevant international classification of diseases (ICD)-9 and -10 diagnostic and procedural codes. We compared baseline characteristics and in-hospital outcomes of patients with oHCM who underwent SM vs ASA. A p-value < 0.001 was considered statistically significant. We identified 15,119 patients with oHCM who underwent septal reduction therapies, of whom 57.4% underwent SM, and 42.6% underwent ASA. Patients who underwent SM had higher all-cause mortality (OR: 1.8 (1.3–2.5)), post-procedure ischemic stroke (OR: 2.3 (1.7–3.2)), acute kidney injury (OR: 1.4 (1.2–1.7)), vascular complications (OR: 3.6 (2.3–5.3)), ventricular septal defect (OR: 4.4 (3.2–6.1)), cardiogenic shock (OR: 1.7 (1.3–2.3)), sepsis (OR: 3.2 (1.9–5.4)), and left bundle branch block (OR: 3.5 (3–4)), compared to ASA. Patients who underwent ASA had higher post-procedure complete heart block (OR: 1.3 (1.1–1.4)), right bundle branch block (OR: 6.3 (5–7.7)), ventricular tachycardia (OR: 2.2 (1.9–2.6)), supraventricular tachycardia (OR: 1.6 (1.4–2)), and more commonly required pacemaker insertion (OR: 1.4 (1.3–1.7)) (p < 0.001 for all) compared to SM. This nationwide analysis evidenced that patients undergoing SM had higher in-hospital mortality and periprocedural complications than ASA; however, those undergoing ASA had more post-procedure conduction abnormalities and pacemaker implantation. The implications of these findings warrant further investigation regarding patient selection strategies for these therapies.