Post-operative atrial fibrillation (POAF) is common after coronary artery bypass graft (CABG) surgery, occurring in 20% to 40% of patients and significantly increasing morbidity. The hemoglobin, albumin, lymphocyte, and platelet (HALP) score, a composite nutritional-inflammatory index, is a prognostic marker in cardiovascular disease. However, its predictive value for POAF remains unestablished. We aimed to evaluate the predictive performance of 5 nutritional-inflammatory indices (HALP, Naples score, Systemic Immune-Inflammation Index [SII], neutrophil percentage-to-albumin ratio [NPAR], and C-reactive protein-albumin-lymphocyte [CALLY] index) for POAF and internally validate a novel prediction model incorporating HALP. Among 448 patients undergoing CABG, POAF occurred in 131 (29.2%). The HALP score demonstrated the highest discriminative ability (area under curve [AUC] 0.812), significantly (P < .001) outperforming Naples (AUC 0.676), NPAR (AUC 0.730), SII (AUC 0.726), and CALLY (AUC 0.684). Adding HALP to the Least Absolute Shrinkage and Selection Operator (LASSO)-derived base model significantly improved discriminative ability (AUC 0.813-0.897; P < .001) and net clinical benefit across threshold probabilities. The combined model achieved a bootstrap-corrected AUC of 0.885 with a calibration slope of 0.909, reflecting excellent internal validity. HALP was the strongest POAF predictor in the combined model. The HALP-integrated model showed excellent performance, offering a practical tool for preoperative POAF risk stratification.

Chronic limb-threatening ischemia (CLTI) carries 1-year mortality of 20% to 25%, comparable with many solid-organ malignancies. Technically successful revascularization, defined by anatomical patency, does not reliably deliver pain relief, restored function, or sustained quality of life. This narrative review synthesizes landmark randomized trials (BEST-CLI, BASIL-1, BASIL-2) and current European and United States guidelines, grading every claim with a scheme in which population indirectness downgrades design strength. We examine 4 domains of morbidity persisting after anatomically successful revascularization: mechanistically heterogeneous pain; functional and quality-of-life decline; psychological burden; and sustained health care use, including chronic opioid use (approximately 35%), unhealed wounds at 1 year (10%-32%), and unplanned 30-day readmission (approximately 25%). No patient-reported outcome measure has been validated specifically for CLTI or used as a co-primary trial endpoint. We propose an accountability gap: the under-measured transfer of unresolved morbidity from vascular services to primary care. We state it as a falsifiable prediction about the discrimination of patency rather than prevalence, with a pre-specified effect size, explicit treatment of death as a competing risk, and a core outcome battery justified against COSMIN criteria. Patient co-production is the indispensable next step.

Infective endocarditis (IE) in patients with malignancy represents a high-risk clinical cohort, yet nationwide data on outcomes and predictors of mortality remain limited. Using the United States National Inpatient Sample (2016-2022), we identified hospitalizations involving IE and a malignancy diagnosis. Inpatient mortality, complications, and temporal trends were analyzed overall and across malignancy subtypes, causative organisms, and prosthetic valve status. Survey-weighted multivariable logistic regression was performed across the full IE cohort. Of 635 715 IE hospitalizations, 44 060 (6.9%) involved a malignancy diagnosis. Inpatient mortality was higher in this group than among IE hospitalizations without malignancy (13.5% vs 9.8%; P < .001), and malignancy remained associated with mortality after adjustment (adjusted odds ratio 1.29; 95% CI 1.19-1.39; P < .001). The proportion of IE hospitalizations involving malignancy increased from 6.7% in 2016 to 7.7% in 2022. Fungal infection, shock, acute kidney injury, and stroke were associated with mortality. Prosthetic-valve IE had lower mortality than non-prosthetic-valve IE (7.7% vs 13.9%; P < .001). These findings identify a high-risk, heterogeneous phenotype and support earlier diagnostic evaluation and coordinated oncology, cardiology, and infectious diseases management.

Apolipoprotein A (ApoA) family members-ApoA-I, ApoA-II, ApoA-IV, and ApoA-V-play important roles in the vasculature that extend beyond lipid transport to regulate lipid-immune crosstalk, vascular homeostasis, and triglyceride metabolism. ApoA-I mediates reverse cholesterol transport, yet its cardioprotective capacity depends on functional integrity rather than HDL-cholesterol levels alone. ApoA-II, ApoA-IV, and ApoA-V exhibit context-dependent roles ranging from enhancing cholesterol efflux and triglyceride clearance to modulating inflammation, oxidative stress, endothelial activation, and thrombosis. Post-translational modifications such as oxidation, glycation, and citrullination within inflammatory milieus can convert protective ApoA proteins into dysfunctional or proinflammatory mediators. Genetic variations within APOA gene clusters have clarified the causal contribution of triglyceride-rich lipoproteins to atherosclerotic risk, shifting emphasis from HDL quantity toward lipoprotein quality and remnant cholesterol burden. In this comprehensive review, we synthesize structural, genetic, mechanistic, and clinical evidence to evaluate the position of the 4 ApoA proteins as context-dependent modulators of cardiovascular disease. We highlight the dualistic nature of their actions and examine failed clinical trials of ApoA-I infusions and mimetic peptides. We conclude by discussing how shifting focus from HDL quantity toward lipoprotein quality and preservation of ApoA functional integrity may inform more precise approaches to residual cardiovascular risk and triglyceride-driven atherogenesis.

This single-center retrospective case series assessed early ulnar artery patency by Doppler ultrasonography (DUS) after coronary angiography via distal ulnar access (DUA), described flow evolution in patients with follow-up, and reported access-related complications. Thirty-eight consecutive patients with a day-3 DUS after coronary angiography via DUA between September 2023 and March 2024 were included. All procedures were performed by 1 operator using a short 6F sheath and 5000 IU intra-arterial heparin. Flow was categorized as thrombosis/no flow, monophasic, or triphasic; the primary endpoint was day-3 non-triphasic flow, and month-1 and month-3 DUS were selective. Mean age was 58.8 ± 10.1 years and 47.4% were male; 21.1% underwent same-session percutaneous coronary intervention. On day 3, thrombosis/no flow occurred in 18.4% (7/38), monophasic flow in 5.3% (2/38), and triphasic flow in 76.3% (29/38); non-triphasic flow was 23.7% (9/38). Month-1 DUS (n = 35) showed no thrombosis/no flow and 94.3% triphasic flow; month-3 DUS (n = 4) was triphasic in all. No clinically relevant hematoma, neuropathy, hand ischemia, or functional impairment was documented. After coronary angiography via DUA, day-3 non-triphasic flow occurred in 23.7%; selective follow-up suggested recanalization without major clinical complications, but limits generalizability.

Epicardial adipose tissue (EAT) is a specialized visceral fat depot that directly interfaces with the myocardium. Under physiological conditions, EAT exhibits a beige-like thermogenic phenotype with enhanced angiogenesis and an anti-inflammatory secretome, contributing to cardioprotection. However, metabolic stress associated with obesity and type 2 diabetes mellitus disrupts this homeostasis, promoting EAT whitening, vascular dysfunction, hypoxia, fibrosis, and chronic inflammation, ultimately leading to adverse cardiovascular outcomes. Asprosin, a recently characterized fasting-induced adipokine, is an important regulator of systemic glucose metabolism, appetite, and insulin resistance. Experimental evidence suggests that asprosin suppresses adipose browning by downregulating thermogenic pathways while promoting adipogenesis and lipid accumulation. This review proposes an integrated asprosin-EAT whitening-angiogenesis axis as a conceptual framework linking EAT dysfunction and cardiovascular disease. Asprosin may contribute to phenotypic remodeling of epicardial adipose tissue through mechanisms involving impaired adipose browning, altered angiogenesis, and vascular dysfunction. Further investigation of the local and paracrine actions of asprosin within EAT is required to determine its potential as a biomarker and therapeutic target for cardiometabolic disease.

Contrast-associated acute kidney injury (CA-AKI) is a serious complication associated with increased morbidity and mortality in patients with acute coronary syndrome (ACS) undergoing coronary angiography. The C-reactive protein-albumin-lymphocyte (CALLY) index is a novel biomarker reflecting inflammatory and nutritional status. This retrospective study evaluated the prognostic value of the CALLY index calculated at hospital admission for predicting CA-AKI in 1516 patients with ACS. CA-AKI developed in 267 patients (17.6%). Patients who developed CA-AKI had significantly lower CALLY index values (0.35 ± 0.16 vs 0.84 ± 0.30; P < .001). In separate multivariable logistic regression analyses adjusted for baseline clinical and procedural confounders, the CALLY index emerged as an independent predictor of CA-AKI (Odds ratio [OR] 0.592 per 0.1-unit increase; 95% CI 0.525-0.668; P < .001). Receiver operating characteristic curve analysis demonstrated good discriminatory capacity for the CALLY index (Area Under the Curve [AUC] = 0.822), significantly outperforming conventional clinical scores and other inflammatory indices (DeLong test P < .001). Furthermore, adding the CALLY index to the Mehran risk score significantly improved reclassification metrics (Net Reclassification Improvement [NRI] = 14.2%, Integrated Discrimination Improvement [IDI] = 0.048; P < .001). The CALLY index serves as a simple, practical, and effective score for early CA-AKI risk stratification in ACS.

Coronary artery calcification (CAC) is a critical determinant of cardiovascular morbidity and mortality. Current research identifies CAC as an active biological process driven by vascular smooth muscle cell (VSMC) osteogenic transdifferentiation, chronic inflammation, oxidative stress, and metabolic dysregulation. These pathological changes are orchestrated by complex signaling networks that promote mineral deposition in the arterial wall. Emerging pharmacological interventions, including denosumab, vitamin K2, and SNF472, have demonstrated potential in attenuating CAC progression by targeting these specific pathways. Conversely, widely prescribed medications such as statins exhibit complex, dual effects on calcification, necessitating careful clinical evaluation. This review synthesizes the core molecular mechanisms underlying CAC and critically evaluates current and emerging pharmacological strategies, providing mechanistic insights to guide future precision management.