Background: Although the cardiometabolic index (CMI) has gained recognition as a new tool for evaluating metabolic health, the relationship between CMI and cardiovascular disease (CVD) remains unclear. This research sought to explore the potential association between CMI and CVD.Methods: Participants from the 2007–2018 National Health and Nutrition Examination Survey (NHANES) were selected. Multivariable logistic regression analyses and smooth curve fitting were utilized to investigate this relationship, along with subgroup evaluations and interaction analyses.Results: This study included 12,837 subjects and the prevalence of CVD was 11.83%. After full adjustment, participants presenting with an increase of one unit in Ln-transformed CMI associated a 15% higher odds of CVD prevalence (OR = 1.15, 95% CI: 1.05–1.26). In the fully adjusted model, individuals falling into the highest CMI quartile (Quartile 4) demonstrated substantially 35% higher odds than those in the lowest CMI quartile (Quartile 1) (OR = 1.35, 95% CI: 1.11–1.66). In addition, there was no nonlinear relationship between CMI and CVD in our selected sample. This positive association was not greatly influenced by any of the stratifications.Conclusions: Among US adults, having higher CMI levels is substantially associated with higher odds of CVD prevalence. This finding suggests that regular monitoring of CMI levels could enable physicians to initiate early interventions, potentially slowing the progression of CVD. However, in order to corroborate our findings, further prospective investigations are still required.

Cardiac organoids offer sophisticated 3D structures that emulate key aspects of human heart development and function. This review traces the evolution of cardiac organoid technology, from early stem cell differentiation protocols to advanced bioengineering approaches. We discuss the methodologies for creating cardiac organoids, including self-organization techniques, biomaterial-based scaffolds, 3D bioprinting, and organ-on-chip platforms, which have significantly enhanced the structural complexity and physiological relevance of in vitro cardiac models. We examine their applications in fundamental research and medical innovations, highlighting their potential to transform our understanding of cardiac biology and pathology. The integration of multiple cell types, vascularization strategies, and maturation protocols has led to more faithful representations of the adult human heart. However, challenges remain in achieving full functional maturity and scalability. We critically assess the current limitations and outline future directions for advancing cardiac organoid technology. By providing a comprehensive analysis of the field, this review aims to catalyze further innovation in cardiac tissue engineering and facilitate its translation to clinical applications.

A 37-year-old man suffered irreversible profound symptomatic bradycardia requiring a pacemaker 3 days after beginning tizanidine/loxoprofen combination therapy for neck pain. This combination therapy is prescribed frequently for joint pain; however, combining loxoprofen with tizanidine could increase the risk of symptomatic bradycardia that is both permanent and severe. Similar cases have not been reported. This case suggests that tizanidine should be used cautiously when combined with loxoprofen, and drug interaction screening should be performed.

Diabetic cardiomyopathy (DCM), as a devastating complication of diabetes mellitus (DM), arises from a complex interplay between systemic metabolic derangements and myocardial vulnerability. While hyperglycemia, lipotoxicity, and insulin resistance are established drivers of cardiac dysfunction, the precise mechanisms linking these metabolic insults to cardiac dysfunction remain elusive. Recent evidence suggests that the dysregulation of mitochondrial calcium homeostasis plays a critical role in integrating diabetic metabolic stress and cardiomyocyte fate. This review synthesizes recent advances in understanding how mitochondrial calcium mishandling—encompassing impaired uptake, excessive release, and buffering failure—orchestrates the pathological triad of bioenergetic deficit, oxidative stress, and cell death in DCM. We delve into the molecular mechanisms underpinning this dysregulation, highlighting its interplay with the diabetic metabolic milieu. Furthermore, we critically evaluate novel therapeutic strategies targeting mitochondrial calcium fluxes, including the inhibition of the mitochondrial calcium uniporter (MCU), the activation of the mitochondrial Na ⁺ /Ca ²⁺ /Li ⁺ exchanger (NCLX), and the modulation of the mitochondrial permeability transition pore (mPTP), discussing their clinical translation potential and existing challenges. By reframing DCM through the lens of mitochondrial calcium homeostasis, this review not only synthesizes current knowledge but also provides a critical comparison of emerging therapeutic strategies and evaluates the formidable challenges in their clinical translation, thereby bridging the gap between endocrine metabolism and cardiac pathophysiology and offering nuanced perspectives for biomarker discovery and stage-specific interventions.

Background: Zolpidem is a non-benzodiazepine hypnotic widely used to manage insomnia. Zolpidem-triggered atrial fibrillation (AF) in patients with cardiomyopathy has never been reported before. Case presentation: A 40-year-old man with Duchenne muscular dystrophy-related cardiomyopathy attempted suicide and developed new-onset AF after zolpidem overdose. One year before admission, the patient visited our clinic due to chest discomfort and fatigue after daily walks for 1 month; both electrocardiography (ECG) and 24-hour Holter ECG results did not detect AF. After administration of cardiac medication (digoxin 0.125 mg/day, spironolactone 40 mg/day, furosemide 20 mg/day, bisoprolol 5 mg/day, sacubitril/valsartan 12/13 mg/day), he felt better. AF had never been observed before this admission via continuous monitoring during follow-up. Sixteen days before admission, the patient saw a sleep specialist and started zolpidem tartrate tablets (10 mg/day) due to insomnia for 6 months; ECG results revealed no significant change. The night before admission, the patient attempted suicide by overdosing on 40 mg of zolpidem after an argument, which resulted in severe lethargy. Upon admission, his ECG revealed new-onset AF, necessitating immediate cessation of zolpidem. Nine hours into admission, AF spontaneously terminated into normal sinus rhythm. Results from the ECG on the following days and the 24-hour Holter ECG at 1-month follow-up showed that AF was not detected. Conclusions: This study provides valuable clinical evidence indicating that zolpidem overdose may induce AF in patients with cardiomyopathy. It serves as a critical warning for clinicians when prescribing zolpidem, particularly for patients with existing heart conditions. Further large-scale studies are needed to validate this finding and to explore the mechanisms between zolpidem and AF.

Objective: To evaluate the utility of the preoperative neutrophil percentage-to-albumin ratio ( N PAR) for predicting perioperative major adverse cardiovascular events (MACE) in patients with stable coronary artery disease (SCAD) undergoing non-cardiac surgery. Methods: In this retrospective cohort study, we included all adult SCAD patients who underwent non-cardiac surgery at the Fourth Affiliated Hospital of Zhejiang University School of Medicine between October 2020 and October 2024. The primary endpoint was the occurrence of MACE during the perioperative period, defined as a composite of all-cause mortality, cardiac arrest, myocardial infarction, heart failure, or stroke occurring intraoperatively or during the postoperative hospital stay. We used multivariable logistic regression to assess the independent association between NPAR and MACE risk. To explore potential nonlinearity, we fitted smooth curves and performed threshold-effect analysis. Mediation analysis quantified the proportion of the NPAR–MACE relationship explained by estimated glomerular filtration rate (eGFR). Incremental predictive value was evaluated by comparing the area under the receiver operating characteristic curve (AUC), net reclassification improvement (NRI), and integrated discrimination improvement (IDI) before and after adding NPAR to established risk models. Feature selection was conducted using the Boruta algorithm, and predictive performance was further validated with an XGBoost model interpreted via Shapley Additive Explanations (SHAP). Results: Of 1,771 patients, 90 (5.1%) experienced MACE. The MACE subgroup had a higher mean NPAR than those without events (19.4 ± 5.3 vs. 15.9 ± 3.5; P < 0.001). Each 1-unit increase in NPAR was associated with a 20% higher risk of MACE (OR 1.20; 95% CI 1.10–1.30). A J-shaped relationship emerged, with an inflection point at NPAR 13.7 (P_threshold = 0.005). eGFR mediated 8.4% of the NPAR–MACE association. NPAR alone yielded an AUC of 0.721. Adding NPAR to the Revised Cardiac Risk Index raised the AUC from 0.679–0.755 (NRI 0.599; IDI 0.035; all P < 0.01). The XGBoost model achieved an AUC of 0.773, and SHAP analysis identified NPAR as the most influential predictor. Conclusions: Preoperative NPAR is an independent, readily available predictor of perioperative MACE in SCAD patients. Incorporation of NPAR into existing risk models significantly enhances predictive accuracy and may inform targeted perioperative management strategies.