Aim: This study aims to evaluate the effectiveness of prolonged Holter monitoring in detecting atrial fibrillation (AF) and other arrhythmias in patients following ischemic stroke. We seek to establish the optimal duration of monitoring that maximizes detection rates while considering clinical feasibility and cost-effectiveness.

Materials and Methods: We conducted a systematic review of recent literature, analyzing data from randomized clinical trials and observational studies that assessed the yield of AF detection through various durations of Holter monitoring. Key metrics included detection rates of AF and other relevant arrhythmias, along with patient outcomes related to therapeutic interventions initiated based on monitoring results.

Conclusions: This review highlights the crucial role of prolonged Holter monitoring, particularly 7-day monitoring, in detecting paroxysmal atrial fibrillation (AF) among ischemic stroke survivors, especially those with cryptogenic strokes. Extended monitoring significantly improves AF detection, enabling timely anticoagulation therapy and better stroke prevention. While challenges like patient compliance and cost-effectiveness remain, integrating prolonged Holter monitoring into standard care could enhance diagnostic accuracy and reduce recurrent stroke risk.

Currently, at least 22 species of Bartonella are known to cause diseases in humans, with Bartonella henselae being the main one. Among the clinical manifestations associated with bartonellosis, cutaneous vasculitis is rare, but it can be severe. We report the case of a 9-year-old child who presented with cervical lymphadenopathy, arthritis, epididymitis, and cutaneous vasculitis as clinical manifestations of systemic bartonellosis, with positive detection of B. henselae in blood and skin fragment using species-specific conventional polymerase chain reaction (PCR) techniques. Vasculitis caused by Bartonella spp. occurs due to the endothelial tropism of the bacteria and can mimic systemic vasculitis with positive anti-neutrophil cytoplasmic antibodies (ANCA). Furthermore, we found just one previous report about epididymitis related to B. henselae infection, and arthritis is also considered an unusual manifestation of the infection. This case emphasizes the need to consider bartonellosis among differential diagnoses when faced with presentations of purpura, cutaneous vasculitis, arthritis, or epididymitis.

Despite the widespread pediatric use of linezolid, data on its hematologic toxicity-particularly among children exposed to anticancer chemotherapy-remain limited and inconsistent. This study aimed to evaluate linezolid-induced hematotoxicity through pharmacokinetic analysis, with an emphasis on chemotherapy-exposed pediatric patients. This dual-center prospective study assessed linezolid pharmacokinetics and clinical profiles in chemotherapy-stratified pediatric cohorts, examining associations with hematologic toxicity. Among 229 pediatric patients (65 with cancer), hematologic toxicity occurred in 43.2%, with significantly higher risks of leukopenia (hazard ratio [HR] 20.29, 95% confidence interval [CI]: 3.98-103.38), neutropenia (HR 2.60, 95% CI: 1.00-6.77), and thrombocytopenia events (HR 7.08, 95% CI: 2.19-22.92) in cancer patients. Median linezolid trough and peak concentrations were 2.60 mg/L (interquartile range [IQR] 1.42-4.06) and 12.00 mg/L (IQR 9.5-14.19), respectively. Among cancer patients, trough concentrations above 7 mg/L elevated leukopenia (HR 6.33, 95% CI: 1.36-29.42) and anemia event (HR 8.72, 95% CI: 1.98-38.37) risk. Prolonged therapy exceeding 14 days elevated the risk of anemia events (HR 2.17; 95% CI: 1.08-4.35), while durations beyond 28 days also increased the risk of neutropenia events (HR 3.58; 95% CI, 1.37-9.32). At equivalent daily doses, twice-daily dosing resulted in higher peak concentrations (19.65 vs 13.67 mg/L; P = 0.020) and a greater incidence of anemia events (62.50% vs 25.00%; P = 0.033) compared to thrice-daily regimens. Linezolid frequently causes hematologic toxicity in children, particularly in chemotherapy recipients. Risk is also driven by high concentrations (peak > 15 mg/L, trough > 7 mg/L in cancer patients), prolonged therapy, and twice-daily dosing, necessitating careful monitoring and dose optimization.

The aim of the study was to investigate the underlying molecular mechanisms by which Naloxone enhances neurological function after ischemic stroke (IS). The permanent middle cerebral artery occlusion (PMCAO) model was utilized to simulate ischemic stroke in mice. Neurological function was assessed through behavioral scoring, and infarct volume as well as brain water content were measured to evaluate the extent of ischemic damage. Histopathological changes in the hippocampus were analyzed using hematoxylin and eosin staining, while neuronal apoptosis was quantified using TUNEL staining. An oxygen-glucose deprivation (OGD) injury model was established in HT22 cells, with cell viability assessed by MTT assay, apoptosis measured by flow cytometry, and lactate dehydrogenase release used to evaluate cellular toxicity. Proinflammatory cytokines were measured by enzyme-linked immunosorbent assay. The miR-30a-5p and Follistatin-like 1 (FSTL1) were quantified by RT-qPCR, and Western blotting was performed to detect FSTL1 protein levels as well as key apoptotic markers. Bioinformatic analysis, luciferase reporter assays, and RNA pulldown assays were conducted to confirm the direct interaction between miR-30a-5p and FSTL1. We found that Naloxone demonstrated a dose-dependent improvement in neurological function in PMCAO mice, as evidenced by reduced infarct volume, diminished cerebral edema, and attenuation of neuronal apoptosis and inflammation. Naloxone treatment significantly enhanced the viability of HT22 cells subjected to OGD, while also reducing apoptosis and inflammatory damage. Furthermore, Naloxone upregulated miR-30a-5p expression, and this upregulation contributed to the amelioration of OGD-induced cellular injury. The protective effects of Naloxone were partially reversed by silencing miR-30a-5p. miR-30a-5p directly targeted FSTL1, and silencing FSTL1 mitigated the reversal effect of miR-30a-5p inhibition on Naloxone's neuroprotective action. We conclude that Naloxone exerts its neuroprotective effects in ischemic stroke by upregulating miR-30a-5p, which inhibits the expression of FSTL1, ultimately improving neurological function and reducing brain injury in ischemic stroke models.

Endothelin-1 (ET-1) contributes to control of blood pressure (BP) and body fluid homeostasis. Blocking prohypertensive ET-1 receptors appeared promising treatment but the critical disturbing side-effect was oedema. Epoxyeicosatrienoic acids (EETs) have natriuretic and vasodilatory activity, hence they could find some therapeutical potential for patients with hypertension and end organ damage. We evaluated the effectiveness of atrasentan (ATR) combined with 14,15-EET analog, EET-A, on BP, kidney function and heart morphology, and ATR-dependent oedema in conscious spontaneously hypertensive rats (SHR). Systolic (SBP), mean and diastolic BP were measured by telemetry in SHR receiving in drinking water: ATR (5 mg/kg/day; n=6), EET-A (10 mg/kg/day; n=6), ATR+EET-A (n=6) or control solvent (C; n=5) for two weeks. Urine and blood sampling, and 24-h observations in metabolic cages were performed weekly. At the end animals were euthanized and organs were harvested. In the second protocol effectiveness of single intragastric drug application on renal electrolyte and water transport was tested. After two weeks of ATR+EET-A treatment SBP decreased significantly more (-13±2 mmHg; p<0.05) than after ATR alone (-3±1 mmHg). Decreases in plasma sodium (-9 mmol/l) and osmolality (-3 mosm/l) were significant in ATR group only, associated with the greatest increase in body weight. In ATR+EET-A and EET-A alone groups organ weights were significantly lower than with ATR alone. Our results suggest that addition of EET-A prolongs the hypotensive effect of ATR and prevents post-ATR water retention. Importantly, EET-A given orally, alone or combined with ATR, shows strong cardio- and renoprotective activity.

To explore the clinical efficacy and safety of interventional closure of patent ductus arteriosus (PDA) via femoral venous puncture under echocardiography guidance at high altitude.

From December 2022 to July 2023, 36 patients with PDA at high altitude were prospectively enrolled and underwent closure either under echocardiography guidance or fluoroscopy guidance. Baseline, procedural, and outcome characteristics were compared in intention-to-treat analysis.

The characteristics of patients and PDA were comparable between the two groups. The success rate of occlusion was 100% in both groups. Compared with the traditional fluoroscopy group, the echocardiography group showed a significant reduction in Air Kerma (112.13 ± 77.51 Gy vs. 247.27 ± 123.81 Gy, p = 0.001), Dose Area Product (24.3 [13.6-31.3] Gy·cm² vs. 41.5 [26.9-63.5] Gy·cm², p = 0.015) and intraoperative contrast dose (0 vs. 1.74 ± 1.02 mL/kg, p < 0.001). In the fluoroscopy group, a significant rise in creatinine (60.47 ± 14.02 umol/L vs. 40.93 ± 14.94 umol/L, p < 0.001) and urea nitrogen levels (6.03 ± 1.12 mmol/L vs. 4.80 ± 0.81 mmol/L, p < 0.001) at 24 h postoperatively were detected compared to preoperative levels, whereas no such changes were detected in the echocardiography group. Except for one patient in the fluoroscopy group lost to 1-year follow-up, no adverse events were reported in either group.

At high altitude, echocardiography-guided percutaneous PDA closure offers comparable efficacy to traditional methods, with minimal X-ray exposure and no contrast-induced kidney injury.

The trial is registered at http://www.chictr.org.cn (ChiCTR2400090901).

Stroke, a vascular disorder affecting the nervous system, is the third-leading cause of death and disability combined worldwide. One in every four people aged 25 and older will face the consequences of this condition, which typically causes loss of limb function, among other disabilities. The proposed review analyzes the mechanisms of stroke and their influence on the disease outcome, highlighting the critical role of rehabilitation in promoting recovery of the upper limb (UL) and enhancing the quality of life of stroke survivors. Common outcome measures and the specific targeted UL features are described, along with emerging supplementary therapies found in the literature. Stroke survivors often develop compensatory strategies to cope with limitations in UL function, which must be detected and corrected during rehabilitation to facilitate long-term recovery. Recent research on the automated detection of compensatory movements has explored pressure, wearable, marker-based motion capture systems, and vision sensors. Although current approaches have certain limitations, they establish a strong foundation for future innovations in post-stroke UL rehabilitation, promoting a more effective recovery.

To better define the importance of the amyloidogenic p.V142I TTR allele across the life span of a carrier, we leveraged data from All of Us to provide a generalizable assessment of the population-level burden of cardiovascular risk and estimate the age at disease onset.

We included self-identifying Black participants in All of Us who provided genomic data (N=77 767). The exposure of interest was p.V142I TTR carrier status (N=2213). Outcomes included incident heart failure (HF), atrial fibrillation, and carpal tunnel syndrome.

The median (interquartile range) age at enrollment was 56 (42-64) years. For the subset with genetic ancestry data (N=50 516), the p.V142I TTR carrier frequency was 3.5% (N=1771) among those with African ancestry. After adjustment for age and traditional risk factors, p.V142I TTR carrier status was associated with a greater risk of HF (odds ratio, 1.56 [95% CI, 1.22-1.99]; P=0.001), atrial fibrillation (odds ratio, 1.3 [95% CI, 1.08-1.90]; P=0.013), and carpal tunnel syndrome (odds ratio, 1.94 [95% CI, 1.43-2.63]; P<0.001).The risks increased in the sixth decade of life. In carriers, the attributable risk of the variant for HF, atrial fibrillation, and carpal tunnel syndrome was 27%, 26%, and 43%, respectively. While traditional HF risk factors did not modify the association of carrier status with HF (P-interaction >0.05 for all), their presence substantially augmented the risk of HF over a lifetime.

p.V142I TTR carriers are at an increased risk of HF and atrial fibrillation, beginning during the sixth decade of life. HF risk rises in a dose-dependent manner with other nonamyloid-related HF risk factors, highlighting the importance of aggressive treatment of HF risk factors among carriers. These observations also confirm the clinical relevance of the p.V142I TTR variant for individuals of African ancestry and underscore the importance of efforts to increase diagnoses, implement TTR-targeted therapies, and evaluate screening strategies for variant transthyretin cardiac amyloidosis.

There are two major distributions of late gadolinium enhancement (LGE) in the context of hypertrophic cardiomyopathy (HCM): intramural LGE and LGE at right ventricular insertion points (RVIPs). However, the clinical significance of intramural LGE has not been well established.

A total of 117 consecutive patients with HCM (61 male; median age, 58.8 years) confirmed by cardiovascular magnetic resonance (CMR) were enrolled, and classified into three groups: (1) no LGE (n = 48), (2) intramural LGE (n = 49), and (3) RVIP LGE (n = 20).

Intramural LGE was detected in 41% of patients with HCM. HCM patients with intramural LGE had greater left ventricular (LV) wall thickness (LVWT) and greater LV mass than those without LGE (all p < 0.05). Furthermore, HCM patients with intramural LGE had a more depressed LV ejection fraction (LVEF) and more impaired global radial strain (GRS), global circumferential strain (GCS), and global longitudinal strain (GLS) than did those with RVIP LGE and those without LGE (all p < 0.05). Multivariate logistic regression analysis revealed that young age and severely thickened LVWT were associated with intramural LGE in patients with HCM (all p < 0.05). Furthermore, negative correlations were observed between intramural LGE and GRS, GCS, and GLS (all p < 0.001).

Intramural LGE is associated with more severe HCM phenotypes, including a greater LVWT, LV mass and extent of LGE; a reduced LVEF; and impaired myocardial strain. These findings indicate that intramural LGE may be a noninvasive biomarker for risk stratification in patients with HCM.

Intramyocardial hemorrhage (IMH) after emergency percutaneous coronary intervention (PCI) in ST-segment elevation myocardial infarction (STEMI) patients is a significant predictor of major adverse cardiovascular events. However, current research lacks a simple and visual predictive model for IMH occurrence.

Our study aims to construct a Nomogram model to predict IMH occurrence.

Patients with STEMI who underwent PCI at Yichang Central People's Hospital from August 2023 to September 2024 and had CMR 2-10 days post-PCI were included. They were divided into IMH and Non-IMH groups. Risk factors for IMH were identified using Random Forest, single-factor, and multifactor Logistic regression analyses. The constructed nomogram prediction model was evaluated using receiver operating characteristic (ROC) curves, calibration curves, and clinical decision analysis (DCA) curves. Bootstrap resampling was used for internal validation.

IMH occurred in 43 patients (Non-IMH:53). Ischemic time, preoperative CK-MB level, and preoperative Myo level were identified as independent risk factors for IMH, while RCA occlusion was a protective factor. A nomogram model based on these four variables was established to predict the risk of IMH occurrence. The model's ROC curve had an area under the curve (AUC) of 0.865, indicating excellent discriminative ability; the calibration curve had a good fit (p = 0.16); the DCA curve showed high clinical applicability. After internal validation, the AUC of the ROC curve was 0.873 (95% CI:0.754-0.921).

The Nomogram model constructed based on four clinical risk factors has good predictive value and clinical applicability, providing an effective reference for predicting the risk of IMH occurrence in STEMI patients after PCI.