Bidirectional ventricular tachycardia is a rare electrocardiographic (ECG) finding, associated with a restricted group of clinical conditions, particularly hereditary channelopathies.

An 11-year-old girl, asymptomatic from a cardiovascular point of view, was identified by family screening after detection in her father of a pathogenic variant in the KCNJ2 gene. The admission ECG showed bidirectional ventricular tachycardia. Clinical investigation revealed periodic paralysis and skeletal dysmorphisms, confirming a diagnosis of Andersen-Tawil syndrome. Pharmacological treatment significantly reduced the arrhythmic burden, with reverse ventricular remodeling at follow-up.

This case illustrates the central role of ECG as a diagnostic tool in rare cardiovascular diseases, allowing early recognition, targeted genetic investigation, and prevention of arrhythmia-induced cardiomyopathy.

Bidirectional ventricular tachycardia is a distinct ECG pattern that should raise suspicion of Andersen-Tawil syndrome and warrants genetic evaluation with cascade family screening. In this patient, the combination of propafenone and beta-blocker therapy was associated with suppression of bidirectional ventricular tachycardia, significant reduction in ventricular arrhythmic load, and reversal of tachycardiomyopathy, suggesting a potential therapeutic alternative when flecainide is not available.

Stroke remains a leading cause of death and disability worldwide. Endothelial dysfunction plays a central role in both acute ischemic injury and subsequent recovery. In this study, we investigated the protective effects and underlying mechanisms of Dl-3-n-butylphthalide (NBP) on human brain microvascular endothelial cells (HBMECs) subjected to oxygen-glucose deprivation (OGD), an in vitro model of ischemic stroke.

HBMECs were divided into three groups: control (normoxia), OGD (10 h hypoxia, followed by reoxygenation for different durations (0-24 h), and then a subsequent 24 h incubation), and NBP-treated OGD (10 μmol/L NBP during reoxygenation). Cell viability and apoptosis were assessed by Cell Counting Kit 8 (CCK8), lactate dehydrogenase (LDH) release, and flow cytometry. Mitochondrial function was evaluated using MitoTracker fluorescence. Molecular mechanisms were examined using Western blot, quantitative real-time PCR (qRT-PCR), immunofluorescence, and enzyme-linked immunosorbent assay (ELISA), focusing on the hypoxia-inducible factor-1α (HIF1α)/vascular endothelial growth factor (VEGF) angiogenic pathway and cyclooxygenase-2 (COX2)-mediated inflammatory response.

NBP at 10 μmol/L significantly improved HBMEC viability (37.5% increase, p < 0.01), reduced apoptosis (p < 0.01), and restored mitochondrial membrane potential (p < 0.05) following OGD injury. Mechanistically, NBP demonstrated dual pathway modulation by: (1) promoting angiogenesis-related gene expression through HIF1α upregulation and subsequent increase in vascular endothelial growth factor receptor 2 (VEGFR2) and endothelial nitric oxide synthase (eNOS) expression (p < 0.05); and (2) suppressing inflammation via COX2 downregulation with concurrent reduction of downstream mediators including inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNFα), interleukin-1β (IL-1β), and Thromboxane B₂ (TXB₂, p < 0.05). This coordinated regulation created a favorable microenvironment balancing pro-angiogenic signals with anti-inflammatory effects.

NBP exerts multi-targeted protection on HBMECs after ischemic injury through associated with the activation of HIF1α/VEGF-mediated angiogenesis and suppression of COX2-driven inflammation. This dual modulation strategy, targeting both vascular repair and inflammatory control, provides preliminary in vitro mechanistic insights that warrant further validation in vivo and in clinical settings.

Stroke has long been a leading cause of death and long-term disability worldwide. In recent years, more and more research has revealed that microglial responses to ischemic injury are highly heterogeneous and exhibit dynamic evolution over time, across brain regions, and under different metabolic states. This endows microglia with a dual regulatory role in both neurotoxicity and neuroprotection after ischemia: on one hand, they drive inflammatory responses, exacerbating secondary neuronal damage, blood-brain barrier disruption, and synaptic loss; on the other hand, they orchestrate debris clearance, vascular rebuilding, and neural repair. The traditional pro-inflammatory versus anti-inflammatory dichotomy is no longer sufficient to fully describe their complex functions. In this review we summarize recent advances in understanding the dual regulatory roles of microglia after ischemic stroke, with a focus on key mechanisms such as metabolic reprogramming, lipid metabolism regulation, inflammasome activation, and epigenetic modification. Furthermore, emerging therapeutic strategies targeting microglia and the challenges they face are discussed.

Previous studies have shown that Heliox, a mixture of 32% oxygen and 68% helium administered at a warm temperature, is effective in treating ischemic brain injury caused by cerebral arterial air embolism. At the same time, therapeutic hypothermia has been shown to lead to a favorable neurological outcome in patients in the acute phase of ischemic stroke; however, there are no published data on the use of Heliox at room temperature after ischemic stroke. All published data indicate only the efficacy of heated Heliox. The most effective temperature regimen for Heliox inhalation to prevent neurological deficits in stroke remains unknown.

Three Heliox inhalation temperature regimens were studied at 20-22 °C, 40-50 °C, and 60-70 °C. The mixture was administered immediately after inducing ischemic stroke in awake rats using a model of cerebral arterial air embolism. Respiratory and cardiovascular function, as well as body temperature, coordination, muscle strength, and serum calcium binding protein B (S100B) concentrations were studied 24 hours after embolization. A brain histopathological study was also performed.

Inhalation of heated Heliox (40-50 °C and 60-70 °C) immediately after cerebral arterial air embolism was shown to be an effective method for maintaining respiratory and cardiovascular function and body temperature, for preventing the development of foci of ischemic brain damage on 2,3,5-triphenyltetrazolium chloride (TTC)-stained sections of the brain, and for partially preserving coordination, muscle strength, locomotor activity, and for a partial reduction in serum S100B concentration during the acute phase of ischemic stroke in rats compared to the untreated group with cerebral arterial air embolism (CAE). Unheated Heliox had a negative effect on experimental animals, and decreased a survival rate to 62.5%.

Heated Heliox has an equally positive effect at temperatures of 40-50 °C and 60-70 °C, and significantly alleviated the symptoms of ischemic stroke during the acute phase. In contrast, unheated Heliox at room temperature (20-22 °C) had a negative effect on the course of ischemic stroke in rats.

Publicly reported 30-day acute myocardial infarction (AMI) mortality rates are widely used to benchmark hospital performance. However, these measures may lack validity when they include deaths among patients with do-not-resuscitate (DNR) orders or those receiving palliative care-groups for whom mortality may be expected and goal-concordant.

We analyzed the national 100% Medicare Inpatient Standard Analytic File and Medicare Beneficiary Summary file to assess 30-day AMI mortality rates stratified by DNR status (absent, present-on-admission, and postadmission) and palliative care involvement. We then conducted a retrospective chart review of all 30-day AMI mortalities at a single academic medical center (2019-2025), applying Global Registry of Acute Coronary Events and a Palliative Performance Scale scores to identify unpreventable deaths, which we defined as a Global Registry of Acute Coronary Events >190.5 or Palliative Performance Scale ≤40%. Global Registry of Acute Coronary Events is a risk-stratification tool using clinical and laboratory variables whereas the Palliative Performance Scale is a bedside functional status and palliative care assessment quantifying patient's self-care ability.

Across n=467 259 total AMI encounters, mean (SD) age was 75.1 (10.5), and the population was 44% female. Thirty-day mortality was 10.4% (39 112/376 062) among patients without DNRs, 43.1% (26 181/60 719) in those with present-on-admission DNR, and 72.1% (21 984/30 478) in those with postadmission DNR. Among 9.2% (43 090/467 259) of encounters with palliative care, there was a 76.9% mortality rate (33 151/43 090). Hazard ratios for mortality were 5.25 (95% CI, 5.17-5.33) for present-on-admission DNR and 10.73 (95% CI, 10.55-10.91) for postadmission DNR as compared with encounters without DNRs. Among n=24 AMI mortalities at our institution, 71% (17/24) had DNRs, and 33% (8/24) met the unpreventable death criteria.

The validity of 30-day AMI mortality metrics may be undermined by their inclusion of high-acuity, end-of-life patients, which may disincentivize hospitals from delivering appropriate, patient-centered care. Removal of DNR or palliative cases from performance measures should be explored to better identify opportunities for reducing preventable deaths.

Large commercial laboratories serve millions of patients and generate billions of test results annually. The objective of our study was to assess the potential use of commercial laboratory lipid testing for population health monitoring.

Lipid levels from commercial laboratory testing of adult patients in Dallas County, TX, were compared with those from DHS-2 (Dallas Heart Study Phase-2)-a population-based cohort study in Dallas County-over the same period (September 2007-September 2009). Sensitivity analysis excluded those with International Classification of Diseases-Tenth Revision codes listing diabetes or cardiovascular disease as the indication for testing. The associations between abnormal lipid levels (high-density lipoprotein cholesterol <50 mg/dL in women and <40 mg/dL in men, low-density lipoprotein cholesterol ≥130 mg/dL, triglycerides ≥150 mg/dL) and residency in any of 76 ZIP codes was assessed in the commercial laboratory population using logistic regression adjusting for age and sex.

The distribution plots of high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides were broadly similar in a commercial laboratory population (n=59 419; median age [interquartile range], 48 [33-58] years; 56% women) and DHS-2 (n=3147; median age [interquartile range], 50 [42-58] years; 60% women). Median high-density lipoprotein cholesterol was 1 mg/dL lower (95% CI 0.6-2), low-density lipoprotein cholesterol was 5 mg/dL lower (95% CI 3-6), and triglycerides were 12 mg/dL higher (95% CI 9-14) in the commercial laboratory population versus DHS-2. Similar results were observed in a sensitivity analysis that excluded those with diabetes or cardiovascular disease. Higher probabilities of abnormal levels of all 3 lipids were observed for 5 ZIP codes (odds ratios [95% CI] ranged from 1.07 [1.001-1.15] to 1.84 [1.48-2.28]).

Within the same geographic region, the differences between lipids observed in commercial laboratory testing and in a population-based cohort were negligible (high-density lipoprotein cholesterol) to moderate (low-density lipoprotein cholesterol, triglycerides). This proof-of-concept study suggests that commercial laboratory testing may be useful for monitoring population lipid levels and assessing regional and temporal variation.

The risk of recurrence remains high among patients with coronary heart disease (CHD). Life's Simple 7 (LS7), a composite indicator of cardiovascular health, has been associated with a lower risk of incident CHD, but its prognostic value among patients with CHD remains unclear. We aimed to examine the association between temporal changes in LS7 and recurrent CHD.

Data were from the US ARIC study (Atherosclerosis Risk in Communities). LS7 scores were assessed at Visit 1 (1987-1989) and Visit 3 (1993-1995). LS7 changes were evaluated by change in LS7 category (from poor/fair [0-6] to moderate/ideal [7-14] or from moderate/ideal to poor/fair), cumulative LS7 score (as quartiles), and change in LS7 score (as quartiles). Recurrent CHD was identified through December 31, 2018. Cox models assessed the association between changes in LS7 and recurrent CHD risk.

Among 1330 participants (mean [SD] age, 55.2 [5.6] years, 50.2% female) included in transition analyses, 561 (42.2%) experienced recurrent events during 21 359.2 person-years of follow-up. Participants whose LS7 score improved from poor/fair to moderate/ideal showed a reduced risk of recurrent CHD (hazard ratio, 0.54 [95% CI, 0.40-0.74]), whereas those whose score declined from moderate/ideal to poor/fair exhibited an increased risk (hazard ratio, 1.82 [95% CI, 1.44-2.30]). Both a higher cumulative LS7 score and a greater increase in LS7 score were associated with a lower risk of recurrent CHD (hazard ratio, 0.38 [95% CI, 0.30-0.49] for Q4 versus Q1 of cumulative score and hazard ratio, 0.51 [95% CI, 0.38-0.68] for Q4 versus Q1 of Δscore).

Deterioration in LS7 during follow-up was associated with an increased risk of recurrent CHD, whereas improvement in LS7 was associated with a reduced risk. These findings underscore the importance of preserving and improving cardiovascular health and support the potential value of longitudinal cardiovascular health assessment in the ongoing management of patients with CHD.

Sirtuins (SIRTs) involvement in different biological pathways opens a promising scenario for the development of related ligands to be evaluated as therapeutic agents in different diseases, such as cancer, neurodegenerative disorders, diabetes, cardiovascular and autoimmune diseases. The continuous elucidation of several SIRT2-ligand complexes fostered the discovery of novel and more selective SIRT2 inhibitors (SIRT2Is). Among them, SIRT2 in the presence of SirReal2 analogues was the most investigated. We recently reported pyrazolo-pyrimidine compounds (1-5) as SIRT2Is (1, SIRT2 % inhibition = 81.2%, at 150 μM). Herein, combined ligand- and structure-based approaches enabled us to filter a further series of pyrazolo-pyrimidine-based analogues (6-16) endowed with improved SIRT2 inhibitory activity in comparison to 1-5. The applied molecular modelling studies revealed superimposable molecular interaction fields (MIFs) and protein-ligand contacts compared with the reference SIRT2Is. Subsequent biochemical and biological assays validated the reported strategy and pointed to compounds 11 and 15 (SIRT2 IC₅₀ = 0.3 and 0.1 μM, respectively) as the most promising SIRT2Is, to be further investigated as anticancer agent.

Cerebral-cardiac syndrome (CCS) is a complication commonly observed following an ischemic stroke, which results in increased morbidity and mortality. Timely diagnosis of CCS is of prognostic significance. This study investigates the significance of multiple cardiovascular biomarkers for CCS in patients with acute ischemic stroke (AIS).

This study retrospectively analyzed 177 patients with AIS admitted to Yongchuan People's Hospital of Chongqing from March 2022 to March 2023. Plasma levels of BNP (B-type natriuretic peptide), cTnI (cardiac Troponin I), Myo (myoglobin), CK-MB (creatine kinase isoenzyme), D-Dimer (DD), FDP (fibrin degradation product), and CRP (C-reactive protein) were measured. Multivariable Firth's penalized logistic regression was used to identify independent risk factors for CCS, and receiver operating characteristic analysis and bootstrap validation were performed to evaluate the diagnostic performance.

CCS occurred in 97 patients (54.8%). BNP, DD, cTnI, Myo, and CK-MB were significantly elevated in the CCS group compared to the non-CCS group (all p < 0.001). After adjustment for covariates, age (OR = 1.047, p = 0.036), BNP (OR = 1.028, p < 0.001), and Myo (OR = 1.003, p = 0.048) remained as independent risk factors. The combined model incorporating age, BNP, and Myo yielded an area under the curve of 0.945 (95% CI: 0.914-0.977), with bootstrap-adjusted AUC = 0.941, indicating excellent discriminatory ability of the model and strong concordance with the clinical diagnosis.

Age, BNP, and Myo constitute a robust diagnostic model for the early identification of CCS in AIS patients. This panel may facilitate timely risk stratification and intervention in the clinical management of CCS.

Risk stratification using validated scoring systems is fundamental to contemporary cardiovascular medicine, underpinning diagnosis, treatment selection, and prognostic assessment. This review provides a comprehensive overview of the major risk scores used across a broad spectrum of cardiovascular diseases, such as atrial fibrillation, acute coronary syndrome, and others, highlighting their development, clinical applications, and evolving roles in guideline-directed care. Importantly, predictive performance alone does not guarantee clinical benefit. We therefore examine evidence from randomized implementation trials evaluating whether risk score-guided management improves clinical outcomes and discuss the future role of artificial intelligence in reshaping cardiovascular risk assessment by integrating dynamic, individualized prediction with actionable clinical decision support.