Cardiac Markers Research Articles

Delving into biomarkers and predictive modeling for CVD mortality: a 20-year cohort study

Accurate prediction of cardiovascular disease (CVD) mortality is essential for effective treatment decisions and risk management. Current models often lack comprehensive integration of key biomarkers, limiting their predictive power. This study aims to develop a predictive model for CVD-related mortality using a machine learning-based feature selection algorithm and assess its performance compared to existing models. We analyzed data from a cohort of 4,882 adults recruited between 1999 and 2004, followed for up to 20 years. After applying the Boruta algorithm for feature selection, key biomarkers including NT-proBNP, cardiac troponins, and homocysteine were identified as significant predictors of CVD mortality. Predictive models were built using these biomarkers alongside demographic and clinical variables. Model performance was evaluated using the concordance index (C-index), sensitivity, specificity, and accuracy, with internal validation conducted through bootstrap sampling. Additionally, decision curve analysis (DCA) was performed to assess clinical benefit. The combined model, incorporating both biomarkers and demographic variables, demonstrated superior predictive performance with a C-index of 0.9205 (95% CI: 0.9129–0.9319), outperforming models with demographic variables alone (C-index: 0.9030 (95% CI: 0.8938–0.9147)) or biomarkers alone (C-index: 0.8659 (95% CI: 0.8519–0.8826)). Cox regression analysis further identified key predictors of CVD mortality, including elevated AST/ALT, TyG, BUN, and systolic blood pressure, with protective factors such as higher chloride and iron levels. Nomogram construction and DCA confirmed that the combined model provided substantial net benefit across various time points. The integration of cardiac biomarkers, lipid profiles, and inflammatory markers significantly improves the accuracy of predictive models for CVD-related mortality. This novel approach offers enhanced prognostication, with potential for further optimization through the inclusion of additional clinical and lifestyle data.

Cardioprotective Potential of Moringa Oleifera Leaf Extract Loaded Niosomes Nanoparticles - Against Doxorubicin Toxicity In Rats.

Doxorubicin (DOX) is one of the most potent anticancer drugs that has ubiquitous usage in oncology; however, its marked adverse effects, such as cardiotoxicity, are still a major clinical issue. Plant extracts have shown cardioprotective effects and reduced the risk of cardiovascular diseases. The current study is intended to explore the cardioprotective effect of ethanolic Moringa oleifera extracts (MOE) leaves loaded into niosomes (MOE-NIO) against DOXinduced cardiotoxicity in rats. MOE niosomes nanoparticles (NIO-NPs) were prepared and characterized by TEM. Seventy male Wistar rats were randomly divided into seven groups: control, NIO, DOX, DOX+MOE, DOX+MOE-NIO, MOE+DOX, and MOE-NIO+DOX. DOX (4 mg/kg, IP) was injected once per week for 4 weeks with daily administration of MOE or MOENIO (250 mg/kg, PO) for 4 weeks; in the sixth and seventh groups, MOE or MOE-NIO (250 mg/kg, PO) was administered one week before DOX injection. Various parameters were assessed in serum and cardiac tissue. Pre and co-treatment with MOE-NIO have mitigated the cardiotoxicity induced by DOX as indicated by serum aspartate aminotransferase (AST), creatine kinase - MB(CK-MB) and lactate dehydrogenase (LDH), cardiac Troponin 1(cTn1) and lipid profile. MOE-NIO also alleviated lipid peroxidation (MDA), nitrosative status (NO), and inflammatory markers levels; myeloperoxidase (MPO) and tumor necrosis factor-alpha (TNF-α) obtained in DOX-treated animals. Additionally, ameliorated effects have been recorded in glutathione content and superoxide dismutase activity. MOE-NIO effectively neutralized the DOXupregulated nuclear factor kappa B (NF-kB) and p38 mitogen-activated protein kinases (p38 MAPK), and DOX-downregulated nuclear factor-erythroid 2-related factor 2 (Nrf2) expressions in the heart. It is concluded that pre and co-treatment with MOE-NIO could protect the heart against DOX-induced cardiotoxicity by suppressing numerous pathways including oxidative stress, inflammation, and apoptosis and by the elevation of tissue antioxidant status. Thus, it may be reasonable to suggest that pre and co-treatment with MOE-NIO can provide a potential cardioprotective effect when doxorubicin is used in the management of carcinoma.

Inhibition of NETs prevents doxorubicin-induced cardiotoxicity by attenuating IL-18-IFN-γ-Cx43 axis induced cardiac conduction abnormalities.

Doxorubicin-induced cardiotoxicity (DIC) is one of the most severe side effects of doxorubicin, yet the underlying mechanisms remain incompletely understood. Our results showed that Neutrophil extracellular traps (NETs) accumulated in plasma and cardiac tissue after doxorubicin treatment. The inhibition of NETs formation by Pad4 gene ablation significantly attenuated doxorubicin-induced arrhythmia, prolonged survival time and reduced the levels of Troponin T (cTnT) and creatine kinase MB (CK-MB) in mice. In addition, reductions in left ventricular fractional shortening and ejection fraction induced by doxorubicin were more severe in WT mice than in Pad4-/- mice. Immunostaining and qPCR analyses revealed that NETs activated macrophages to release pro-inflammatory cytokines such as IL-18, IL-1β, and TNF-α. IL-18, in turn, activated T cells to produce IFN-γ, which, along with TNF-α, downregulated the expression of Cx43, thereby inducing cardiac conduction abnormalities. We identify that IL-18-IFN-γ-Cx43-induced cardiac conduction abnormalities triggered by neutrophil extracellular traps is the key molecular and cellular determinants of DIC. Furthermore, targeting NETs formation using ozone therapy significantly alleviated DIC. This study highlights the critical role of NETs in the development of DIC and proposes ozone therapy as a potential therapeutic strategy for treating DIC.

Cardiovascular MRI-derived Right Atrial Strain for Improved Risk Stratification in Patients with Severe Aortic Stenosis.

Purpose To assess the prognostic implications of cardiac MRI-derived imaging markers in individuals with severe aortic stenosis (AS). Materials and Methods This prospective study (German Clinical Trials Register, DRKS00024479) enrolled individuals with severe AS who underwent cardiac MRI before transcatheter aortic valve replacement (TAVR) from January 2017 to March 2022. Image analyses included myocardial volumes, cardiac MRI feature tracking-derived left atrial (LA) and right atrial (RA) as well as left ventricular (LV) and right ventricular (RV) strain, myocardial T1 mapping, and late gadolinium enhancement analyses. Cardiovascular (CV) mortality was defined as primary clinical end point. Cox proportional hazards models were used to determine the association between cardiac MRI-derived parameters and CV mortality. Results The final analysis included 145 participants (median age, 80 years [IQR, 75-83 years]; 91 male). Participants who experienced CV death during follow-up had significantly enlarged RV end-diastolic volumes (median, 82.9 [IQR, 70.8-96.0] mL/m2 vs 62.8 [54.7-76.0] mL/m2; P < .001) and impaired strain values of all cardiac chambers compared with those who survived (LV global longitudinal strain [GLS], -18.1% [-13.1% to -20.4%] vs -22.5% [-16.1% to -27.3%], P = .02; RV GLS, -22.9% [-18.6% to -25.4%] vs -27.9% [-22.9% to -32.0%], P = .002; LA atrial reservoir strain [Es], 9.5% [7.2%-15.4%] vs 14.3% [9.0%-18.1%], P = .04; RA Es, 12.4% [6.8%-14.4%] vs 16.2% [11.2%-22.1%], P < .001). RA reservoir strain independently helped predict CV mortality after adjustment for other cardiac MRI markers and clinical parameters of heart failure (hazard ratio, 0.82 [95% CI: 0.71, 0.95]; P = .008). Within the subgroup of participants with high extracellular volume values, RA strain further identified participants with AS at high risk for CV mortality (P = .001 on log-rank testing). Conclusion In individuals with AS undergoing TAVR, several cardiac MRI parameters were significantly associated with CV mortality. RA strain was an independent predictor of CV mortality and may provide more optimized patient management. Keywords: Cardiac MRI, Aortic Stenosis, TAVR, Risk Assessment, Strain Analyses German Clinical Trials Register no. DRKS00024479 Supplemental material is available for this article. © RSNA, 2025.

Lipoprotein(a) and the risk of type I cardiorenal syndrome in patients with coronary artery disease: A retrospective clinical study

ObjectiveThe present study aimed to investigate the correlation between lipoprotein(a) (Lp-a) and coronary artery disease (CAD) complicated by type I cardiorenal syndrome (CRS). MethodsWe conducted a retrospective analysis of patients diagnosed with CAD admitted to the Department of Cardiovascular Medicine at Shaoxing Central Hospital from January 2021 to December 2022, with chief complaints of “chest distress and dyspnea.” Patient demographic data, biochemical indicators (including blood lipid levels and serum creatinine), cardiac function markers (such as pro-brain natriuretic peptide, pro-BNP), echocardiography, and coronary angiography results were collected. Patients were categorized into two groups based on estimated glomerular filtration rate (e-GFR): the CRS group (e-GFR < 60 mL/min/1.73 m2) and the simple heart failure group (SHF group, e-GFR ≥ 60 mL/min/1.73 m2). A comparative analysis of baseline characteristics, lipid profiles, ejection fraction (LVEF), left atrial size (LA), end-diastolic interventricular septal thickness (IVSd), left ventricular end-diastolic dimension (LVEDD), and left ventricular end-systolic dimension (LVESD) between the two groups was performed. Multivariable logistic regression analysis was applied to assess the association between serum lipoprotein(a) (Lp-a) levels and the occurrence of CRS. ResultsA total of 269 patients were included, comprising 149 males and 120 females with an average age of 76.0 ± 11.4 years. Significant differences were observed between the CRS and SHF groups in terms of age, history of hypertension, diabetes, myocardial infarction, serum triglycerides, Lp-a, and creatinine (all P < 0.05). Spearman’s correlation analysis revealed an inverse relationship between Lp-a and e-GFR (r = -0.588, P < 0.05). Multivariable logistic regression analysis indicated that Lp-a (OR = 1.980, 95 % CI: 1.269–2.992, P = 0.027) and age (OR = 1.584, 95 % CI: 0.955–1.913, P = 0.006) were positively associated with the development of CRS. ConclusionSerum Lp-a levels are positively correlated with the occurrence of CRS, potentially serving as an independent risk factor for CRS.

When to consider takotsubo cardiomyopathy in menopausal elderly woman presenting chest pain

Background: An elderly menopausal woman presenting with chest pain in the emergency department may have coronary artery disease (CAD), Takotsubo cardiomyopathy, or other conditions. It is crucial to conduct a thorough diagnostic evaluation in menopausal elderly woman. Case illustration: A 77-year-old postmenopausal woman presenting with first-onset chest pain after having familial issues and severe psychological stress was admitted to the emergency department. She had no identifiable risk factors for CAD, and her physical examination revealed no significant abnormalities. The electrocardiogram (ECG) indicated non-specific ST-segment elevation in leads V3-V6. Serial ECGs showed an evolution of ST-segment elevation that did not align with the typical pattern observed in STEMI. Despite the elevation in cardiac enzymes in the previous hospital, unfortunately, serial cardiac enzymes were inconsistently normal in our hospital. Therefore, these findings implied that the patient's condition might not be ACS, and we cannot rule out the possibility of Takotsubo syndrome. The patient underwent coronary angiography (DCA) and The DCA results revealed normal coronary with suspicion of apical ballooning of the left ventricle as observed from cine angiography. Subsequent echocardiography demonstrated apical akinesis with basal hyperkinesis, the large area of dysfunctional myocardium extending beyond the territory of a single coronary artery and characteristic apical ballooning resembling an octopus trap, consistent with the diagnosis of Takotsubo syndrome. The patient was managed conservatively with supportive care. Her symptoms improved, and she was discharged after five days. Conclusion: This case highlights the importance of considering takotsubo cardiomyopathy in menopausal elderly woman with no risk factor of CAD presenting with chest pain after having psychological stress. Keywords: Takotsubo Syndrome, Acute Coronary Syndrome, octopus trap, stress induced cardiomyopathy, Cathecolamine induced

Identifying echocardiographic predictors of late gadolinium enhancement in severe aortic stenosis patients undergoing transcatheter aortic valve implantation: insights from cardiac MRI

Abstract Background Aortic stenosis (AS) is prevalent among the elderly. Accurate prognostic assessment in AS is crucial for optimizing patient management and outcomes. Identifying factors associated with Late Gadolinium Enhancement (LGE), a cardiac MRI marker, can help in risk stratification. LGE-positive individuals have a poorer prognosis, including a twofold increased risk of mortality and adverse cardiovascular events. Purpose The purpose of this study was to identify echocardiographic predictors of LGE in patients with severe AS. Methods Data from 58 patients with severe AS scheduled for transcatheter aortic valve implantation (TAVI) were analyzed. Echocardiograms and MRI scans were performed within two weeks before TAVI. The average age of the patients was 81.5 years, and 60% were male. LGE was present in 16 patients (27.6%). Univariate logistic regression identified significant echocardiographic factors associated with LGE, which were then included in a multivariate analysis. Results Univariate analysis showed significant echocardiographic factors: large left atrial volume (LAD &amp;gt;34 ml/m²) (P = 0.0116), septal mitral annular velocity (e' septal) (P = 0.0281), left ventricular mass index (LVMi) (P = 0.0350), and left atrium size (P = 0.0453). Multivariate analysis indicated large left atrial volume (Coeff = 0.636), septal mitral annular velocity (Coeff = -0.563), left ventricular mass index (Coeff = 0.126), and left atrium size (Coeff = 0.345) were associated with LGE. Measures of AS severity, including aortic valve area (AVA), peak aortic velocity (Vmax), and mean pressure gradient (mean PG), were not significantly associated with LGE. Conclusion Large left atrial volume, septal mitral annular velocity, left ventricular mass index, and left atrium size are echocardiographic factors associated with LGE in patients with severe AS. These predictors could assist clinicians in identifying high-risk patients and improving management strategies.

Fermented Houttuynia Cordata Juice Exerts Cardioprotective Effects by Alleviating Cardiac Inflammation and Apoptosis in Rats with Lipopolysaccharide-Induced Sepsis

Background/Objectives: Sepsis-induced cardiac dysfunction is a major problem that often leads to severe complications and a poor prognosis. Despite the growing awareness of its impact, effective treatment options for sepsis-induced cardiac dysfunction remain limited. To date, fermented products of Houttuynia cordata (HC), known for its rich bioactive properties, have shown potential in modulating inflammatory and oxidative stress pathways. However, treatment with fermented HC juice (FHJ) in lipopolysaccharide (LPS)-induced sepsis in rats has not been investigated. Methods: Rats were pretreated with FHJ at doses of 200 mg/kg and 400 mg/kg for 2 weeks. After that, the rats were injected with a single dose of LPS (10 mg/kg), and 12 h after injection, they developed sepsis-induced cardiac dysfunction. Then, cardiac function, oxidative stress, inflammation, apoptosis, and cardiac injury markers were determined. Results: Pretreatment with FHJ at doses of 200 mg/kg and 400 mg/kg prevented LPS-induced cardiac dysfunction in rats by attenuating cardiac inflammation (IL-1β, TLR-4, and NF-κB levels), oxidative stress (MDA levels), and apoptosis (cleaved-caspase 3 and Bax/Bcl-2 expression) and reducing markers of cardiac injury (LDH and CK-MB levels). Conclusions: These results suggest that FHJ could be a potential therapeutic agent for sepsis-induced heart disease.

Effect of olive olive extracts in myocardial and vascular function of patients with chronic cononary syndromes

Abstract Introduction In a recent study, we demonstrated that the administration of an olive oil supplement enriched with HT (Olivomed) reduces oxidative stress and inflammatory biomarkers, improves endothelial and arterial function, and facilitates the diastolic function of the left ventricle after a short treatment period in patients with chronic coronary syndromes. Objetive Wehypothesized that the administration of an oral supplement, Olivomed SMART, containing olive oil extract enriched with oleuropein (OL), hydroxytyrosol (HT) and oleocanthal (OLEO), can reduce oxidative burden and further improve cardiac and vascular markers in patients with chronic coronary syndromes. Method Thus, in a prospective, randomized, crossover, double-blind, placebo-controlled clinical trial, we randomized 15 patients with chronic coronary syndromes to an oral supplement of olive oil extract enriched with OL, HT, and OLEO in a ratio of 2:1:3 or a placebo for one month. We measured before treatment, one month after using the placebo, and one month after administering the olive supplement: a) the Perfused Boundary Region (PBR) related inversely to the thickness of the endothelial glycocalyx in sublingual arterioles (range 5–25 μm), a marker inversely related to glycocalyx thickness, b) endothelial-dependent vasodilation (FMD) of the brachial artery, c) flow reserve in the anterior descending (CFR) with Doppler echocardiography, d) pulse wave velocity (PWV), central systolic blood pressure (cSBP), e) concentration of malondialdehyde (MDA), an oxidative stress marker. Results It appears that the administration of the Olivomed SMART supplement significantly improves vascular markers FMD and CFR compared to baseline, while no changes are induced by the placebo (Table 1). Olivomed SMART improves diastolic function, as shown by improved values of E’, E/e’, DT, LVGLS. No significant no marker indicates any difference compared to baseline (Table 2). The administration of the Olivomed SMART supplement significantly reduced levels of the oxidative stress marker MDA and oxidized LDL cholesterol in serum compared to baseline. In contrast, no statistically significant changes were observed after placebo administration (Table 3). Comparing the action of Olivomed and Olivomed SMART on the main vascular, echocardiographic, and biochemical markers relative to baseline values before treatment, the following table (Table 4) shows significant changes after the administration of Olivomed SMART in left ventricular longitudinal strain values and glycocalyx integrity in vessels ranging 20-25 μm. Conclusion Comparing Olivomed and Olivomed SMART, it appears that the beneficial effects on vascular and cardiac properties are largely due to the action of HT, while the newer combined formulation seems to provide additional benefits in endothelial function of arterioles, coronary artery function, and myocardial strain through the reduction of oxidative stress.

Clinical Features and Inhospital Outcomes of Takotsubo (Stress) Cardiomyopathy: Ten Years’ Experience from a Tertiary Care Center in South India

Abstract Background: Takotsubo cardiomyopathy is a syndrome which is characterized by transient regional systolic dysfunction, principally, of the left ventricle (LV), mimicking myocardial infarction (MI), but in the absence of angiographic evidence of obstructive coronary artery disease or acute plaque rupture. Aims and Objectives: In the present study we estimated clinical profile and assess the clinical course and short-term outcome of takotsubo cardiomyopathy. Materials and Methods: This was a single-center retrospective study conducted between April 01, 2013, and May 31, 2023. Cases were patients who were admitted in the Department of Cardiology with a diagnosis of takotsubo cardiomyopathy. Descriptive statistics were obtained for all variables and entered in MS Excel and analyzed with SPSS (SPSS for Windows, version 16.0, Chicago, IL, USA) in the study, and appropriate statistical tests like P value were employed to ascertain the significance. Results: Over 10 years (2012-2022), 55 patients of South Asian ethnicity with a diagnosis of takosubo cardiomyopathy were treated at this 2,858-bed tertiary-care hospital. Out of the study population 89.1% were female. Hypertension was seen in 58.2%, Diabetes Mellitus was seen in 45.5% and Dyslipidaemia was seen in 61.8 % of the patients. Stress factor or a precipitating event, was found in majority of the patients (63.6%). The mode of presentation was such that 63% presented with typical chest pain, 70.9% had dyspnoea, 9.1% had palpitation and 7.3% had syncope. The Cardiac enzymes were raised in 56 % patients. Coronary angiogram was done in all the patients which showed normal coronaries in 89.1% and non-flow limiting Coronaries in 10.9%. Of the study population, 25 (45.5%) patients had developed acute heart failure during their hospital stay and 17 (30.9%) patients had developed new arrhythmias. After Univariate and multivariate analysis to find the predictors of heart failure, evidence of right ventricular dysfunction was found to be an independent risk factor for developing acute heart failure. [OR = 4.14 ,95% CI (1.34 to 12.8)] and initial presentation as palpitation was an independent risk factor for developing new arrythmia. [OR =3.86 ,95% CI (1.16 to 8.84)]. Acute renal failure occurred in 6(10.9%) and there was no occurrence of cerebrovascular accident. The mean ± SD duration of hospital stay of the entire study cohort was of 4.09 ± 2.396 days. The overall mortality in this cohort was 2 (3.6%). At mean follow up time of 5.3 ± 1.4 years two patients died due to cerebrovascular accidents. 41 patients (74%) were asymptomatic, and 5 (9%) patients had intermittent episodes of dyspnoea. 2 (3.4%) patients were found to have paroxysmal atrial fibrillation episodes. At the echocardiographic follow up the mean ejection fraction improved to 56 ± 4%. Conclusions: The present study showed the high morbidity of TTS, diagnosed according to the new Inter-TAK criteria, in a tertiary center in India, especially during hospitalization, even though the overall prognosis is usually good. Often there is a preceding emotional or physical trigger, however absence of a trigger does not preclude a diagnosis of Takotsubo cardiomyopathy. Presence of RV failure had higher chances of acute heart failure and index presentation of palpitation had higher occurrence of arrythmias.

Severe central nervous system injury in 9 children with COVID-19

PurposeTo investigate the clinical features and prognosis of severe central nervous system (CNS) injury in children caused by coronavirus disease 2019 (COVID-19).MethodWe retrospectively studied confirmed pediatric cases of COVID-19 complicated with CNS injury.ResultsNine patients diagnosed with COVID-19 complicated with severe CNS injury were admitted to the pediatric intensive care unit of the Affiliated Hospital of Jining University from December 1, 2022 to January 12, 2023. Of the nine patients, seven were male (77.78%). Five children were aged ≥ 10 years, and the others were 1–2 years old. All children had fever, eight had convulsions, seven had progressed to multiple organ failure, and all suffered varying degrees of coma. Most of the children had elevated interleukin-6 (100%), lactic acid (100%), alanine transaminase (87.5%), aspartate transaminase (87.5%), creatine kinase MB (87.5%), and lactate dehydrogenase (85.7%) levels. Four children had cerebrospinal fluid proteinnacell separation. The cranial imaging results of five children were abnormal. One child had lost his vital signs when admitted to hospital, and the remaining eight received hormonal shock, human immunoglobulin transfusion, antinainfection, cranial pressure reduction, and tracheal intubation, among others, during hospitalization. Ultimately, eight children died, and the remaining child has serious neurological sequelae and is undergoing rehabilitation.ConclusionsSevere CNS injury caused by COVID-19 has an acute onset, rapid progression, high disability rate, and high fatality rate. A low cerebrospinal fluid protein level may be a protective factor for children with severe nervous system injury caused by COVID-19.

Astragaloside IV Alleviates Myocardial Fibrosis After Myocardial Infarction Through SIRT3/β-catenin/PPARγ Signaling Pathway

Background Myocardial fibrosis following myocardial infarction (MI) is linked to decreased cardiac function and heart failure. Astragaloside IV (AST IV), a component of traditional Chinese medicine, has shown promise in animal studies for improving cardiac function. Purpose This study intends to investigate the role of AST IV in MI and its correlation with the sirtuin-3 (SIRT3)/β-catenin/peroxisome proliferator-activated receptor gamma (PPARγ) signaling pathway. Methods After the establishment of an animal model of MI, 60 rats were divided into a control group, model group (MI group), positive control group (sham group), low-dose AST IV group (0.8 mg/100 g), and high-dose AST IV group (3 mg/100 g). The animals were injected once a day for 4 consecutive weeks. To further investigate the mechanism of action of AST IV, another nine rats from the model group were randomly divided into the 3TYP group (5 mg/100 g), SKL2001 group (20 µmol/L, 10 mL/kg), and T0070907 group (0.15 mg/100 g), with three rats in each group. The rats in each group were intervened once a day by intraperitoneal injection and once a day by gavage for 4 consecutive weeks. Hemodynamics, cardiac function, ventricular weight, and infarct area were assessed at 1, 2, and 4 weeks post-surgery. Myocardial collagen content in the non-infarcted area was measured, the expression rate of transforming growth factor-beta and ED-positive cells was calculated, and reverse transcription polymerase chain reaction was used to detect SIRT3, β-catenin, and PPARγ mRNA expression. Results The left ventricular ejection fraction, short-axis shortening rate, and left ventricular mass in the model group were decreased obviously. AST IV treatment decreased systolic blood pressure, +dp/dtmax, –dp/dtmax, and left ventricular end-diastolic pressure, as well as reduced myocardial collagen deposition in rat hearts ( p &lt; 0.05). AST IV inhibited the SIRT3/β-catenin/PPARγ signaling pathway when alleviating myocardial fibrosis. Intervention with SIRT3 blocker 3-TYP, β-catenin agonist SKL2001, and PPARγ blocker T0070907 reversed the inhibitory effect of AST IV on the signaling pathway. Conclusion AST IV exhibits significant anti-fibrotic effects, effectively reducing collagen deposition in the MI model, improving cardiac function parameters, and decreasing markers such as creatine kinase-MB. It significantly regulates SIRT3, β-catenin, and PPARγ to exert cardioprotective effects. The key mechanism involves inhibiting the SIRT3/β-catenin/PPARγ, offering an innovative strategy for post-MI treatment.

Assessment of the Association Between Clinical and Laboratory Parameters and Past Coronavirus Infection in Patients with Coronary Artery Restenosis

Understanding the risk factors for coronary in-stent restenosis is particularly important in patients with coronavirus disease (COVID-19). Such patients require careful monitoring, priority treatment, and prevention.The aim of our study was to assess the association between clinical and laboratory parameters and previous coronavirus infection in patients with coronary artery restenosis.Materials and methods. A cross-sectional study was conducted on a continuous sample of patients with coronary artery disease who underwent repeated myocardial revascularization in the period from 2020 to 2023 (931 patients). 420 patients in the main group had coronary artery stent restenosis, of which 162 (38.5 %) had suffered from coronavirus infection (CVI). The control group included 511 patients with repeated myocardial revascularization without stent restenosis, of whom 107 (20.9 %) had undergone CVI. Laboratory tests included troponin I, D-dimer, creatine kinase (CK), creatine kinase-MB (CK-MB), serum creatinine and glucose, C-reactive protein (CRP), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and fibrinogen, IgG and IgM antibodies to coronavirus and RNA detection by polymerase chain reaction. Statistical calculations were performed using SPSS version 20.0 software.Results: It was established that there were statistically significantly higher levels of IgG antibodies to coronavirus and C-reactive protein in the main study group compared to the control group. When dividing the study groups into subgroups of individuals with and without previous CVI, statistically significant differences in troponin levels were found (p&lt;0.001): between the level in the group with restenosis and CVI compared to groups without restenosis with CVI, with restenosis without CVI, and in groups with revascularization without CVI and with restenosis without CVI. The levels of D-dimer, CPK, CPK-MB, CRP, and APTT had statistically significant differences in the groups with previous CVI compared to the groups without CVI. The results of multiple regression analysis indicated a statistically significant positive relationship in the study groups between the development of myocardial infarction and such indicators as CRP, blood glucose, low-density lipoproteins (LDL), previous CVI, as well as a negative relationship with left ventricular ejection fraction and high-density lipoproteins (HDL). The role of these predictors in the development of myocardial infarction was confirmed using ROC analysis.Conclusion: The results of our study indicated a relationship between previous coronavirus infection and an increased risk of coronary artery restenosis in patients with previous myocardial revascularization.

Dihydromyricetin Protects Against Hypoxia/Reoxygenation Injury in Cardiomyocytes by Activating miR-34a-Mediated Notch1 Pathway.

Dihydromyricetin (Dih), a naturally occurring flavonoid, has been identified to exert a protective effect against ischemia/reperfusion injury. However, the detailed mechanisms remain unclear. Here we investigated the biological role of Dih in preventing hypoxia/reoxygenation (H/R) injury in cardiomyocytes. The results showed that Dih protected cardiomyocytes against H/R-induced apoptosis, as proved by improved cell viability and decreased lactate dehydrogenase (LDH) release, cell apoptosis percentage, and caspase-3/7 activity. H/R-induced oxidative stress in cardiomyocytes was also prevented by Dih with increased activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT), and decreased levels of malondialdehyde (MDA) and reactive oxygen species (ROS). Treatment with Dih prevented H/R-induced increase in the activities of myocardial enzymes aspartate aminotransferase (AST), creatine kinase-MB (CK-MB), and creatine kinase (CK). miR-34a expression was upregulated after H/R stimulation, which could be attenuated by Dih pretreatment. Besides, miR-34a overexpression attenuated the protective effects of Dih against H/R-caused increase in apoptosis, oxidative stress, and myocardial enzyme activities. Next, we demonstrated that Notch1 was a target molecule of miR-34a. Notch1 overexpression reversed the role of miR-34a in regulating the cardioprotective effect of Dih on H/R injury. These observations indicated that the cardioprotective effect of Dih against H/R injury was mediated by the miR-34a/Notch1 signaling. Dih may be a candidate agent for improving the clinical efficacy of cardiac ischemia/reperfusion injury treatment.

Use of Coronary CTA to Triage Patients With Low to Intermediate Risk for CADs in an Acute Care Facility Can Help Lower Healthcare Costs When Compared With the Current Standard of Care: A Retrospective Study.

Acute chest pain is one of the most common reasons for ED visits in the United States. Most patients are eventually admitted to the hospital to "rule out ACS" even when there are no significant EKG abnormalities or elevated cardiac enzymes. In addition to undergoing expensive tests while in the hospital, patients are also exposed to iatrogenic harm thereby worsening the overall healthcare costs. Meanwhile, the use of coronary computed tomography angiography (CTA) as a "gatekeeper" diagnostic test for patients with low to intermediate risk for coronary artery diseases (CADs) has significantly lowered hospital admissions and associated costs. However, coronary CTA may not be helpful for all classes of patients. Therefore,this study seeks to determine if the distribution ofpatients presenting to the ED withchest pain in an acute care facility will justify an investment in coronary CTA and contribute to lowering healthcare costs. Patients' data between July 2022 and June 2023 were considered in our analysis. Results revealed that a significant number of patients who presented to the ED for chest pain and were subsequently admitted to the hospital for further work-up would have benefited from coronary CTAscreening without any need for further inpatient work-up. Also, cost analysis showed that the use of coronary CTA would have helpedsignificantly lower healthcare costs in this facility.

Preconditioning with acteoside ameliorates myocardial ischemia‑reperfusion injury by targeting HSP90AA1 and the PI3K/Akt signaling pathway.

The present study aimed to investigate the cardioprotective effects of acteoside (AC) on myocardial ischemia‑reperfusion injury (MIRI). To meet this aim, a network pharmacological analysis was conducted to search for key genes and signaling pathways associated with AC and MIRI. The infarct size of the rat heart was evaluated using 2,3,5‑triphenyltetrazolium chloride staining, and the serum levels of creatine kinase MB isoenzyme, cardiac troponin I, malondialdehyde and superoxide dismutase were subsequently detected in an in vivo experiment. The inhibitory effect of AC on oxidative stress was further confirmed by assessing the intracellular accumulation of reactive oxygen species (ROS). Hematoxylin and eosin staining was subsequently carried out to observe cardiac histopathological damage. The anti‑apoptotic effects of AC were determined using terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling assay and Hoechst 33342 staining, and the expression levels of apoptosis‑associated proteins in the myocardial tissue were assessed using immunohistochemical analysis. In addition, cell viability was determined using a Cell Counting Kit‑8 assay, and the expression levels of key target proteins associated with AC and MIRI were detected by western blot analysis. The results suggested that pretreatment with AC could mitigate MIRI‑induced myocardial damage, oxidative stress and apoptosis. The anti‑apoptotic effects of AC were associated with elevated Bcl‑2 levels, and reduced caspase‑3 and Bax expression levels in myocardial tissue. In vitro, AC pretreatment both led to an increased rate of cell survival and alleviated oxidative stress, as demonstrated by a decreased level of intracellular ROS accumulation. Moreover, guided by the network pharmacological analysis, heat‑shock protein 90AA1 (HSP90AA1) and the phosphoinositide 3‑kinase (PI3K)/serine‑threonine protein kinase (Akt) signaling pathway emerged as key targets for the action of AC against MIRI. Furthermore, the western blot analysis results showed that pretreatment with AC led to a significant increase in the activity of the PI3K/Akt signaling pathway, in addition to increased expression levels of glycogen synthase kinase‑3β and HSP90AA1. Taken together, the findings of the present study revealed that AC may exert cardioprotective effects on MIRI through suppressing apoptosis and oxidative stress by regulating the expression and activity of key proteins.

In vivo and in silico study of europinidin against streptozotocin-isoproterenol-induced myocardial damage via alteration of hs-CRP/CPK-MB/Caspase-3/Bcl-2 pathways

Europinidin is a novel anthocyanidin found in the petals of Plumbago europea that exhibits several physiological effects. Research was conducted to assess europinidin’s cardioprotective efficacy in a diabetic and myocardial infarction (MI) experimental model. Rat was injected through the intraperitoneal administration of 45 mg/kg of streptozotocin (STZ), while MI was induced by subcutaneously administering 85 mg/kg of isoproterenol (ISP) at 24 and 48 h prior to the sacrifice procedure. Europinidin 10 and 20 mg/day was administered orally for 4 weeks after validation of diabetes (glucose > 250 mg/dl) on the 7th day. Experimental rats were randomly allocated to control, STZ-ISP control, STZ-ISP + europinidin-10 mg, STZ-ISP + europinidin-20 mg and europinidin 20 mg perse group. Biochemicals parameters including anti-diabetic (Glucose, HbA1c, serum insulin), cardiac markers (hs-CRP, CPK-MB), dyslipidaemia (lipid analysis), anti-inflammatory (IL6, TNF-α and IL-β), oxidative stress (MDA) and antioxidant (SOD, CAT and GSH), kidney function (creatinine), liver function (AST) and pancreatic function (lipase) along with apoptosis markers (Bcl-2, caspase-3) were evaluated. In addition, histopathological indices of heart injury were investigated. In addition, molecular docking (AUTODOCK Tools 1.5.6.) and dynamics were performed. Europinidin (10 and 20 mg/day) reduced blood glucose, HbA1c, hs-CRP, and CPK-MB. It improved serum insulin, blood lipid profile and reduced inflammatory cytokines (IL-6, TNF-α, IL-β), oxidative stress and increased antioxidant enzymes (SOD, CAT and GSH). Europinidin also protected renal, hepatic functions and restored apoptosis markers (increased Bcl-2, decreased caspase-3 levels). Histopathological analysis demonstrated a reduced extent of myocardial necrosis and fibrosis. Europinidin binds in silico to proteins 1NME, 1I0E, 3I2Y and 4AQ3 with energies of -7.038, -6.682, -8.6 and − 8.761 kcal/mol, respectively. While molecular dynamics simulation studies supported the interactions of europinidin with important therapeutic target proteins. Europinidin demonstrates significant cardioprotective and anti-diabetic potential in a diabetic MI experimental model.

Effect of rapamycin-eluting stents on in-stent restenosis and early inflammatory response in coronary artery narrowing animal models

Objectiveit was to evaluate the efficacy and safety of rapamycin-eluting stents at different doses in the treatment of coronary artery narrowing in miniature pigs.Methodsa total of 20 miniature pigs were randomly assigned into four groups: S1 group (low-dose rapamycin-coated stent, 55 µg/mm2), S2 group (medium-dose rapamycin-coated stent, 120 µg/mm2), S3 group (high-dose rapamycin-coated stent, 415 µg/mm2), and D0 group (bare metal stent). The stent size was 3.0 mm × 18 mm, with an over-expansion ratio of 1.1. Each group consisted of five pigs. Stent implantation was followed by euthanasia and tissue collection after 1 month. Vascular measurements, inflammatory response scores, cardiovascular injury scores, endothelialization scores, liver and kidney function indices, and myocardial injury markers were compared among the groups.Resultsthe neointimal thickness in the S2 and S3 groups was significantly lower than that in the S1 and D0 groups (S1 group: 24.08 ± 3.95, S2 group: 1.86 ± 0.28, S3 group: 2.72 ± 0.74, D0 group: 22.85 ± 3.15, P < 0.05). The residual lumen area in the S2 and S3 groups was significantly larger than that in the S1 and D0 groups (S1 group: 2.73 ± 0.51, S2 group: 4.25 ± 0.78, S3 group: 3.91 ± 0.73, D0 group: 2.91 ± 0.44, P < 0.05). The neointimal area in the S2 and S3 groups was significantly smaller than that in the S1 and D0 groups (S1 group: 3.44 ± 0.84, S2 group: 1.78 ± 0.25, S3 group: 2.07 ± 0.41, D0 group: 3.43 ± 0.72, P < 0.05). The degree of lumen narrowing in the S2 and S3 groups was significantly lower than that in the S1 and D0 groups (S1 group: 44.25 ± 3.66%, S2 group: 14.19 ± 2.01%, S3 group: 15.29 ± 2.45%, D0 group: 21.79 ± 3.51%, P < 0.05). The inflammation scores of coronary artery walls in the S2 and S3 groups of miniature pigs were markedly lower than those in the S1 and D0 groups (P < 0.05). The cardiovascular injury scores (P = 0.072) and endothelialization scores (P = 0.085) differed slightly among the four groups (P > 0.05). Post-operative liver function indicators (alanine transaminase, aspartate transaminase), kidney function indicators (blood urea nitrogen, serum creatinine), and myocardial injury markers (creatine kinase, creatine kinase-MB) also showed neglectable differences among the four groups (P > 0.05).Conclusionmedium and high doses of rapamycin-eluting stents effectively inhibit neointimal hyperplasia and local vascular inflammatory response in miniature pigs without causing damage to liver and kidney functions or myocardial cells. These stents demonstrate high efficacy and safety. Rapamycin-coated coronary stents, as an effective treatment for coronary artery stenosis, may achieve further improvement in therapeutic efficacy through optimization of drug dosage and stent design.

Dichloroacetate: A metabolic game-changer in alleviating macrophage inflammation and enhancing recovery after myocardial infarction.

Dichloroacetate (DCA) has shown potential in modulating cellular metabolism and inflammation, particularly in cardiac conditions. This study investigates DCA's protective effects in a mouse model of myocardial infarction (MI), focusing on its ability to enhance cardiac function, reduce inflammation, and shift macrophage polarization from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype. An acute MI model was created using left anterior descending coronary artery ligation. Mice were assigned to four groups: normal control, MI control, MI + 50 mM DCA, and MI + 100 mM DCA. Cardiac fibrosis and injury were assessed through H&E staining. Cardiac function was evaluated via echocardiography, and serum levels of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) were measured. Inflammation and apoptosis were analyzed through immunohistochemistry, ELISA, western blotting, and flow cytometry in heart tissue and RAW264.7 cells. Additionally, macrophage polarization and relevant signaling pathways were examined. DCA significantly improved cardiac function in MI mice, evidenced by reduced myocardial injury and lower CK-MB and LDH levels. It also decreased inflammatory cytokines (TNF-α, IL-6 and IL-1β) and facilitated macrophage polarization from M1 to M2. Western blotting revealed that DCA inhibited iNOS and COX2 while enhancing Arg1 expression, alongside improved mitochondrial function and reduced apoptosis. Additionally, by injecting AAV-PDHK4 (pyruvate dehydrogenase kinase) into MI mice, we found that DCA effectively inhibited the progression of MI through the suppression of PDHK4. DCA protects against myocardial infarction by enhancing cardiac function, reducing inflammation, and promoting macrophage polarization, likely through inhibition of PDHK4 and NF-κB pathways, positioning it as a potential therapeutic strategy for cardiac repair post-MI.

Comparison of thromboelastographic profiles and clinical characteristics in children with severe Mycoplasma pneumoniae pneumonia

BackgroundThis study aimed to compare Thromboelastographic (TEG) profiles and clinical characteristics between severe Mycoplasma pneumoniae (MP) pneumonia patients with normal and abnormal TEG parameters.MethodsThe clinical data of 133 children with severe MP pneumonia were retrospectively analyzed. Patients were divided into normal (n = 76) and abnormal (n = 57) TEG groups. Demographic characteristics, clinical manifestations, laboratory findings, imaging features, bronchoscopy results, treatment, complications, and outcomes were compared between groups.ResultsThe abnormal TEG group (42.9%) had longer fever duration (median: 8.5 vs. 7.0 days, P &amp;lt; 0.001) and hospital stay (median: 11.5 vs. 10.0 days, P = 0.003). They also showed higher levels of C-reactive protein (median: 30.2 vs. 20.1 mg/L, P &amp;lt; 0.001), lactate dehydrogenase (median: 334.5 vs. 276.0 U/L, P = 0.001), and D-dimer (median: 1.2 vs. 0.5 μg/ml, P &amp;lt; 0.001). HRCT revealed more lobar consolidation or multilobar involvement (36.8% vs. 18.4%, P = 0.016), and bronchoscopy showed more mucous plug obstruction (28.1% vs. 10.5%, P = 0.008) in the abnormal TEG group. TEG parameters indicated a hypercoagulable state with shorter R time (P &amp;lt; 0.001), shorter K time (P &amp;lt; 0.001), and higher MA (P = 0.003). The abnormal TEG group had higher incidences of coagulopathy (P &amp;lt; 0.001), cardiac involvement (elevated cardiac enzymes: 36.8% vs. 17.1%, P = 0.009; pericardial effusion: 10.5% vs. 1.3%, P = 0.017), and plastic bronchitis (P = 0.006). They also required longer azithromycin courses (median: 15 vs. 14 days, P = 0.026).ConclusionChildren with severe MP pneumonia and abnormal TEG profiles have more severe clinical manifestations, higher inflammatory markers, more extensive lung involvement, and a higher incidence of complications. TEG may help identify high-risk patients and guide management in severe MP pneumonia.