Cardiac Biomarkers Research Articles

Novel cardiac extracellular matrix biomarkers in STEMI: Associations with ischemic injury and long-term mortality.

We aimed to determine whether serum levels of proteins related to changes in cardiac extracellular matrix (ECM) were associated with ischemic injury assessed by cardiac magnetic resonance (CMR) and mortality in patients with ST-elevation myocardial infarction (STEMI). The concentrations of six ECM-related proteins (periostin, osteopontin, syndecan-1, syndecan-4, bone morphogenetic protein 7, and growth differentiation factor (GDF)-15) were measured in serum samples from patients on Day 1 and Month 4 after STEMI (n = 239). Ischemic injury was assessed by myocardial salvage index, microvascular obstruction, infarct size, and left ventricular function measured by CMR conducted during the initial admission (median 2 days after admission) and after 4 months. All-cause mortality was recorded after a median follow-up time of 70 months. Levels of periostin increased from Day 1 to Month 4 after hospitalization, while the levels of GDF-15, osteopontin, syndecan-1, and syndecan-4 declined. At both time points, high levels of syndecan-1 were associated with microvascular obstruction, large infarct size, and reduced left ventricular ejection fraction, whereas high levels of syndecan-4 at Month 4 were associated with a higher myocardial salvage index and less dilatation of the left ventricle. Higher mortality rates were associated with periostin levels at both time points, low syndecan-4 levels at Month 4, or high GDF-15 levels at Month 4. In patients with STEMI, we found an association between serum levels of ECM biomarkers and ischemic injury and mortality. The results provide new insight into the role ECM components play in ischemic injury following STEMI and suggests a potential for these biomarkers in prognostication after STEMI.

Dual delivery of carbon monoxide and doxorubicin using haemoglobin-albumin cluster: proof of concept for well-tolerated cancer therapy.

A serious concern of doxorubicin (DOX) therapy is that it causes severe adverse effects, particularly cardiotoxicity. Carbon monoxide (CO) possesses powerful cytoprotective effects against drug-induced organ injury and is expected to ameliorate DOX-induced cardiotoxicity. In this study, a dual carrier of DOX and CO (CO-HemoAct-DOX) was fabricated based on a haemoglobin-albumin cluster (HemoAct), which is a protein cluster with a haemoglobin core structure wrapped by serum albumin. CO-HemoAct-DOX was synthesised by binding CO to a haemoglobin core and covalently conjugating (6-maleimidocaproyl)hydrazone derivative of DOX to an albumin shell. The average DOX/cluster ratio was about 2.6. In the in vitro cytotoxicity assay against cancer cells, the anti-tumour activity of CO-HemoAct-DOX was 10-fold lower than that of DOX in a 2D-cultured model, whereas CO-HemoAct-DOX suppressed the growth of tumour spheroids to the same extent as DOX in the 3D-cultured model. In colon-26 tumour-bearing mice, CO-HemoAct-DOX achieved DOX delivery to the tumour site and alleviated tumour growth more effectively than DOX. Furthermore, CO-HemoAct attenuated DOX-induced cardiomyocyte atrophy in H9c2 cells and elevated the levels of cardiac biomarkers in mice exposed to DOX. These results suggest that the dual delivery of CO and DOX using HemoAct is a promising strategy as an anti-tumour agent to realise well-tolerated cancer therapy with minimal cardiotoxicity.

Review of the Diagnostic and Prognostic Values of Cardiac Markers in Diabetes

Abstract Introduction Cardiovascular disease is a leading cause of mortality in people with diabetes (PWD). We aimed to explore the role of troponin T (TnT) and probrain natriuretic peptide (proBNP) as screening and prognostic indicators of cardiovascular morbidity and mortality in PWD in the existing literature. Methods This review paper is a focused narrative nonsystematic review of the literature which examined relevant publications pertinent to the significance of cardiac biomarkers. We aimed to investigate the diagnostic value of cardiac TnT (cTnT) and cTnI in addition to proBNP in diabetes and the prognostic value of cTnT and proBNP in diabetic and nondiabetic patients. The process of searching through literature was conducted from December 2022 to April 2023. Searches were done across PubMed and Google Scholar databases to identify relevant articles published from January 2001 to April 2023. The selected were entered into EndNote 20 software to extract the title and abstract. Results A total of 75 articles were identified in Google Scholar in addition to 32 articles from PubMed. After a thorough review, only a total of 22 articles were selected, pointing out those which discussed the pathophysiology and diagnostic, prognostic, and screening values of the types of Tn and proBNP markers. The value of TnT in PWD, specifically T2D, is threefold higher than in healthy patients. Individuals with high levels of high-sensitivity (hs) cTnI or cTnT were at the highest mortality risk. Nonetheless, N-terminal (NT)-proBNP and TnT function independently as predictors of unfavorable outcomes. Conclusions TnT is an important early screening tool prognostic indicator. Elevated TnT was associated with an increased risk of cardiovascular events in PWD. hs-cTn may help diabetes-related clinical care for older persons by identifying those at high mortality risk; furthermore, in diabetic individuals, NT-pro-BNP appears to be 92% sensitive and 90% specific for the diagnosis of heart failure.

Transcriptomics coupled with proteomics reveals osimertinib-induced myocardial mitochondrial dysfunction

Osimertinib, an irreversible epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) used for cancer treatment, can cause significant cardiac toxicity. However, the specific mechanism of osimertinib-induced cardiotoxicity is not fully understood. In this study, we administered osimertinib to mice and neonatal rat ventricular myocytes (NRVMs). We observed significant structural and functional damage to the hearts of these mice, along with a marked increase in cardiac injury biomarkers and accompanying ultrastructural damage to mitochondria. We integrated 4D label-free protein quantification and RNA-Seq methods to analyze the sequencing data of NRVMs under osimertinib treatment (0 and 2.5 μM). Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis evidenced that differentially expressed genes (DEGs)and differentially expressed proteins (DEPs) were distinctly enriched for oxidative phosphorylation (OXPHOs). Simultaneously, osimertinib primarily affected the contents of adenosine triphosphate (ATP). Further investigations revealed that osimertinib disrupts the functions of the ATP synthase (complex V), leading to a reduction in ATP production. Taken together, our data demonstrated that osimertinib causes mitochondrial dysfunction, which in turn leads to the onset of cardiac toxicity.

EFFICACY AND SAFETY OF NICORANDIL FOR PERIPROCEDURAL MYOCARDIAL INJURY IN PATIENTS UNDERGOING PCI

Coronary artery disease (CAD) remains a leading cause of morbidity and mortality globally, with percutaneous coronary intervention (PCI) being a typical therapeutic approach. Objectives: In this comparative study, we aimed to investigate the efficacy and safety of nicorandil for periprocedural myocardial injury in patients undergoing PCI. Methods: This comparative study was conducted at Ayub Teaching Hospital from September 2023 to December 2023. Data from 90 patients was recruited for the research using inclusion and exclusion screening standards. Our study was performed on 90 patients treated with percutaneous coronary intervention (PCI). Patients from Group 1 were different from those in Group 2. Group A: the critical study parameters will switch between those patients who received nicorandil and Group B: non-nicorandil patients. Baseline demographic data, past medical history, and relevant laboratory values and clinical characteristics were documented for all patients. In addition, an intraoperative laboratory investigation was conducted, including cardiac biomarkers. Results: Research data were drawn from 90 patients whose gender wasn't a factor based on the research protocol. In Group A, the mean age of the patients was 62 years. Players in group A played for 4 ± 8.5 years. In team B, the players had a slightly longer experience and played for 63. Humans on Earth could do the same, and it could significantly impact future generations: ± 7. 9 years. Of 58 men and 32 women in the control group, there were two persons and persons in the experimental group, respectively. Only one stent differed between the two groups; however, the number was similar. 8 ± 0. 6 mmol/l in the tricorandil group and 1. +9 ± 0 in Case 1. Patients in the Nicorandil group displayed the lowest level of heart problem-causing protein (troponin) at the peak (5. There is a statistically significant 1.8-fold (2 ng/mL versus seven ng/mL) decline in serum lysozyme levels in the group administered rhG-CSF. The treatment group exhibited a substantial increase in haemoglobin levels (t(12) = 3. 74, p-value <0.005) with a mean difference of 0. 5 ± 2 ng/mL. 001, 95% CI: 2. 1 to 3. 5). Conclusion: It is concluded that nicorandil shows positive results for the efficacy (the ability of a drug to bring the desired effect) and safety of the drug in reducing myocardial injury and in maintaining the function of myocardial during percutaneous coronary intervention in patients.

Prognostic utility of point-of-care measured bioadrenomedullin in patients presenting with acute heart failure at the emergency department

Abstract Funding Acknowledgements None. Background Acute heart failure (AHF) is a severe condition that is frequently encountered in the emergency department (ED). We aimed to investigate the role of bioadrenomedullin (bio-ADM)- a molecule previously shown to be associated with clinical congestion- as an early prognostic marker for short-term outcomes in patients presenting with AHF in the ED. Methods Seventy-six AHF patients were prospectively enrolled upon ED presentation. Clinical, echocardiography, standard laboratory and cardiac biomarker assessments were performed. Bio-ADM was measured from whole blood sample using a commercially available point-of-care immunoassay. We examined prognostic utility of bio-ADM for predicting 30-day mortality. Results Study group consisted of 61% males, of mean(±SD) age 71±13years, systolic blood pressure (SBP) 140±41mmHg, categorized according to AHF clinical phenotypes as 15(20%) pulmonary edema, 53(70%) decompensated chronic HF and 8(10%) cardiogenic shock. Median (IQR) creatinine, NTproBNP, hsTroponinT and bio-ADM were: 1.15(0.90-1.83)mg/dl, 5094(2836-12816)pg/ml, 38(24-91)pg/ml and 52.3(45-113)pg/ml, respectively. Levels of bio-ADM were higher in patients with cardiogenic shock compared to acute pulmonary edema and decompensated chronic HF [median (IQR): 266.8(101.9-500)pg/ml, 49.8(45-67.5)pg/ml and 47.4(45-97.5)pg/ml, respectively], (p=0.019). Log(bio-ADM) was significantly correlated with SBP (Spearman rho= -0.387, p=0.003), logCreatinine (rho=0.430, p<0.001), log(NTproBNP) (rho=0.430, p=0.003) and log(hsTroponinT) (rho= 0.386, p=0.003). During 30-days follow-up, 15 patients died. In ROC analysis, a bio-ADM cutoff of 64.8pg/ml predicted 30-day mortality with 75% sensitivity and 65% specificity (AUC 0.763, p=0.017). In a multivariable Cox proportional hazards model that included log(bio-ADM), log(NTproBNP) and logCreatinine and adjusted for AHF phenotype, only log(bio-ADM) seemed to be independently prognostic of 30-day mortality (HR,95%CI: 5.80, 0.97-34.66, p=0.054). Conclusions In a broad AHF population, point-of-care bio-ADM measured upon presentation at the ED is associated with worse clinical and biochemical AHF profiles and may provide independent prognostic information for 30-day mortality.30-day mortality by bio-ADM ≥ vs <64.8

Cardiac biomarkers for diagnosing Takotsubo syndrome.

Cardiac biomarkers for diagnosing Takotsubo syndrome.

Empagliflozin to prevent progressive adverse remodelling after myocardial infarction (EMPRESS-MI): rationale and design.

Patients with a reduced left ventricular ejection fraction (LVEF) following an acute myocardial infarction (MI) are at risk of progressive adverse cardiac remodelling that can lead to the development of heart failure and death. The early addition of a sodium-glucose cotransporter 2 (SGLT2) inhibitor to standard treatment may delay or prevent progressive adverse remodelling in these patients. EMpagliflozin to PREvent worSening of left ventricular volumes and Systolic function after Myocardial Infarction (EMPRESS-MI) is a randomized, double-blind, placebo-controlled, multi-centre trial designed to assess the effect of empagliflozin on cardiac remodelling evaluated using cardiovascular magnetic resonance (CMR) in 100 patients with left ventricular systolic dysfunction following MI. Eligible patients were those ≥12h and ≤14days following acute MI, with an LVEF <45% by CMR. Patients were randomized to empagliflozin 10mg once a day or matching placebo. The primary outcome will be change in left ventricular end-systolic volume indexed to body surface area over 24weeks from randomization. Secondary endpoints include measures of left ventricular and atrial volumes, left ventricular mass, LVEF, and circulating cardiac biomarkers. EMPRESS-MI will assess the effect of the SGLT2 inhibitor empagliflozin on cardiac remodelling in patients with left ventricular systolic dysfunction after an acute MI.

Abstract PO5-15-01: Prospective Biomarker Assessment of Cardiotoxicity Among Ethnically Diverse Women with Early Breast Cancer

Abstract Background: Approximately 4.1 million women in the United States are living with breast cancer1. Cardiac dysfunction is a significant adverse effect of commonly used breast cancer therapies like doxorubicin (D) and trastuzumab (T). The cardiotoxicity (CTox) associated with these agents manifests as a reduction in left ventricular ejection fraction (LVEF) with or without signs and symptoms of heart failure. Purpose: The objective of this study is to evaluate serum cardiac and inflammatory biomarkers over time and their association with CTox development. Methods: A total of 133 newly diagnosed stage I-III invasive breast cancer patients were enrolled in a prospective clinical trial (2013-2017) and received standard of care T and/or D based systemic therapy. They underwent serial echocardiograms every 6 months for two years and then based on clinical need for a total of six years. CTox was defined as a &amp;gt;10% drop in LVEF, and/or LVEF &amp;lt; 50%. Biomarker data was collected at baseline, 12 and 24 months and included both cardiac biomarkers (Troponin-I, TN-I and amino terminal B-type natriuretic peptide, NT-proBNP) and measures of inflammation (C-reactive protein, CRP). Of the 32 with CTox patients, 15 had adequate serum samples and were matched with 15 patients without CTox (N=30), controlling for age, race, and treatment regimen prior to serum sample analysis. Results: The mean LVEF at baseline was similar between CTox and non-CTox patients (64% vs 62%, p=0.342). However, over the course of 12 and 24 months, CTox patients experienced a statistically significant decrease in LVEF compared to their baseline values (55% and 56%, respectively, p &amp;lt; 0.001). At baseline, CTox patients had higher CRP levels compared to non-CTox (13.4 mg/L vs 3.35 mg/L), however this difference did not reach statistical significance (P &amp;gt;0.05). Although this difference seemed to narrow at 12 months (3.88 mg/L vs 1.52 mg/L, p&amp;lt; 0.05) and 24 months (6.85 mg/L vs 2.36 mg/L, p&amp;lt; 0.05), CTox patients consistently had higher mean CRP levels. Mean TN-I levels increased at both 12 and 24 months compared to baseline (CTox 1.13 ng/L, 7.13 ng/L, 4.13 ng/L vs non-CTox 0.800 ng/L, 8.13 ng/L, 4.60 ng/L, p&amp;lt; 0.05) but there were no significant differences between the two groups (p &amp;gt;0.05). While baseline NT-proBNP levels did not differ significantly between the CTox and non-CTox patients, there were statistically significant increases in CTox patients at 12 and 24 months (205 pg/mL vs 74 pg/mL, and 200 pg/mL vs 96 pg/mL, p &amp;lt; 0.01, respectively). Conclusion: In a well characterized, diverse, matched subset of patients with early breast cancer who were prospectively followed with serial echocardiograms, distinct biomarker patterns were observed. Measures of inflammation (CRP) at baseline were different and these changes appeared to diminish over time. While the cardiac biomarker TN-I appeared to increase in both +CTox and -CTox group over time, only those with differential NT-proBNP elevations were associated with cardiotoxicity. 1Lisa Gallicchio, PhD and others, Estimation of the Number of Individuals Living With Metastatic Cancer in the United States, JNCI: Journal of the National Cancer Institute, Volume 114, Issue 11, November 2022, Pages 1476–1483 Citation Format: Shahzaad Jahangier, Rubina Qamar, Maharaj Singh, Vinay Thohan, James Weese, Bijoy Khandheria, Anna Kamke-Jordan. Prospective Biomarker Assessment of Cardiotoxicity Among Ethnically Diverse Women with Early Breast Cancer [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO5-15-01.

Abstract PO4-12-07: INSTITUTIONAL EXPERIENCE IN PATIENTS WITH EARLY BREAST CANCER WHO RECEIVED CARDIOTOXIC THERAPY IN CARDIONCOLOGY UNIT

Abstract Introduction: Early breast cancer (eBC) is the most frequent malignancy diagnosed in women worldwide; fortunately, survival is increasing related to early diagnosis and the incorporation of new drugs. In this scenario, preventing long-term toxicities become essential. Cardiac adverse events related to anthracyclines or trastuzumab such as reduction in left ventricular (LV) systolic function and clinical heart failure (HF), are well known and are the leading cause of morbidity in breast cancer survivors. Cardioprotective strategies and early diagnoses of asymptomatic cardiac dysfunction are essential to optimized management and prevention of overt cardiovascular (CV) disease. We made a specific cardiac assessment within an Oncocardiology multidisciplinary Unit in patients receiving anticancer therapies. We present the experience in patients with eBC treated with anthracyclines, trastuzumab or both in the past five years. Materials and Methods: We conducted an institutional, interventional, prospective study in patients who received anthracyclines, trastuzumab or both according to the standard of care (SoC) in eBC. Basal CV risk stratification included lipid profile, glycated haemoglobin, high-sensitive troponin T (hs-TnT) and N-terminal ProB-type natriuretic peptide (NT-ProBNP) was done. Image assessment was done by echocardiogram (echo), including myocardial deformation assessed by speckle tracking (STRAIN). Follow-up was done according to anthracycline or trastuzumab therapy with echo and cardiac biomarkers during the systemic therapy and at the end of anticancer treatment, 1, 2 and 5 years after. Patients with uncontrolled CV risks factors according to local protocol, asymptomatic cardiac dysfunction defined as decreased strain (&amp;gt;15% compared with baseline) or increased cardiac biomarkers (Hs-TnT &amp;gt;14 at baseline or x3 basal value during the follow-up; NT-ProBNP &amp;gt; 300 in patients with &amp;lt; 50y; &amp;gt; 600 in patients between 50-75-y or &amp;gt;900 in patients &amp;gt; 75 years or older) or patients who develop heart failure during the treatment or follow-up were referred to cardiologist. Results: between 2018 and 2022, 1125 patients were diagnosed with eBC in our institution, and 435 patients received systemic treatment with anthracyclines, trastuzumab or both. During the study period, 165 of these patients were referred to the cardio-oncologist. 60% received treatment with anthracyclines, 36% with trastuzumab and 4.1% with both. The median age was 58(±23.2), 60% had previous CV risk factors. The main reason to refer patients to the cardio-oncologist was asymptomatic cardiac dysfunction and uncontrolled CV risk factors. (Table 1). 60% of patients initiated angiotensin-converting-enzyme inhibitors or Beta-blockers, and only two patients stopped anticancer therapy due to severe cardiac dysfunction. The period of high risk of developing cardiotoxicity was the first year after the end of treatment. Conclusion: multidisciplinary evaluation within a cardio-oncology unit is useful to optimize CV risk factors and to detect asymptomatic cardiac dysfunction in patients receiving cardiotoxic drugs. Table 1. Main reasons to refer patients to cardiologist. Citation Format: Tamara Martos, Laia Carla Belarte-Tornero, Mireia Ble, Eva Gimeno, Laura Sanhauja, Felicidad Martines-Medina, Maria Martinez-García, Maria Castro-Henriques, Joan Albanell, Sonia Servitja. INSTITUTIONAL EXPERIENCE IN PATIENTS WITH EARLY BREAST CANCER WHO RECEIVED CARDIOTOXIC THERAPY IN CARDIONCOLOGY UNIT [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO4-12-07.

Modeling the Impact of Biomarker-Guided Versus ASCVD Risk-Guided Drug Treatment in US Adults With Stage 1 Hypertension: The National Health and Nutrition Examination Survey, 1999 to 2004.

Guidelines recommend antihypertensive medication for adults with both stage 1 hypertension (systolic blood pressure, 130-139 mm Hg or diastolic blood pressure, 80-89 mm Hg) and 10-year atherosclerotic cardiovascular disease (ASCVD) risk ≥10%. Cardiac biomarkers could facilitate a more targeted approach to the treatment of stage 1 hypertension. We studied 1999 to 2004 National Health and Nutrition Examination Survey participants aged ≥20 years with untreated stage 1 hypertension without heart failure or ASCVD. hs-cTnI (high-sensitivity cardiac troponin I) and hs-cTnT (high-sensitivity cardiac troponin T) and NT-proBNP (N-terminal pro-B-type natriuretic peptide) were measured in stored serum. We used the Pooled Cohort Equations to predict 10-year ASCVD risk. All participants had linked mortality follow-up through December 31, 2019. Overall, 17.5% of US adults (32.2 million) had untreated stage 1 hypertension. Among these 32.2 million persons, 15.7% had ASCVD risk ≥10%, 5.6% had elevated hs-cTnI, 4.7% had elevated hs-cTnT, and 9.5% had elevated NT-proBNP. Among adults aged 65 to 79 years with untreated stage 1 hypertension, 80.5% had ASCVD risk ≥10%, 13.0% had elevated hs-cTnI, 15.2% had elevated hs-cTnT, and 29.4% had elevated NT-proBNP. Less than half of the adults aged ≥80 years with untreated stage 1 hypertension had elevated biomarkers. The cardiovascular disease mortality rates among all adults with untreated stage 1 hypertension and with either ASCVD risk ≥10%, elevated hs-cTnI, elevated hs-cTnT, or elevated NT-proBNP were 7.51, 7.74, 8.75, and 5.87 per 1000 person-years, respectively. Cardiac biomarkers may be more selective for informing risk-based treatment decisions in stage 1 hypertension, particularly among adults aged ≥65 years.

Cardiac biomarkers in patients with hypoplastic left heart syndrome and Fontan circulation: The effects of aerobic exercise training on single ventricle circulation

Cardiac biomarkers in patients with hypoplastic left heart syndrome and Fontan circulation: The effects of aerobic exercise training on single ventricle circulation

Elevated CA125 levels using ABEI-based assay in heart failure: Correlation with disease severity and cardiac biomarkers

Elevated CA125 levels using ABEI-based assay in heart failure: Correlation with disease severity and cardiac biomarkers

Integrated serum pharmacochemistry with network pharmacology and pharmacological validation to elucidate the mechanism of Yiqitongmai decoction (YQTMD) against myocardial infarction

Ethnopharmacological relevanceYiqitongmai decoction (YQTMD), a classic TCM, has been widely used in clinical treatment for MI. However, it is still difficult to clarify the potential active compounds and pharmacological mechanisms of it in treating MI. Aim of the studyTo explore the active ingredients, pharmacological effects, potential targets and mechanisms of YQTMD against MI. Materials and MethodsSerum pharmacochemistry by UPLC-MS/MS was applied to analyze the phytochemical components in serum from YQTMD. These components were then used to predict the potential targets using network pharmacology approach and molecular dynamics simulations, and then the protective effect of them on H9c2 cells following hypoxic conditions was assessed. Afterwards, the pharmacological effects of YQTMD on MI in mice were tested by determining electrocardiogram (ECG), echocardiography, cardiac biomarkers, oxidative stress, inflammation and pathophysiological changes. The protein levels involving STAT3 signal were detected using western blot and immunofluorescence assays. Furthermore, STAT3 inhibitor Sttatic was employed to further elucidate the underlying mechanisms. ResultsTotally, 26 compounds derived from YQTMD were identified in mice serum, and 201 genes associated with the compounds were collected. The compounds including safflomin A, ferulic acid, gypenoside XVII, ginsenoside Rg1 and glycyrrhizic acid were identified as the critical compounds of YQTMD to regulate STAT3 pathway.In vitro, compounds combination significantly enhanced the viability of H9c2 cells and reduced ROS level compared to model cells. The in vivo results showed that YQTMD effectively reduced myocardial injury, as evidenced by the decreased serum cardiac injury markers, reduction in the size of myocardial infarct, restoration of abnormal alterations in ECG and decrease in cardiomyocyte apoptosis. Additionally, YQTMD attenuated MI-induced cardiac dysfunction, alleviated pathological changes, reduced MDA levels, and enhanced SOD and GSH levels compared with model mice. Significantly, the levels of IL-6, IL-1β, and TNF-α were observed to decrease in the YQTMD group. The expression levels of key proteins (p-STAT3, HIF-1α, NOX2, TLR5 and Caspase3) in STAT3 pathway were also regulated by YQTMD. However, the cardioprotective effects of YQTMD on MI were attenuated by STAT3 inhibitor Sttatic. ConclusionsThis study investigated the active ingredients and potential mechanisms of YQTMD for MI treatment based on serum pharmacochemistry and network pharmacology approaches, revealing that YQTMD exerts its therapeutic effects on MI by alleviating oxidative stress, inflammation and apoptosis through adjusting STAT3 signaling pathway.

The management of heart failure patients in a value-based healthcare system: The role of cardiac biomarkers

The management of heart failure patients in a value-based healthcare system: The role of cardiac biomarkers

Characterization of clinical serum cardiac biomarker levels in individuals with Friedreich ataxia

Friedreich ataxia is a progressive autosomal recessive neurodegenerative disorder characterized by ataxia, dyscoordination, and cardiomyopathy. A subset of patients with Friedreich ataxia have elevated levels of serum cardiac troponin I, but associations with disease outcomes and features of cardiomyopathy remain unclear. In this study, we characterized clinically obtained serum cardiac biomarker levels including troponin I, troponin T, and B-type natriuretic peptide in subjects with Friedreich ataxia and evaluated their association with markers of disease. While unprovoked troponin I levels were elevated in 36% of the cohort, cTnI levels associated with a cardiac event (provoked) were higher than unprovoked levels. In multivariate linear regression models, younger age predicted increased troponin I values, and in logistic regression models younger age, female sex, and marginally longer GAA repeat length predicted abnormal troponin I levels. In subjects with multiple assessments, mean unprovoked troponin I levels decreased slightly over time. The presence of abnormal troponin I values and their levels were predicted by echocardiographic measures of hypertrophy. In addition, troponin I levels predicted long-term markers of clinical cardiac dysfunction over time to a modest degree. Consequently, troponin I values provide a marker of hypertrophy but only a minimally predictive biomarker for later cardiac manifestations of disease such as systolic dysfunction or arrhythmia.

Evaluating the progression of acute coronary syndrome through the association of cardiac biomarkers with biochemical tests

Evaluating the progression of acute coronary syndrome through the association of cardiac biomarkers with biochemical tests

Changes in blood metabolomes as potential markers for severity and prognosis in doxorubicin-induced cardiotoxicity: a study in HER2-positive and HER2-negative breast cancer patients.

We aimed to compare the changes in blood metabolomes and cardiac parameters following doxorubicin treatment in HER2-positive and HER2-negative breast cancer patients. Additionally, the potential roles of changes in blood metabolomes as severity and prognostic markers of doxorubicin-induced cardiotoxicity were determined. HER2-positive (n = 37) and HER2-negative (n = 37) breast cancer patients were enrolled. Cardiac function assessment and blood collection were performed at baseline and 2weeks after completion of doxorubicin treatment in all patients, as well as at three months after completion of doxorubicin treatment in HER2-negative breast cancer patients. Blood obtained at all three-time points was processed for measuring cardiac injury biomarkers. Blood obtained at baseline and 2weeks after completion of doxorubicin treatment were also processed for measuring systemic oxidative stress and 85 metabolome levels. Cardiac injury and systolic dysfunction 2weeks after completion of doxorubicin treatment were comparable between these two groups of patients. However, only HER2-negative breast cancer patients exhibited increased systemic oxidative stress and cardiac autonomic dysfunction at this time point. Moreover, 33 and 29 blood metabolomes were altered at 2weeks after completion of doxorubicin treatment in HER2-positive and HER2-negative breast cancer patients, respectively. The changes in most of these metabolomes were correlated with the changes in cardiac parameters, both at 2weeks and 3months after completion of doxorubicin treatment. The changes in blood metabolomes following doxorubicin treatment were dependent on HER2 status, and these changes might serve as severity and prognostic markers of doxorubicin-induced cardiotoxicity. The study was conducted under ethical approval from the Institutional Review Board of the Faculty of Medicine, Chiang Mai University (Registration number: MED-2563-07001; Date: April 28, 2020). The study also complied with the Declaration of Helsinki.

Clinical characteristics of patients with high extracellular volume fraction evaluated by cardiac computed tomography for coronary artery evaluation

Abstract Aim To evaluate the distribution of extracellular volume fraction detected via computed tomography, clinical characteristics of high extracellular volume fraction detected via computed tomography, and the rate of incidental detection of cardiac amyloidosis in patients undergoing cardiac computed tomography for coronary artery evaluation. Methods and Results This study included 874 consecutive patients (mean age, 74.4 ± 7.1 years; men, 65%), comprising men aged ≥60 years and women aged ≥70 years, who had undergone cardiac computed tomography between January 2020 and September 2022. The mean extracellular volume fraction detected via computed tomography was 29.7 ± 5.2%, and 108 patients (12.4%) had an extracellular volume fraction detected via computed tomography of ≥35%. Older age (75.9 ± 8.2 years vs. 74.2 ± 6.9 years; P = 0.042), male sex (75.9% vs. 63.0%; P = 0.007), impaired left ventricular ejection fraction, increased high-sensitivity cardiac troponin T and B-type natriuretic peptide levels, and increased left ventricular thickness showed significant associations with an extracellular volume fraction detected via computed tomography of ≥35%. Cardiac amyloidosis was diagnosed incidentally in 15 patients based on an increase in extracellular volume fraction detected via computed tomography. The prevalence of cardiac amyloidosis was 1.7% (15/874) and 14.3% (15/105) in the entire study population and in patients with an extracellular volume fraction detected via computed tomography of ≥35%, respectively. An increase in the extracellular volume fraction detected via computed tomography was suggestive of cardiac amyloidosis. Conclusion Elevated extracellular volume fraction detected via computed tomography, associated with elevated cardiac biomarker levels and myocardial structural changes, may lead to the incidental diagnosis of cardiac amyloidosis.

Clinical implications of septic cardiomyopathy: A narrative review.

Sepsis is caused by the body's dysregulated response to infection, which can lead to multiorgan injury and death. Patients with sepsis may develop acute cardiac dysfunction, termed septic cardiomyopathy, which is a global but reversible dysfunction of both sides of the heart. This narrative review discusses the mechanistic changes in the heart during septic cardiomyopathy, its diagnosis, existing treatment options regarding severity and course, and emerging treatment approaches. Although no standardized definition for septic cardiomyopathy exists, it is described as a reversible myocardial dysfunction that typically resolves within 7 to 10 days. Septic cardiomyopathy is often diagnosed based on electrocardiography, cardiac magnetic resonance imaging, biomarkers, and direct invasive and noninvasive measures of cardiac output. Presently, the treatment of septic cardiomyopathy is similar to that of sepsis, primarily focusing on acute interventions. Treatments for cardiomyopathy often include angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and diuretics. However, because of profound hypotension in sepsis, many cardiomyopathy treatments are contraindicated in patients with septic cardiomyopathy. Substantial efforts have been made to study the pathophysiological mechanisms and diagnostic options; however, the lack of a uniform definition for septic cardiomyopathy is challenging for physicians when considering treatments. Another challenge for physicians is that the treatment for septic cardiomyopathy has only focused on acute intervention, whereas the treatment for other cardiomyopathies has been provided on a long-term basis. A better understanding of the underlying mechanisms of septic cardiomyopathy may contribute to the development of a unified definition of the condition and novel treatment options.