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Cardiotoxicity

Cardiotoxicity refers to the adverse effects of substances, drugs, or other agents on the heart and cardiovascular system.
It can manifest as arrhythmias, myocardial damage, hypertension, or other cardiovascular complications.
Understanding and mitigating cardiotoxicity is crucial in drug develoment and safety assessment.
The PubCompare.ai platform leverages AI to help researchers optimize their cardiotoxicity studies by locating relevant literature, protocols, and products, while enhancing reproducibility and accuracy.
This powerful tool can take your cardiotoxicity research to new heights.

Most cited protocols related to «Cardiotoxicity»

1
ESMO Consensus Recommendations for Cardio-Oncology

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Publication 2020
Adult Anabolism ARID1A protein, human Blood Vessel Cardiac Events Cardiotoxicity Cardiovascular System Conferences Europeans Immunotherapy Neoplasms Pharmaceutical Preparations Pharmacotherapy Therapeutics
2
Harmonized Cardiomyopathy Surveillance Recommendations

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Publication 2015
Abdomen Adult Anthracyclines Anthraquinones Cardiologists Cardiomyopathies Cardiotoxicity Cardiovascular System Carotid Artery Diseases Chest Child Clinical Reasoning Congenital Abnormality Coronary Artery Disease Daunorubicin Diastole Doxorubicin Electric Conductivity Epidemiologists Epirubicin Fibrosis Genetic Heterogeneity Heart Heart Failure Idarubicin Leukemia Malignant Neoplasms Mediastinum Mitoxantrone Neoplasms North American People Nurses Oncologists Pericardium Pharmacotherapy Population Group Radiation Oncologists Radiotherapy Stenosis Survivors of Childhood Cancer Systole Therapeutics Whole-Body Irradiation
3
Calcium Flux Assay in Cardiomyocytes
Calcium flux in cardiomyocytes was assessed using the instructions provided by the EarlyTox Cardiotoxicity Kit from Molecular Devices, LLC (Table 1). Briefly, cells in 25 μL medium per well were equilibrated for 2 h at 37°C in the presence of 25 μL of prewarmed calcium dye reagent. Before treatment with test chemicals, basal calcium flux was recorded at 515–575 nm following excitation at 470–495 nm for 100 s in 0.125 s read intervals using the FLIPR tetra plate reader (Molecular Devices). The exposure time per read was 0.05 s, the gain was set to 2,000, and the excitation intensity was set to 30%. The instrument temperature was kept at a constant 37°C. Test chemicals (12.5 μL of 5× concentration working solutions) at the appropriate concentrations were added simultaneously to all wells using the instrument-specific automated liquid handler. Between subsequent readings at 10, 30, 60, and 90 min, cells were incubated at 37°C and 5% CO2.
Grimm F.A., Iwata Y., Sirenko O., Bittner M, & Rusyn I. (2015). High-Content Assay Multiplexing for Toxicity Screening in Induced Pluripotent Stem Cell-Derived Cardiomyocytes and Hepatocytes. Assay and Drug Development Technologies, 13(9), 529-546.
Publication 2015
Calcium Cardiotoxicity Cells Medical Devices Myocytes, Cardiac Tetragonopterus
4
Concentration-Response Modeling for Toxicity Assessment

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Publication 2013
Cardiotoxicity Robins Sulfoxide, Dimethyl
5
Cardiotoxicity of Cancer Therapy Cohort Study
The Cardiotoxicity of Cancer Therapy (CCT) study is an ongoing, prospective, longitudinal cohort study of breast cancer participants at the Rena Rowan Breast Cancer Center at the University of Pennsylvania (Philadelphia, PA). This study was approved by the Institutional Review Board of the University of Pennsylvania and all participants provided informed consent.
The study protocol has been previously described.19 (link) Briefly, participants were eligible to be included if they were at least 18 years of age, diagnosed with breast cancer, and treated with doxorubicin and/or trastuzumab therapy. The only exclusion criterion was pregnancy; participants with an abnormal baseline LVEF were not excluded. Treatment regimens were determined by the treating oncologist and classified into 3 primary categories: 1) doxorubicin (240 mg/m2) with concurrent cyclophosphamide, followed by paclitaxel (Dox); 2) trastuzumab with docetaxel and either cyclophosphamide or carboplatin (Tras); and 3) doxorubicin (240 mg/m2) with concurrent cyclophosphamide, followed by trastuzumab and paclitaxel (Dox+Tras).
Detailed clinical data, verified via physician medical records, and the MD Anderson Symptom Inventory – Heart Failure (MDASI-HF) survey assessing HF symptoms on a scale of 0–10, were obtained at baseline and followup.20 (link) Echocardiograms were also performed at standardized time intervals according to the prescribed treatment regimen.19 (link) In the Dox group, echocardiography was performed at baseline, at completion of paclitaxel (approximately 4 months after initiation of chemotherapy), and annually. In the Tras group, echocardiography was performed at baseline, every 3 months during trastuzumab, and annually. In the Dox+Tras group, echocardiography was performed at baseline, after doxorubicin (approximately 2 months after initiation of chemotherapy), every 3 months during trastuzumab, and annually.
The current analyses were limited to those participants enrolled between August 2010 and August 2015 who had a baseline assessment of cardiac function and at least 1 followup echocardiogram, and include echocardiography data up to 3.2 years after initiation of therapy.
Narayan H.K., Finkelman B., French B., Plappert T., Hyman D., Smith A.M., Margulies K.B, & Ky B. (2017). Detailed Echocardiographic Phenotyping in Breast Cancer Patients: Associations with Ejection Fraction Decline, Recovery, and Heart Failure Symptoms over 3 Years of Followup. Circulation, 135(15), 1397-1412.
Publication 2017
Carboplatin Cardiotoxicity Cyclophosphamide Docetaxel Doxorubicin Echocardiography Ethics Committees, Research Heart Heart Failure Malignant Neoplasm of Breast Malignant Neoplasms Oncologists Paclitaxel Pharmacotherapy Physicians Pregnancy Sorbus Therapeutics Trastuzumab Treatment Protocols Tretinoin

Most recents protocols related to «Cardiotoxicity»

1
Toxicity Assessment of Cy5.5-Coated Nanoparticles
The toxicity of repeated and high dose of CNPs treatment was assessed by histological and hematological analyses. Briefly, Cy5.5-CNPs (10, 22.5 or 90 mg/kg) were intravenously injected into BALB/c mice with single- or multi-dosage (three times). On day 7 after treatments, major organs (liver, lung, spleen, kidney, brain and heart) were collected from mice, and structural abnormalities in organ tissues were assessed by staining with H&E. In the case of hematological analyses, blood samples were collected from the mice on day 7 and centrifuged at 2200 rpm to obtain plasma. The following factors in blood samples were measured; alanine aminotransferase (ALT), blood urea nitrogen (BUN), alkaline phosphatase (ALP), aspartate Aminotransferase (AST), creatine kinase (CK) and troponin I. The cardiotoxicity by Cy5.5-CNPs was further analyzed after multiple-dosage. The heart tissues were collected from mice after treatment with 10, 22.5 or 90 mg/kg of Cy5.5-CNPs three times. The accumulation of Cy5.5-CNPs in heart tissues was observed using a Leica TCS SP8 confocal laser-scanning microscope. Collagen fiber in heart tissues were stained with Masson's trichrome. Briefly, heart tissues were incubated in Bouin's fixative for 30 min at 56 °C, and the nuclei were co-stained with Weigert's iron hematoxylin. Then, cytoplasm was stained with Biebrich scarlet-acid fuchsin, and then differentiated in phosphomolybdic–phosphotungstic acid. The collagen matrix in heart tissues was stained with aniline blue solution. The collagen in heart tissues were quantitatively analyzed using an Image Pro software, and collagen contents were presented in proportion to the total area of heart tissues.
Chang H., Yhee J.Y., Jeon S., Shim M.K., Yoon H.Y., Lee S, & Kim K. (2023). In vivo toxicity evaluation of tumor targeted glycol chitosan nanoparticles in healthy mice: repeated high-dose of glycol chitosan nanoparticles potentially induce cardiotoxicity. Journal of Nanobiotechnology, 21, 82.
Publication 2023
Aftercare Alkaline Phosphatase aniline blue Aspartate Transaminase Biebrich Scarlet BLOOD Brain Cardiotoxicity Cell Nucleus Collagen Congenital Abnormality Creatine Kinase CY5.5 cyanine dye Cytoplasm D-Alanine Transaminase Fibrosis Fixatives Heart Iron Kidney Liver Lung Mice, Inbred BALB C Microscopy, Confocal Mus Phosphotungstic Acid Plasma Spleen Tissues Troponin I Urea Nitrogen, Blood vascular factor
2
Non-Inferiority Cardiac Surveillance in HER2+ Breast Cancer
The proportion of patients who develop a cardiac event at 12 months will be estimated together with an exact 95% confidence interval. Based upon our preliminary data of early-stage HER2-positive patients treated with non-anthracycline trastuzumab-based regimens, the estimated cardiac event rate is 1.2% (95% CI 0.1–4.1%) [21 ]. The null hypothesis of the current study is that a reduced cardiotoxicity surveillance strategy is non-inferior to routine standard-of-care surveillance by a prespecified margin in the cardiac event rate of 2.9%. This non-inferiority margin corresponds to the difference between the observed cardiac event rate from our preliminary data and the upper bound of the 95% confidence interval. With 190 patients, we will have 84% power to reject the null hypothesis using a one-sided exact test with a significance level of 0.052. We will reject the null hypothesis if no more than 3 participants develop a cardiac event. If 4 or more cardiac events are observed during any point in the trial, the study will stop.
Yu A.F., Dang C.T., Jorgensen J., Moskowitz C.S., DeFusco P., Oligino E., Oeffinger K.C., Liu J.E, & Steingart R.M. (2023). Rationale and design of a cardiac safety study for reduced cardiotoxicity surveillance during HER2-targeted therapy. Cardio-oncology, 9, 13.
Publication 2023
Anthracyclines Cardiac Events Cardiotoxicity ERBB2 protein, human Patients Rate, Heart Trastuzumab Treatment Protocols
3
Reduced Cardiac Monitoring in HER2+ Breast Cancer
This is a single-arm prospective trial (ClinicalTrials.gov Identifier: NCT03983382) with a primary objective to evaluate the cardiac safety of a reduced cardiotoxicity surveillance strategy (every 6 months) in patients with HER2-positive breast cancer treated with a non-anthracycline HER2-targeted treatment regimen. Secondary objectives include the following: 1) to measure the change in LVEF and global longitudinal strain (GLS) after 6 and 12 months of treatment compared to baseline; 2) to estimate the incidence of asymptomatic LVEF decline; 3) to estimate the incidence of early interruption of HER2-targeted treatment; and 4) to determine feasibility of a reduced cardiotoxicity surveillance strategy.
Yu A.F., Dang C.T., Jorgensen J., Moskowitz C.S., DeFusco P., Oligino E., Oeffinger K.C., Liu J.E, & Steingart R.M. (2023). Rationale and design of a cardiac safety study for reduced cardiotoxicity surveillance during HER2-targeted therapy. Cardio-oncology, 9, 13.
Publication 2023
Anthracyclines Cardiotoxicity erbb2 Gene Heart Malignant Neoplasm of Breast Patients Safety Treatment Protocols
4
Cardiac Safety in HER2+ Breast Cancer
The study will be conducted in HER2-positive breast cancer patients (stage I-IV) receiving a non-anthracycline-based chemotherapy regimen in combination with a HER2-targeted agent (e.g. trastuzumab, pertuzumab, or ado-trastuzumab emtansine). The primary exclusion criteria are: (1) prior treatment with anthracyclines or HER2-targeted therapy; (2) baseline LVEF < 53% (or institutional lower limit of normal); (3) systolic or diastolic blood pressure ≥ 160 mmHg or ≥ 90 mmHg, respectively; and (4) history of heart failure, cardiomyopathy, or other significant CVD associated with increased cardiotoxicity risk (e.g. atrial fibrillation, atherosclerotic cardiovascular disease, significant valvular heart disease, etc.). Following approval by the primary medical oncologist, written informed consent will be obtained from each patient prior to study enrollment. The inclusion and exclusion criteria of this study are presented in Table 1.

Main eligibility criteria

Inclusion criteriaExclusion criteria

1. Female

2. Age ≥ 18 years

3. Pathologically confirmed HER2-positive invasive breast carcinoma (stage I-IV)

4. Anticipated treatment with HER2-targeted therapy for ≥ 12 months

5. Normal LV systolic function (LVEF ≥ institutional lower limit of normal)

6. Willing and able to provide written informed consent and comply with the requirements of the protocol

1. Anticipated treatment with anthracycline chemotherapy

2. Prior treatment with anthracycline chemotherapy

3. History of cardiomyopathy, heart failure, or other clinically significant cardiovascular disease

4. Uncontrolled hypertension, defined as a systolic blood pressure ≥ 160 mmHg and/or diastolic blood pressure ≥ 90 mmHg

Yu A.F., Dang C.T., Jorgensen J., Moskowitz C.S., DeFusco P., Oligino E., Oeffinger K.C., Liu J.E, & Steingart R.M. (2023). Rationale and design of a cardiac safety study for reduced cardiotoxicity surveillance during HER2-targeted therapy. Cardio-oncology, 9, 13.
Publication 2023
Ado-Trastuzumab Emtansine Anthracyclines Atherosclerosis Atrial Fibrillation Breast Carcinoma Cardiomyopathies Cardiotoxicity Cardiovascular System Combination Drug Therapy Congestive Heart Failure Eligibility Determination erbb2 Gene High Blood Pressures Malignant Neoplasm of Breast Oncologists Patients pertuzumab Pressure, Diastolic Systole Systolic Pressure Trastuzumab Treatment Protocols Valve Disease, Heart
5
Phase Ib/II Study of Immunotherapy
The primary endpoint of the Phase Ib study was dose-limiting toxicity (DLT), with the intention that a Phase II study would be conducted if DLT occurred in fewer than two-sixths of the treated patients, whereas the study would be terminated if DLT occurred in two or more patients. DLT was defined as any of the following adverse events occurring within 21 d of initial drug administration: Grade 4 neutropenia > 7 d; ≥ Grade 3 neutropenia with fever (T ≥ 38.5 °C) lasting > 24 h; Grade 4 thrombocytopenia or Grade 3 thrombocytopenia with bleeding; Grade 4 anemia; ≥ Grade 3 clinically significant nonhematologic toxicity; ≥ Grade 2 immune-related cardiotoxicity, immune-related pneumonia, immune-related ophthalmopathy; and ≥ Grade 3 other immune-related toxicity.
The primary endpoint of the Phase II study was the major pathological response (MPR) rate, with secondary endpoints consisting of the R0 resection rate, pCR rate, safety, disease-free survival (DFS), event-free survival (EFS), and OS. The Becker standard was used to evaluate pathological regression of the primary tumor after surgery. No residual tumor cells were defined as type 1a, less than 10% were defined as type 1b, 10–50% were defined as type 2, and the remainder were defined as type 3. Pathological remission assessed at Grades 1a and 1b was considered to be MPR (including pCR), while pCR was defined as the absence of residual tumor cells (including primary tumors and lymph nodes).
Li Y., Zhou A., Liu S., He M., Chen K., Tian Z., Li Y., Qin J., Wang Z., Chen H., Tian H., Yu Y., Qu W., Xue L., He S., Wang S., Bie F., Bai G., Zhou B., Yang Z., Huang H., Fang Y., Li B., Dai X., Gao S, & He J. (2023). Comparing a PD-L1 inhibitor plus chemotherapy to chemotherapy alone in neoadjuvant therapy for locally advanced ESCC: a randomized Phase II clinical trial: A randomized clinical trial of neoadjuvant therapy for ESCC. BMC Medicine, 21, 86.
Publication 2023
Anemia Cardiotoxicity Cells Eye Disorders Febrile Neutropenia Leukopenia Neoplasms Nodes, Lymph Operative Surgical Procedures Patients Pneumonia Residual Tumor Safety Thrombocytopenia Thrombocytopenia 3

Top products related to «Cardiotoxicity»

1
Earlytox cardiotoxicity kit by Molecular Devices
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The EarlyTox Cardiotoxicity Kit is a laboratory equipment product designed to assess the cardiotoxic potential of test compounds. The kit enables the measurement of various functional parameters, including beat rate and beat pattern, in cardiomyocytes derived from human induced pluripotent stem cells (hiPSCs).
2
Analyzer2200 by INCELL
The Analyzer2200 is a laboratory instrument designed for the analysis of various samples. It offers precise and efficient data collection capabilities to support research and testing activities.
3
Flipr tetra by Molecular Devices
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The FLIPR Tetra is a high-throughput cellular screening system designed for rapid and sensitive detection of cellular responses. It utilizes fluorescence-based detection to measure changes in cellular parameters, such as membrane potential and calcium flux, in real-time. The FLIPR Tetra is capable of simultaneously monitoring multiple wells in a microplate format, making it a versatile tool for a wide range of applications in drug discovery and cell biology research.
4
Dimethyl sulfoxide (dmso) by Merck Group
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DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.
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Formaldehyde solution is a versatile laboratory reagent used for various applications. It is a clear, colorless liquid that contains a concentrated solution of formaldehyde in water. The primary function of this product is to act as a fixative, preservative, and disinfectant in various laboratory procedures.
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Hank s balanced salt solution by Thermo Fisher Scientific
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Hank's Balanced Salt Solution (HBSS) is a commonly used cell culture medium that maintains the pH, osmotic pressure, and ion concentrations required for the survival and growth of cells in vitro. It provides a balanced salt solution with a variety of inorganic salts, glucose, and phenol red as a pH indicator. HBSS is often used as a base for the preparation of more complex cell culture media or as a washing solution for cells.
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Mitotracker orange cmtmros reagent by Thermo Fisher Scientific
MitoTracker Orange CMTMRos is a fluorescent dye used to label and detect mitochondria in live cells. It is a cell-permeant dye that accumulates in active mitochondria, allowing for visualization of mitochondrial morphology and distribution.
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Recombinant oncostatin m by Thermo Fisher Scientific
Recombinant oncostatin M is a cytokine protein produced through recombinant DNA technology. It is a member of the interleukin-6 family of cytokines and plays a role in various biological processes.

More about "Cardiotoxicity"

Cardiotoxicity, a critical concern in drug development and safety assessment, refers to the adverse effects of various substances, medications, or other agents on the heart and cardiovascular system.
This can manifest as a range of complications, including arrhythmias, myocardial damage, hypertension, and other cardiovascular issues.
Understanding and mitigating cardiotoxicity is crucial for ensuring the safety and efficacy of new pharmaceutical products.
The PubCompare.ai platform leverages advanced AI technologies to empower researchers in optimizing their cardiotoxicity studies.
This powerful tool helps users locate relevant literature, protocols, and products, while enhancing the reproducibility and accuracy of their research.
Some key subtopics and related terms in the realm of cardiotoxicity include: - Arrhythmias: Irregular heartbeats or abnormal heart rhythms - Myocardial damage: Injury or harm to the heart muscle - Hypertension: High blood pressure - Cardiovascular complications: Other adverse effects on the heart and blood vessels - EarlyTox Cardiotoxicity Kit: A tool for assessing the cardiotoxic potential of compounds - Analyzer2200: An instrument for analyzing cellular responses to drugs and chemicals - FLIPR Tetra: A high-throughput screening platform for measuring cellular responses - DMSO (Dimethyl sulfoxide): A solvent commonly used in cell-based assays - Formaldehyde solution: A fixative used in histological and cytological analyses - Cisapride monohydrate: A medication that can potentially cause cardiac arrhythmias - Hank's Balanced Salt Solution: A buffer solution used in cell culture and other applications - Penicillin-streptomycin solution: An antibiotic solution used to prevent bacterial contamination - MitoTracker Orange CMTMRos: A fluorescent dye used to stain mitochondria - Recombinant oncostatin M: A cytokine that can have cardioprotective effects By leveraging the insights and tools provided by the PubCompare.ai platform, researchers can take their cardiotoxicity studies to new heights, ensuring the safety and efficacy of the drugs and compounds they are developing.