ABSTRACT
To explore characteristics of outpatients in a single cardio-oncology clinic, patients visiting cardio-oncology clinic of Fuwai Hospital CAMS&PUMC (Beijing, China) from January 2020 to December 2021 were analyzed retrospectively. In total, 330 patients were included, the median age (Q1, Q3) was 58(46, 66) years, and there were 192 females (58.2%). The purposes for visit included an evaluation and treatment of cardiovascular adverse reactions (n=247, 74.8%), pre-antitumor therapy assessment (n=51, 15.5%), and management of primary or metastatic cardiac tumors (n=32, 9.7%). For patients with cardiovascular adverse reactions, the most common tumor type was breast cancer (n=88, 29.5%), followed by gastrointestinal cancer (n=70, 23.5%), and hematological cancers (n=62, 20.8%). Among them, 236 cases (95.5%) had received antitumor drugs in the past; 38 cases (15.4%) had a history of chest radiotherapy; some cases were complicated with hypertension (n=69, 23.2%) and/or hyperlipidemia (n=69, 23.2%); 42 cases (14.1%) had a history of coronary heart disease; and 16 cases (5.4%) were complicated with atrial fibrillation or flutter. Among 32 patients with cardiac tumors, 11 cases (34.4%) had primary malignant tumors; 6 cases (18.8%) had benign tumors; 2 cases (6.3%) had metastatic tumors; and 13 (40.6%) had unknown pathological types. This study explores the epidemiology of cardio-oncology in China and provides clinical insights for the future development of cardio-oncology. In the future, it is still necessary to study the benefits of cardio-oncology clinics and develop standardized indicators to evaluate their benefits.
Subject(s)
Antineoplastic Agents , Breast Neoplasms , Heart Neoplasms , Female , Humans , Antineoplastic Agents/adverse effects , Breast Neoplasms/therapy , Breast Neoplasms/complications , Heart Neoplasms/chemically induced , Heart Neoplasms/complications , Medical Oncology , Retrospective Studies , Male , Middle Aged , AgedSubject(s)
Heart Neoplasms/chemically induced , Lymphoma/chemically induced , Methotrexate/adverse effects , Rheumatic Fever/drug therapy , Aged, 80 and over , Antirheumatic Agents/adverse effects , Biopsy , Diagnosis, Differential , Female , Heart Atria , Heart Neoplasms/diagnosis , Heart Ventricles , Humans , Lymphoma/diagnosis , Magnetic Resonance Imaging, Cine/methods , Myocardium/pathology , Tomography, X-Ray Computed/methodsSubject(s)
Heart Failure/diagnostic imaging , Heart Neoplasms/diagnostic imaging , Heart Ventricles/diagnostic imaging , Lymphoma, Large B-Cell, Diffuse/diagnostic imaging , Abdominal Neoplasms/chemically induced , Abdominal Neoplasms/diagnostic imaging , Abdominal Neoplasms/drug therapy , Aged , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Antirheumatic Agents/adverse effects , Arthritis, Rheumatoid/drug therapy , Cyclophosphamide/administration & dosage , Doxorubicin/administration & dosage , Doxorubicin/analogs & derivatives , Female , Heart Failure/etiology , Heart Neoplasms/chemically induced , Heart Neoplasms/complications , Heart Neoplasms/drug therapy , Humans , Lymph Nodes/diagnostic imaging , Lymph Nodes/pathology , Lymphoma, Large B-Cell, Diffuse/chemically induced , Lymphoma, Large B-Cell, Diffuse/complications , Lymphoma, Large B-Cell, Diffuse/drug therapy , Methotrexate/adverse effects , Prednisolone/administration & dosage , Tomography, X-Ray Computed , Vincristine/administration & dosageSubject(s)
Heart Neoplasms/surgery , Heart Ventricles/surgery , Hemangioma/surgery , Pericardium/surgery , Pulmonary Artery/surgery , Ventricular Outflow Obstruction/surgery , Disease Management , Heart Neoplasms/chemically induced , Heart Neoplasms/diagnostic imaging , Heart Ventricles/diagnostic imaging , Hemangioma/complications , Hemangioma/diagnostic imaging , Humans , Male , Middle Aged , Pericardium/diagnostic imaging , Perioperative Care/methods , Pulmonary Artery/diagnostic imaging , Ventricular Outflow Obstruction/diagnostic imaging , Ventricular Outflow Obstruction/etiologyABSTRACT
We encountered a case of a cardiac hemangioma protruding into the inner cavity of the right ventricle from the right ventricular free wall. The tumor gradually enlarged over 11 years (from 35 mm to 78mm) without presenting any symptoms. However, when it extended to the right ventricular outflow tract, non-sustained ventricular tachycardia occurred, and emergency surgery was required. The tumor was diagnosed as a cavernous benign hemangioma. Complete resection was not possible, and the part involving the right ventricle remained. This residual tumor caused postoperative ventricular arrhythmia, and an implantable cardioverter defibrillator was required. We concluded that non-surgically treated cardiac hemangiomas carry the risk of non-resectability, regardless of malignancy.
Subject(s)
Heart Neoplasms/surgery , Heart Ventricles/surgery , Hemangioma, Cavernous/surgery , Aged, 80 and over , Asymptomatic Diseases , Echocardiography , Female , Heart Neoplasms/chemically induced , Heart Ventricles/diagnostic imaging , Hemangioma, Cavernous/diagnostic imaging , Humans , Time Factors , Tomography, X-Ray ComputedABSTRACT
Cardiac rhabdomyoma (CR) is a rare tumor commonly associated with tuberous sclerosis. They are often detected prenatally or in early infancy. The case of a Nigerian human immunodeficiency virus (HIV)-exposed neonate with CR who presented with supraventricular tachycardia and cardiovascular collapse is presented. The infant was born to a mother on highly active antiretroviral therapy (HAART). The possible role of HIV and HAART in CR etiology and the difficulty in the management of this case are highlighted.
Subject(s)
Anti-HIV Agents/adverse effects , Heart Neoplasms/complications , Infectious Disease Transmission, Vertical/prevention & control , Rhabdomyoma/complications , Tachycardia, Supraventricular/etiology , Amiodarone/therapeutic use , Anti-Arrhythmia Agents/therapeutic use , Anti-HIV Agents/therapeutic use , Fatal Outcome , Heart Neoplasms/chemically induced , Humans , Infant, Newborn , Male , Rhabdomyoma/chemically induced , Risk Factors , Tachycardia, Supraventricular/diagnosis , Tachycardia, Supraventricular/drug therapySubject(s)
Dust , Environmental Exposure/adverse effects , Mesothelioma/chemically induced , Mesothelioma/epidemiology , Minerals , Age Factors , Age of Onset , Aluminum Silicates/adverse effects , Aluminum Silicates/chemistry , Asbestos/adverse effects , Geology , Heart Neoplasms/chemically induced , Heart Neoplasms/epidemiology , Humans , Mesothelioma/prevention & control , Minerals/adverse effects , Minerals/chemistry , Nevada/epidemiology , Occupational Exposure/adverse effects , Pericardium , Peritoneal Neoplasms/chemically induced , Peritoneal Neoplasms/epidemiology , Pleural Neoplasms/chemically induced , Pleural Neoplasms/epidemiology , Sex FactorsSubject(s)
Heart Neoplasms/pathology , Heart Transplantation , Immunosuppression Therapy/adverse effects , Lymphoproliferative Disorders/pathology , Adult , Antineoplastic Agents/therapeutic use , Boronic Acids/therapeutic use , Bortezomib , Female , Heart Neoplasms/chemically induced , Heart Neoplasms/drug therapy , Humans , Immunosuppressive Agents/administration & dosage , Lymphoproliferative Disorders/chemically induced , Lymphoproliferative Disorders/drug therapy , Plasmacytoma , Pyrazines/therapeutic useSubject(s)
Antibodies, Monoclonal/toxicity , Antibodies, Neoplasm/toxicity , Heart Neoplasms/etiology , Mycosis Fungoides/drug therapy , Mycosis Fungoides/pathology , Aged , Alemtuzumab , Antibodies, Monoclonal/therapeutic use , Antibodies, Monoclonal, Humanized , Antibodies, Neoplasm/therapeutic use , Female , Heart Neoplasms/chemically induced , Heart Neoplasms/pathology , Humans , Mycosis Fungoides/diagnosis , Neoplasm InvasivenessSubject(s)
Heart Neoplasms/diagnostic imaging , Kidney Transplantation , Lymphoma, B-Cell/diagnostic imaging , Lymphoma, Large B-Cell, Diffuse/diagnostic imaging , Pancreas Transplantation , Pericarditis/etiology , Ventricular Outflow Obstruction/etiology , Adult , Diagnosis, Differential , Echocardiography, Transesophageal , Heart Neoplasms/chemically induced , Heart Neoplasms/complications , Humans , Immunosuppressive Agents/adverse effects , Lymphoma, B-Cell/chemically induced , Lymphoma, B-Cell/complications , Lymphoma, Large B-Cell, Diffuse/chemically induced , Lymphoma, Large B-Cell, Diffuse/complications , MaleABSTRACT
OBJECTIVES: The effects of direct intramyocardial injection of the plasmid encoding vascular endothelial growth factor (phVEGF165) in the border zone of myocardial infarct tissue in rat hearts were investigated. BACKGROUND: Controversy exists concerning the ability of VEGF to induce angiogenesis and enhance coronary flow in the myocardium. METHODS: Sprague-Dawley rats received a ligation of the left coronary artery to induce myocardial infarction (MI). At 33.1 +/- 6.5 days, the rats were injected with phVEGF165 at one location and control plasmid at a second location (500 microg DNA, n = 24) or saline (n = 16). After 33.1 +/- 5.7 days, the hearts were excised for macroscopic and histologic analysis. Regional blood flow ratios were measured in 18 rats by radioactive microspheres. RESULTS: phVEGF165-treated sites showed macroscopic angioma-like structures at the injection site while control DNA and saline injection sites did not. By histology, 21/24 phVEGF165-treated hearts showed increased focal epicardial blood vessel density and angioma-like formation. Quantitative morphometric evaluation in 20 phVEGF165-treated hearts revealed 44.4 +/- 10.5 vascular structures per field in phVEGF165-treated hearts versus 21.4 +/- 4.7 in control DNA injection sites (p < 0.05). Regional myocardial blood flow ratios between the injection site and noninfarcted area did not demonstrate any difference between phVEGF,165-treated hearts (0.9 +/- 0.2) and saline-treated hearts (0.7 +/- 0.1). CONCLUSIONS: Injection of DNA for VEGF in the border zone of MI in rat hearts induced angiogenesis. Angioma formation at the injection sites did not appear to contribute to regional myocardial blood flow, which may be a limitation of gene therapy for this application.
Subject(s)
Disease Models, Animal , Endothelial Growth Factors/genetics , Endothelial Growth Factors/therapeutic use , Genetic Therapy/methods , Heart Neoplasms/chemically induced , Hemangioma/chemically induced , Lymphokines/genetics , Lymphokines/therapeutic use , Myocardial Infarction/therapy , Neovascularization, Physiologic/drug effects , Plasmids/genetics , Plasmids/therapeutic use , Animals , Coronary Circulation/drug effects , Drug Evaluation, Preclinical , Endothelial Growth Factors/adverse effects , Genetic Therapy/adverse effects , Heart Neoplasms/pathology , Hemangioma/pathology , Injections , Lymphokines/adverse effects , Myocardial Infarction/pathology , Plasmids/adverse effects , Random Allocation , Rats , Rats, Sprague-Dawley , Vascular Endothelial Growth Factor A , Vascular Endothelial Growth FactorsABSTRACT
We show that a construct designated as MAHEVA, which encodes oncogenes v-myc from MH2 virus and v-erbA from AEV under the control of the LTR of MH2, induces rapidly growing heart rhabdomyosarcomas, when it is injected in E3 but not E5 chick embryos. A similar pathology has previously been observed with MC29, within the same limited time frame. The tumors, which expressed P61-63myc, P75gag-erbA and Pr76gag proteins were detectable from E14 onwards. Compared with MC29, MAHEVA induced a secondary anomaly, not detectable prior to E17. This is the appearance of cartilage nodules within the heart rhabdomyosarcomas. The constant location of these nodules inside the rhabdomyosarcomas and their delayed appearance suggests that the chondrocytes originate from myoblasts prevented from differentiating by the expression of the v-myc product. This interpretation is supported by the appearance of chondrocytes in E3 heart muscle cells infected in vitro with MAHEVA.
Subject(s)
Embryo, Mammalian/drug effects , Embryo, Nonmammalian , Embryonic and Fetal Development/genetics , Oncogene Protein p55(v-myc)/pharmacology , Retroviridae Proteins, Oncogenic/pharmacology , Animals , Cartilage/pathology , Cell Line , Chick Embryo , Drug Synergism , Gene Expression/genetics , Heart Neoplasms/chemically induced , Heart Neoplasms/metabolism , Heart Neoplasms/pathology , Oncogene Protein p55(v-myc)/genetics , Oncogene Protein p55(v-myc)/metabolism , Oncogene Proteins v-erbA , Precipitin Tests , Retroviridae Proteins, Oncogenic/genetics , Retroviridae Proteins, Oncogenic/metabolism , Rhabdomyosarcoma/chemically induced , Rhabdomyosarcoma/metabolism , Rhabdomyosarcoma/pathology , Transcription, Genetic/geneticsABSTRACT
The carcinogenicity of inhaled 1,3-butadiene was evaluated in C57BL/6 x C3H F1 mice exposed to concentrations of this gas ranging from 6.25 to 625 ppm. Butadiene is a high production volume chemical, used mainly in the manufacture of synthetic rubber. In these 2-yr inhalation studies, a potent multisite carcinogenic response was observed, including neoplasms of the lung at concentrations as low as 6.25 ppm. Early occurrence and extensive development of lethal lymphocytic lymphomas in mice exposed to 625 ppm of butadiene reduced the number of animals at risk for the expression of later developing neoplasms at other sites; at lower exposure concentrations, dose responses were demonstrated for hemangiosarcomas of the heart and neoplasms of the lung, forestomach, Harderian gland, preputial gland, liver, mammary gland, and ovary. So far, no long-term studies on butadiene have been conducted at exposure concentrations that have not shown a carcinogenic response. In separate experiments with reduced exposure durations, butadiene induced neoplastic responses at multiple organ sites even after only 13 wk of exposure. Because of the correspondence between these animal data and recent epidemiology findings, there is a worldwide public health need to reevaluate current workplace exposure standards for 1,3-butadiene.
Subject(s)
Butadienes/toxicity , Neoplasms, Experimental/chemically induced , Animals , Dose-Response Relationship, Drug , Female , Heart Neoplasms/chemically induced , Hemangiosarcoma/chemically induced , Leukemia, Lymphocytic, Chronic, B-Cell/chemically induced , Lung Neoplasms/chemically induced , Male , Mice , Mice, Inbred C3H , Mice, Inbred C57BL , Stomach Neoplasms/chemically inducedABSTRACT
1,3-Butadiene (CAS No. 106-99-0) was studied for potential carcinogenicity and chronic toxicity by inhalation in B6C3F1 mice. Groups of 50 mice of each sex were exposed to 0, 625, or 1250 ppm 1,3-butadiene for 6 hr/day, 5 days/week for 60 weeks (male) or 61 weeks (female). The study was scheduled for 104 weeks of exposure but was terminated early because of reduced survival related to induction of a variety of tumors in 1,3-butadiene-exposed mice. A second chronic inhalation study was conducted in which male and female mice were exposed to 0, 6.25, 20, 62.5, 200, or 625 ppm for up to 2 years. Additional groups of 50 male mice were exposed to 625 ppm for 13 or 26 weeks, 312 ppm for 52 weeks, or 200 ppm for 40 weeks, then held without exposure until scheduled sacrifice 104 weeks after initial exposure. 1,3-Butadiene-exposed mice from both studies had increased incidences of malignant lymphomas that were observed as early as week 20 in the first study and week 23 in the second study. The lymphomas were primarily lymphocytic and originated in the thymus, although generalized lymphoma was often present. Exposed mice in both studies developed cardiac hemangiosarcomas that were observed as early as week 32 in the first study and week 41 in the second study. Also present were foci of endothelial hyperplasia in the myocardium that were regarded as early evidence of developing hemangiosarcoma. Alveolar epithelial hyperplasia, alveolar/bronchiolar adenomas and alveolar/bronchiolar carcinomas represented the spectrum of proliferative lung lesions induced by exposure to 1,3-butadiene in both studies. Exposure-related proliferative forestomach lesions observed in both studies included epithelial hyperplasia, squamous cell papillomas, and squamous cell carcinomas. 1,3-Butadiene-exposed female mice in both studies developed mammary gland neoplasms at increased incidences. Most of the mammary tumors were pleomorphic adenocarcinomas, but several adenoacanthomas were also seen. Granulosa cell tumors of the ovary were exposure-related neoplasms in both studies. Occasionally the granulosa cell tumors were malignant as evidenced by vascular invasion or pulmonary metastasis. Although there was an increased incidence of hepatocellular neoplasms in exposed females in the first study, by week 65 of the second study there was not evidence of a clear response of liver neoplasms. The preliminary results of the second study indicate there was induction of tumors similar to those seen in the first study but occurring in response to lower concentrations of 1,3-butadiene.
Subject(s)
Butadienes/toxicity , Carcinogens , Neoplasms, Experimental/chemically induced , Animals , Female , Heart Neoplasms/chemically induced , Heart Neoplasms/pathology , Liver Neoplasms, Experimental/chemically induced , Liver Neoplasms, Experimental/pathology , Lung Neoplasms/chemically induced , Lung Neoplasms/pathology , Lymphoma/chemically induced , Lymphoma/pathology , Male , Mammary Neoplasms, Experimental/chemically induced , Mammary Neoplasms, Experimental/pathology , Mice , Neoplasms, Experimental/pathology , Ovarian Neoplasms/chemically induced , Ovarian Neoplasms/pathology , Stomach Neoplasms/chemically induced , Stomach Neoplasms/pathologyABSTRACT
Two studies on the carcinogenicity of the fungicide captan in animals were reviewed. The results and conclusions, which were based on my examination of the histological sections, showed that captan is highly carcinogenic in rats and mice. Neoplasms at all sites, as well as malignant neoplasms, were increased in both low and high dose captan-treated male and female rats. Benign and malignant neoplasms of the endocrine organs were increased in low and high dose male and female rats ingesting captan. Neoplasms of the adrenal and pituitary glands were increased. Increased incidences of benign and malignant neoplasms, and of malignant neoplasms only, were observed in the reproductive system of female rats ingesting captan. The incidence of these neoplasms was markedly increased in the mammary gland and ovary. Female rats given captan were more susceptible to the development of hepatic neoplasms than were male rats. Captan induced neoplasms of the duodenum in male and female mice. There also were toxic changes in rats. Captan-treated male rats were more susceptible to the induction of chronic renal disease than were female rats. Male rats also had a high incidence of particularly severe testicular atrophy as a result of the ingestion of captan. Such lesions interfere with the health of the rats and with the development of neoplasms.
Subject(s)
Captan/toxicity , Neoplasms, Experimental/chemically induced , Adrenal Gland Neoplasms/chemically induced , Animals , Dose-Response Relationship, Drug , Female , Heart Neoplasms/chemically induced , Kidney Failure, Chronic/chemically induced , Liver Neoplasms/chemically induced , Male , Mammary Neoplasms, Experimental/chemically induced , Ovarian Neoplasms/chemically induced , Pituitary Neoplasms/chemically induced , Rats , Rhabdomyosarcoma/chemically induced , Sarcoma, Experimental/chemically induced , Sex Factors , Testicular Diseases/chemically induced , Uterine Neoplasms/chemically inducedABSTRACT
1,3-butadiene (CAS No. 106-99-0) was evaluated for carcinogenicity and chronic toxicity by inhalation exposure in B6C3F1 mice because of its high production volume, widespread exposure of workers, and the lack of carcinogenicity and toxicity data (NTP Report #228, 1984). Butadiene (BD) had long been considered to have low toxicity. The long-term studies established that BD is a potent mouse carcinogen with multiple organ carcinogenicity (Huff et al. 1985; Melnick et al. 1988). This paper presents morphological descriptions and illustrations of the neoplastic lesions induced by 1,3-butadiene in B6C3F1 mice.
Subject(s)
Butadienes/adverse effects , Mutagens/adverse effects , Neoplasms, Experimental/chemically induced , Adenocarcinoma/chemically induced , Adenocarcinoma/pathology , Adenoma/chemically induced , Adenoma/pathology , Animals , Carcinoma/chemically induced , Carcinoma/pathology , Female , Granulosa Cell Tumor/chemically induced , Granulosa Cell Tumor/pathology , Heart Neoplasms/chemically induced , Heart Neoplasms/pathology , Hemangiosarcoma/chemically induced , Hemangiosarcoma/pathology , Liver Neoplasms/chemically induced , Liver Neoplasms/pathology , Lung Neoplasms/chemically induced , Lung Neoplasms/pathology , Lymphoma/chemically induced , Lymphoma/pathology , Male , Mice , Neoplasms, Experimental/pathology , Ovarian Neoplasms/chemically induced , Ovarian Neoplasms/pathology , Stomach Neoplasms/chemically induced , Stomach Neoplasms/pathologyABSTRACT
10 endocardial tumours (two tumours induced by N-nitrosoethylurea and eight spontaneous) of BD VI rats were examined for protein S-100 using specific antiserum in an immunoperoxidase reaction. The presence of protein S-100 in tumour cells is demonstrated in all cases and is considered as a proof of Schwann cell origin of these tumours.