Colchicine is a drug that has long been used to treat a variety of illnesses; however, it reportedly has adverse effects at apparent toxic doses as well as at lower and therapeutically recommended doses. The typical therapeutic dose of colchicine is up to 2.4 mg daily, although it is sometimes as high as 8–10 mg daily. Here, we describe a case in which the patient showed sudden deterioration and died because of unintentional colchicine poisoning with a relatively small dose. When a colchicine poisoned patient visits the hospital, the physician should identify the patient's colchicine poisoning dose and concomitant drugs. Moreover, the patients should be monitored intensively for 24 to 72 hours and managed with various supportive treatment methods early and actively.
Cardiotoxicity ; Colchicine* ; Humans ; Poisoning* ; Sepsis

Cancer therapeutics-related cardiac dysfunction(CTRCD)is receiving more attention.Risk factors assessment before cancer therapy,cardiac function monitoring during and after cancer therapy,and early detection and treatment of myocardial injury are key to preventing clinical heart failure.The incidence and severity of cardiotoxicity can be reduced by measures such as reducing drug dose,adjusting administration route,and using low toxic drugs.Cardioprotective agents including anti-heart failure drugs and dexrazoxane are important for the prevention and treatment of CTRCD.Patients with advanced heart failure may also benefit from mechanical treatments including cardiac resynchronization therapy and mechanically-assisted ventricular devices.This article reviews the recent advances in the prevention and treatment of CTRCD.
Cardiotoxicity ; Heart ; Heart Diseases ; Humans

Cardiovascular (CV) toxicity associated with anti-cancer treatment is commonly encountered and raises critical problems that often result in serious morbidity or mortality. Most cardiac toxicities are related to the cumulative dose of chemotherapy; however, the type of chemotherapy, concomitant agents, and/or conventional CV risk factors have been frequently implicated in CV toxicity. Approximately half of the patients exhibiting CV toxicity receive an anthracycline-based regimen. Therefore, serologic biomarkers or cardiac imagings are important during anti-cancer treatment for early detection and the decision of appropriate management of cardiotoxicity. However, given the difficulty in determining a causal relationship, a multidisciplinary collaborative approach between cardiologists and oncologists is required. In this review, we summarize the CV toxicity and focus on the role of cardiac imaging in management strategies for cardiotoxicity associated with anti-cancer treatment.
Biomarkers ; Cardiotoxicity ; Diagnosis* ; Drug Therapy ; Echocardiography* ; Humans ; Mortality ; Risk Factors

Cardiotoxicity is smong the main safety problems of drugs in clinical application. In recent years, traditional Chinese medicine has been gradually emphasized and studies on the evaluation of cardiac safety and prevention of cardiotoxicity of Chinese medicine have been on the rise, particularly the cardiotoxic Chinese medicine or the Chinese medicine components targeting cardiotoxicity. As for the research methods for cardiac safety evaluation of Chinese medicine, this review introduces the related clinical indexes and cell and animal models. As to the improvement of heart safety, this study reviews the material basis and mechanism of cardiotoxic Chinese medicines as well as the alleviation of cardiotoxicity by controlling the content of toxic compounds and changing dosage form, processing method, and compatibility of Chinese medicine. In addition, the effective components and mechanisms of prescriptions and active compounds in Chinese medicine for preventing and treating cardiotoxicity induced by chemotherapeutic drugs in recent years were summarized. This review is expected to serve as a reference for cardiac safety evaluation and clinical rational application of Chinese medicine.
Animals ; Cardiotoxicity/prevention & control* ; Drugs, Chinese Herbal ; Medicine, Chinese Traditional

Cardiotoxicity is a well-known complication following treatment with anthracyclines. However, they are still widely used in chemotherapy for breast cancer, lymphoma, leukemia, and sarcoma, among others. Patient clinical characteristics, such as age, sex, comorbidities, anthracycline dose and infusion schedule, and the combined anti-cancer agents used, are diverse among cancer types. It is difficult to recommend guidelines for the prevention or management of anthracycline-induced cardiotoxicity applicable to all cancer types. Therefore, anthracycline-induced cardiotoxicity remains a major limitation in the proper management of cancer patients treated with an anthracycline-combined regimen. Efforts have been extensive to determine the mechanism and treatment of anthracycline-induced cardiotoxicity. Because cardiotoxicity causes irreversible damage to the myocardium, prevention is a more effective approach than treatment of cardiotoxicity after symptomatic or asymptomatic cardiac dysfunction develops. This article will review the pathophysiological mechanisms of anthracycline-induced cardiotoxicity and strategies for protecting the myocardium from anthracycline.
Anthracyclines ; Appointments and Schedules ; Breast Neoplasms ; Cardiotoxicity* ; Comorbidity ; Doxorubicin ; Drug Therapy ; Humans ; Leukemia ; Lymphoma ; Myocardium ; Sarcoma

Bupivacaine is frequently used for pain control and local anesthesia. However, it is associated with certain acute and fatal side effects, although rare, including cardiac and central nervous system toxicities. In particular, bupivacaine-induced cardiac toxicity may be fatal. This condition can be diagnosed as bupivacaine-induced cardiotoxicity by excluding other causes and determining a history of bupivacaine administration. However, in emergency situations, recognizing bupivacaine toxicity can be difficult due to the physician's lack of awareness regarding the condition or in the absence of clear communication regarding the patient's medical history. In the current case report, we describe our experience with strong suspected bupivacaine-induced cardiotoxicity in a patient who underwent cesarean section along with a review of the literature.
Anesthesia, Local ; Bupivacaine* ; Cardiomyopathies* ; Cardiotoxicity ; Central Nervous System ; Cesarean Section* ; Emergencies ; Female ; Humans ; Peripartum Period* ; Pregnancy

PURPOSE: To observe the effectiveness of the practical instruction sheet and the educational video for left-sided breast treatment in a patient receiving deep inspiration breath hold (DIBH) technique. Two parameters, simulation time and patient satisfaction, were assessed through the questionnaire. METHODS: Two different approaches, which were the instruction sheet and educational video, were combinedly used to assist patients during DIBH procedures. The guideline was assigned at least 1 week before the simulation date. On the simulation day, patients would fill the questionnaire regarding their satisfaction with the DIBH instruction. The questionnaire was categorized into five levels: extremely satisfied to dissatisfied, sequentially. The patients were divided into four groups: not DIBH technique, DIBH without instruction materials, the DIBH with instruction sheet or educational video, and DIBH with both of instruction sheet and educational video. RESULTS: Total number of 112 cases of left-sided breast cancer were analyzed. The simulation time during DIBH procedure significantly reduced when patients followed the instruction. There was no significant difference in simulation time on the DIBH procedures between patient compliance via instruction sheet or educational video or even following both of them. The excellent level was found at 4.6 ± 0.1 and 4.5 ± 0.1, for patients coaching via instruction sheet as well as on the educational video, respectively. CONCLUSION: Patient coaching before simulation could potentially reduce the lengthy time in the simulation process for DIBH technique. Practicing the DIBH technique before treatment is strongly advised.
Breast Neoplasms ; Breast ; Cardiotoxicity ; Humans ; Patient Compliance ; Patient Satisfaction ; Unilateral Breast Neoplasms

OBJECTIVETo evaluate the sensitivity of NT-pro-BNP in daunorubicin (DNR) induced myocardial damage by monitoring the level of NT-pro-BNP and myocardial enzymes (CK, CKMB) before and after DNR treatment in childhood acute leukemia (AL) and performing control study.

METHODSSixty-two cases (total 194 samples) which diagnosed as primary AL were enrolled and had received the conventional chemotherapy. According to the cumulative dose of DNR, they were divided into three groups: cumulative dose ≤ 60 mg/m(2) (group A); cumulative dose 60 - 120 mg/m(2) (group B); cumulative dose > 120 mg/m(2) (group C) and 15 cases with idarubicin (IDA) or mitoxantrone (MXR) as altervative to DNR (group D).

RESULTSThere was a significant difference (P = 0.000) in the level of NT-pro-BNP before and after DNR therapy, but did not in the myocardial enzymes activities (CK, P = 0.085 and CKMB, P = 0.076). The level of NT-pro-BNP appeared obviously elevated (P = 0.001) when DNR cumulative dose > 60 mg/m(2). While the level of CKMB did (P = 0.022) until DNR cumulative dose > 120 mg/m(2). In the 15 cases used IDA or MXR as alternative to DNR, the level of NT-pro-BNP fall from (239.9 ± 230.0) ng/L to (137.0 ± 131.9) ng/L (P = 0.024).

CONCLUSION(1) Compared with myocardial enzymes detection, NT-pro-BNP level can predict earlier DNR-induced cardiotoxicity. (2) Selection of the second or third generation anthracycline to treat AL can significantly reduce the cardiotoxicity in children.

Immune checkpoint inhibitors (ICIs) have been changing the paradigm of cancer treatment. However, immune-related adverse effects (irAEs) have also increased with the exponential increase in the use of ICIs. ICIs can break up the immunologic homeostasis and reduce T-cell tolerance. Therefore, inhibition of immune checkpoint can lead to the activation of autoreactive T-cells, resulting in various irAEs similar to autoimmune diseases. Gastrointestinal toxicity, endocrine toxicity, and dermatologic toxicity are common side effects. Neurotoxicity, cardiotoxicity, and pulmonary toxicity are relatively rare but can be fatal. ICI-related gastrointestinal toxicity, dermatologic toxicity, and hypophysitis are more common with anti- CTLA-4 agents. ICI-related pulmonary toxicity, thyroid dysfunction, and myasthenia gravis are more common with PD-1/PD-L1 inhibitors. Treatment with systemic steroids is the principal strategy against irAEs. The use of immune-modulatory agents should be considered in case of no response to the steroid therapy. Treatment under the supervision of multidisciplinary specialists is also essential, because the symptoms and treatments of irAEs could involve many organs. Thus, this review focuses on the mechanism, clinical presentation, incidence, and treatment of various irAEs.
Autoimmune Diseases ; Cardiotoxicity ; Homeostasis ; Incidence ; Myasthenia Gravis ; Organization and Administration ; Specialization ; Steroids ; T-Lymphocytes ; Thyroid Gland

This study aims to explore the toxicity mechanism of Rhododendri Mollis Flos(RMF) based on serum metabolomics and network toxicology. The toxic effect of RMF on normal rats was evaluated according to the symptoms, serum biochemical indexes, and histopathology. Serum metabolomics was combined with multivariate statistical analysis to search endogenous differential metabolites and related metabolic pathways. The toxic components, targets, and signaling pathways of RMF were screened by network toxicology technique, and the component-target-metabolite-metabolic pathway network was established with the help of serum metabolomics. The result suggested the neurotoxicity, hepatotoxicity, and cardiotoxicity of RMF. A total of 31 differential metabolites and 10 main metabolic pathways were identified by serum metabolomics, and 11 toxic components, 332 related target genes and 141 main signaling pathways were screened out by network toxicology. Further analysis yielded 7 key toxic components: grayanotoxin Ⅲ,grayanotoxinⅠ, rhodojaponin Ⅱ, rhodojaponin Ⅴ, rhodojaponin Ⅵ, rhodojaponin Ⅶ, and kalmanol, which acted on the following 12 key targets: androgen receptor(AR), albumin(ALB), estrogen receptor β(ESR2), sex-hormone binding globulin(SHBG), type 11 hydroxysteroid(17-beta) dehydrogenase(HSD17 B11), estrogen receptor α(ESR1), retinoic X receptor-gamma(RXRG), lactate dehydrogenase type C(LDHC), Aldo-keto reductase(AKR) 1 C family member 3(AKR1 C3), ATP binding cassette subfamily B member 1(ABCB1), UDP-glucuronosyltransferase 2 B7(UGT2 B7), and glutamate-ammonia ligase(GLUL). These targets interfered with the metabolism of gamma-aminobutyric acid, estriol, testosterone, retinoic acid, 2-oxobutyric acid, and affected 4 key metabolic pathways of alanine, aspartate and glutamate metabolism, cysteine and methionine metabolism, steroid hormone biosynthesis, and retinol metabolism. RMF exerts toxic effect on multiple systems through multiple components, targets, and pathways. Through the analysis of key toxic components, target genes, metabolites, and metabolic pathways, this study unveiled the mechanism of potential neurotoxicity, cardiotoxicity, and hepatotoxicity of RMF, which is expected to provide a clue for the basic research on toxic Chinese medicinals.
Animals ; Cardiotoxicity ; Chemical and Drug Induced Liver Injury ; Drugs, Chinese Herbal/toxicity* ; Hormones ; Metabolomics ; Rats