Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 6 de 6
Filter
1.
Cancer Research on Prevention and Treatment ; (12): 524-529, 2021.
Article in Chinese | WPRIM | ID: wpr-988578

ABSTRACT

Breast cancer is one of the most common malignant tumors in women. Because of the abundance of diagnosis and treatment methods and the wide application of targeted therapy drugs in recent years, the survival time of breast cancer patients is longer than before and the mortality rate shows a downward trend. However, the incidence of cardiovascular toxicity associated with targeted drug therapy in breast cancer patients is also increasing. This article reviews the research progress of cardiovascular toxicity associated with targeted drug therapy in breast cancer.

2.
Rev. costarric. salud pública ; 28(1): 105-116, ene.-jun. 2019. tab
Article in Spanish | LILACS | ID: biblio-1013980

ABSTRACT

Resumen La cocaína es una sustancia psicoactiva ampliamente utilizada de forma recreativa. El uso indiscriminado de esta sustancia genera múltiples consultas a los servicios de emergencias, principalmente debido a sus efectos cardiovasculares. Los mecanismos fisiopatológicos actúan principalmente en sistema nervioso simpático, cardiomiocito, plaquetas, canales de sodio y potasio, entre otros. El objetivo principal de esta revisión es demostrar los efectos cardiovasculares asociados al uso de la cocaína.


Abstract Cocaine is a psychoactive substance widely used recreationally. The indiscriminate use of this substance generates multiple consultations to the emergency services, mainly due to its cardiovascular effects. The physio pathological mechanisms act mainly in sympathetic nervous system, cardiomyocyte, platelets, sodium and potassium channels, among others. The main objective of this review is to demonstrate the cardiovascular effects associated with the use of cocaine.


Subject(s)
Cannabis/adverse effects , Cardiovascular Diseases/pathology , Cocaine/adverse effects , Coronary Disease , Cardiotoxicity , Chest Pain
3.
Practical Oncology Journal ; (6): 134-138, 2019.
Article in Chinese | WPRIM | ID: wpr-752827

ABSTRACT

Objective The aim of this study was to establish a practical and feasible prevention,and a treatment scheme of cardiovascular toxicity(CVT)induced by chemotherapy in cervical cancer based on known effective measures and to provide scientific guidance and basis for clinical treatment. Methods The risk of pre-chemotherapy CVT and post-chemotherapy CVT were evalua-ted in 164 subjects from November 2016 to January 2018. The Interrupted time series(ITS)model of CVT incidence before and after intervention was established. The CVT biomarkers and results of clinical examination before and after chemotherapy were compared in selected patieds. The effects of measures were evaluated. Results There was no difference in the ITS model of CVT incidence before and after intervention(P>0. 05). Among echocardiography examination results,the E peak velocity of mitral valve and E/A ratio in-creased,and the difference was statistically significant(P<0. 05),LVEF、FS、SV and A peak velocity of mitral valve had no differ-ences(P>0. 05). There were no differences in ECG and double lower extremities arteriovenous ultrasonography results(P>0. 05). The level of sICAM-1,sTM,vWF and h-FABP decreased(P<0. 05),the levels of NO and eNOS increased(P<0. 05);there was no significant difference in the levels of hs-CRP and E-selectin(P>0. 05). Conclusion The comprehensive prevention and treat-ment program established in this study can improve the cervical cancer chemotherapy CVT microscopically, and further research should be carried out by expanding the sample size.

4.
Journal of Cardiovascular Ultrasound ; : 1-25, 2018.
Article in English | WPRIM | ID: wpr-713245

ABSTRACT

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.


Subject(s)
Humans , Biomarkers , Cardiotoxicity , Diagnosis , Drug Therapy , Echocardiography , Mortality , Risk Factors
5.
Korean Journal of Anesthesiology ; : 403-411, 2005.
Article in Korean | WPRIM | ID: wpr-222110

ABSTRACT

BACKGROUND: This study was designed to assess the effects of rilmenidine on the autonomic nervous system, and to evaluate whether it prevents bupivacaine-induced cardiovascular toxicity during intravenous bupivacaine infusion in anesthetized cats. METHODS: Thirty male cats were randomly divided into a control group (n = 15) and a rilmenidine group (n = 15). Following the injection of rilmenidine (10microgram/kg), systolic blood pressures (SBP) and R-R intervals (RRI) were recorded for 5 minutes. Then power spectral analyses of the SBP and RRI, and transfer function analysis were conducted to evaluate the autonomic nervous system. During the infusion of bupivacaine (0.5 mg/kg/min), blood pressures, heart rates, times to reach each events, and bupivacaine doses were measured at the first QRS modification, the first dysrhythmia, at 25% (HR25) and 50% reductions in baseline heart rate, and at 25% and 50% reductions in baseline mean arterial pressure and at final systole. RESULTS: The high frequency (HF) power of heart rate variability (HRV) was significantly elevated in the rilmenidine group versus the control group. Magnitude HF was significantly higher in the rilmenidine group than in the control group. The onset of dysrhythmia correlated significantly with the HFs of HRV and baroreflex sensitivity (BRS). Except for HR25, the rilmenidine group showed significantly higher bupivacaine doses and delayed event onsets versus the control group. CONCLUSIONS: We suggest that pretreatment with rilmenidine delays the onset of dysrhythmia by increasing vagal tone and BRS and by reducing cardiovascular toxicity when bupivacaine is infused continuously to isoflurane anesthetized cats.


Subject(s)
Animals , Cats , Humans , Male , Arterial Pressure , Autonomic Nervous System , Baroreflex , Bupivacaine , Heart Rate , Isoflurane , Systole
6.
Korean Journal of Anesthesiology ; : 1532-1540, 1994.
Article in Korean | WPRIM | ID: wpr-218152

ABSTRACT

This study was performed to evaluate the influence of clonidine pretreatment on the car- diovascular toxic effects of bupivacaine overdose induced by constant intravenous infusion. Thirty male rabbits were used for this study and they were divided into saline pretreatment group(15) and clonidine-pretreatment group(15). The changes of mean arterial pressure, heart rate and electrocardiogram by the bupivacaine-induced toxic effect during intravenous infusion of bupivacaine were observed. The results were as follows; 1. Mean arterial pressure was significantly decreased in clonidine-premedicated group compared with control group (P<0.01) before infusion of bupivacaine, but the times occuring 25% and 50% decrease of mean arterial pressure were significantly prolonged in clonidine group compared with control group (P <0.001 ). 2. Heart rate was significantly decreased in clonidine group compared with control group (P<0.01) before infusion of bupivacaine, but the times occuring 25% and 50% decrease of heart rate were significantly prolonged in clonidine group compared with control group (P< 0.001). 3. The times occuring the first QRS modification and first dysrhythmia and the final systole were significantly prolonged in clonidine group compared with control group (P < 0.001). In conclusion, clonidine given prophylactically delays the cardiotoxicity caused by bupivacaine overdose snd does not accentuate the subsequent hypotension.


Subject(s)
Humans , Male , Rabbits , Arterial Pressure , Bupivacaine , Clonidine , Electrocardiography , Heart Rate , Hypotension , Infusions, Intravenous , Systole
SELECTION OF CITATIONS
SEARCH DETAIL