Left Ventricular Diastolic Dysfunction Induced by Cyclophosphamide in Blood Stem Cell Transplantation.
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Abstract:
Cardiac complications are major limiting factors regarding the success of high-dose chemotherapy supported by blood stem cell transplantation (BSCT). The cardiotoxicity of cyclophosphamide remains obscure relative to that of anthracyclines. The aim of this study was to estimate noninvasively the cardiotoxicity of cyclophosphamide administered during the pretransplant conditioning of BSCT for patients with various hematological diseases. A total of 27 consecutive patients were divided into two groups depending on the conditioning regimen, ie, group A (n=15) which received cyclophosphamide (median dose of 120 mg/kg; range 100 to 200 mg/kg) and group B (n=12) which did not. Ultrasound cardiograms (UCG) and signal-averaged electrocardiograms (SAECG) were recorded in the two groups both preceding and following the BSCT. There were no statistical intergroup or intragroup differences in left ventricular (LV) dimensions or contractile function. Significant (P<0.01) posttransplant increases in interventricular septal wall thickness and Ap/Ep ratio were noted in group A. Moreover, the filtered QRS duration as estimated by SAECG was prolonged (P<0.05) whereas the summated LV voltage (SV1+RV5) was reduced in the posttransplant period only in group A. These results suggest that early cyclophosphamide cardiotoxicity was characterized by LV diastolic rather than systolic dysfunction. These findings may contribute to acute hemodynamic deterioration observed after cyclophosphamide-containing conditioning chemotherapy.Keywords:
Cardiotoxicity
Preload
We report 3 cases of heart transplantation in adults due to chemotherapy-induced cardiotoxicity in a transplant center in Rio de Janeiro, Brazil. All patients received anthracyclines during cancer treatment. We reviewed and discussed the cases with data from the literature, addressing the importance of early diagnosis and treatment of heart failure in cancer survivors. Heart Transplantation in Patients with Chemotherapy-Induced Cardiotoxicity
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Cancer Chemotherapy
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Purpose of review To summarize the relevant peer-reviewed publications over the past year that addressed issues of when to give (or not give) fluid to the critically ill patient. Recent findings Clinical data from several studies underscore the inability of measures of ventricular filling to assess either preload or preload responsiveness. Whereas less invasive monitoring techniques than pulmonary arterial catheterization demonstrate better discrimination with estimates of both preload and preload responsiveness. Measuring dynamic changes in stroke volume, descending aortic flow, and both superior and inferior vena caval diameters during ventilation provides good predictive value in defining preload responsiveness. One study demonstrated that resuscitation protocols keyed to esophageal flow measures improved outcome in postoperative cardiac surgery patients. Summary Preload is not preload responsiveness. Functional measures of preload responsiveness exist and are superior to traditional measures of filling pressures in driving resuscitation in critically ill patients.
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Also termed left ventricular end-diastolic pressure (LVEDP), preload is a measure of the degree of the ventricular stretch when the heart is at the end of diastole. Preload, in addition to afterload and contractility, is one of the three main factors that directly influence stroke volume (SV), the amount of blood pumped out of the heart in one cardiac cycle. Affected by changes in venous tone and circulating blood volume, changes in preload directly affect stroke volume, therefore influencing cardiac output and the overall function of the heart. A thorough understanding of preload, what affects it, and how pharmacological treatments can manipulate preload is essential to understanding overall cardiac physiology.
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Cardiac cycle
Cardiovascular physiology
End-diastolic volume
Venous return curve
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Purpose of review: To summarize the relevant peer-reviewed publications over the past year that addressed issues of when to give (or not give) fluid to the critically ill patient. Recent findings: Clinical data from several studies underscore the inability of measures of ventricular filling to assess either preload or preload responsiveness. Whereas less invasive monitoring techniques than pulmonary arterial catheterization demonstrate better discriminations with estimates of both preload and preload responsiveness. Measuring dynamic changes in stroke volume, descending aortic flow, and both superior and inferior vena caval diameters during ventilation provides good predictive value in defining preload responsiveness. One study demonstrated that resuscitation protocols keyed to esophageal flow measures improved outcome in postoperative cardiac surgery patients. Summary: Preload is not preload responsiveness. Functional measures of preload responsiveness exist and are superior to traditional measures of filling pressures in driving resuscitation in critically ill patients. © 2005 Lippincott Williams & Wilkins.
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Adjuvant Chemotherapy
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Doxorubicin (Dox) is a chemotherapeutic agent widely used for the treatment of numerous cancers. However, the clinical use of Dox is limited by its unwanted cardiotoxicity. Mitochondrial dysfunction has been associated with Dox-induced cardiotoxicity. To mitigate Dox-related cardiotoxicity, considerable successful examples of a variety of small molecules that target mitochondria to modulate Dox-induced cardiotoxicity have appeared in recent years. Here, we review the related literatures and discuss the evidence showing that mitochondria-targeting small molecules are promising cardioprotective agents against Dox-induced cardiac events.
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