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1
Palmer, S. C., J. Carver, L. Jacobs, K. H. Schmitz, C. Fung, E. Mohler, and D. J. Vaughn. "Assessment of coronary heart disease risk in testicular cancer survivors." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 4592. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.4592.
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4592 Background: Testicular cancer survivors (TCS) who receive cisplatin-based chemotherapy (CBCT) are reported to have an increased risk of coronary heart disease (CHD) compared to chemo-naive TCS (J Clin Oncol 21:1513–1523, 2003). We hypothesized that TCS treated with CBCT would demonstrate abnormal objective measures of future CHD risk compared to chemo-naive TCS. Methods: TCS ≥ 2 years from diagnosis underwent evaluation using established objective measures predictive of future CHD risk: body mass index (BMI), Framingham relative risk (RR), flow-mediated endothelium-dependent vasodilation of the brachial artery (FMD), carotid artery intima-media thickness (IMT), serum intercellular adhesion molecule-1 (ICAM-1), and high sensitivity C-reactive protein (hs-CRP). Data were analyzed using parametric and non-parametric statistics as appropriate. Results: 30 TCS who received CBCT and 20 chemo-naive TCS were recruited. The mean age and time from diagnosis were similar between the 2 groups. Both groups demonstrated elevated BMI, increased Framingham RR, and impaired FMD, consistent with an increased risk of CHD. However, there were no statistically significant differences in these measures between the two groups. Carotid IMT, ICAM-1, and hs-CRP were not significantly abnormal and these measures also did not differ between the two groups. Conclusions: TCS demonstrate abnormal objective measures of CHD risk in both CBCT-treated and chemo-naive groups. These data suggest that behavioral interventions to modify CHD risk should target all TCS independent of chemotherapy status. All values reported are mean ± standard deviation [Table: see text] No significant financial relationships to disclose.
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Сергеева, N. Sergeeva, Коломиец, V. Kolomiets, Маль, G. Mal, Алыменко, and M. Alymenko. "Evaluation of Spent Pharmacotherapy in the Patients with Coronary Heart Disease Associated with Pulmonary Tuberculosis by means of the Neural Network." Journal of New Medical Technologies 21, no. 4 (October 8, 2014): 108–12. http://dx.doi.org/10.12737/7281.
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Current, the programs of mass prevention of the cardiovascular diseases, based on preventive medicinal correction of risk factors of cardiovascular diseases, such as hyperlipidemia, arterial hypertension, diabetes mellitus, are developed and realized.
Pulmonary tuberculosis influences on state of blood system, which can be considered as functional disorders of the cardiovascular system caused by tuberculosis. These violations caused by concomitant tuberculosis lung diseases, such as cardiovascular and other diseases of the respiratory system. Specific (tuberculosis) damages of the heart and blood vessels are rare and currently their influence on pathomorphosis of tuberculosis isn’t expressed. Modern schemes of treatment of coronary heart disease and hypertension are also applicable to patients with Pulmonary tuberculosis. Effective treatment of coronary heart disease and hypertension in patients with tuberculosis by means of the drugs, allows to normalize the function of the cardiovascular system and to carry out long-chemotherapy by anti-TB drugs and cures of tuberculosis. The study showed the ability to predict the degree of lipid-lowering effect in patients with coronary heart disease in combination with infiltrative tuberculosis of the lungs that can provide the right choice of drug in lipid-lowering therapy.
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Bachmeyer, Claude, Hervé Joly, and Roland Jorest. "Early Myocardial Infarction during Chemotherapy for Testicular Cancer." Tumori Journal 86, no. 5 (September 2000): 428–30. http://dx.doi.org/10.1177/030089160008600513.
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A 36-year-old man with testicular cancer had an acute myocardial infarction during the first course of chemotherapy with bleomycin, etoposide and cisplatin. Since the patient had no significant risk factors for coronary heart disease, the infarction was likely to be attributable to the chemotherapy regimen. The physiopathological mechanisms of this causal relationship are discussed here.
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Ozben, Beste, Ramazan Kurt, Huseyin Oflaz, Murat Sezer, Mert Basaran, Taner Goren, and Sabahattin Umman. "Acute Anterior Myocardial Infarction After Chemotherapy for Testicular Seminoma in a Young Patient." Clinical and Applied Thrombosis/Hemostasis 13, no. 4 (October 2007): 439–42. http://dx.doi.org/10.1177/1076029607303334.
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Testicular cancer is the most common solid tumor among young men aged 15 to 35 years. Combination chemotherapy with cisplatin, etoposide, and bleomycin remains the mainstay of treatment. We present a 27-year-old man who presented with an acute anterior myocardial infarction during the second course of chemotherapy for seminoma. Because the patient had no significant risk factors for coronary heart disease, the infarction was likely caused by the chemotherapy regimen.
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Hader, Shelby N., Natalya Zinkevich, Laura E. Norwood Toro, Alison J. Kriegel, Amanda Kong, Julie K. Freed, David D. Gutterman, and Andreas M. Beyer. "Detrimental effects of chemotherapy on human coronary microvascular function." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 4 (October 1, 2019): H705—H710. http://dx.doi.org/10.1152/ajpheart.00370.2019.
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Chemotherapy (CT) is a necessary treatment to prevent the growth and survival of cancer cells. However, CT has a well-established adverse impact on the cardiovascular (CV) system, even years after cessation of treatment. The effects of CT drugs on tumor vasculature have been the focus of much research, but little evidence exists showing the effects on the host microcirculation. Microvascular (MV) dysfunction is an early indicator of numerous CV disease phenotypes, including heart failure. The goal of this study was to evaluate the direct effect of doxorubicin (Dox) on human coronary MV function. To study the effect of CT on the cardiac MV function, flow-mediated dilation (FMD), pharmacologically-induced endothelial dependent dilation to acetylcholine (ACh), and smooth muscle-dependent dilation to papaverine were investigated. Vessels were freshly isolated from atrial appendages of adult patients undergoing cardiopulmonary bypass surgery or from cardiac tissue of pediatric patients, collected at the time of surgery to repair congenital heart defects. Isolated vessels were incubated in endothelial culture medium containing vehicle or Dox (100 nm, 15–20 h) and used to measure dilator function by video microscopy. Ex vivo treatment of adult human coronary microvessels with Dox significantly impaired flow-mediated dilation (FMD). Conversely, in pediatric coronary microvessels, Dox-induced impairment of FMD was significantly reduced in comparison with adult subjects. In both adult and pediatric coronary microvessels, ACh-induced constriction was reversed into dilation in the presence of Dox. Smooth muscle-dependent dilation remained unchanged in all groups tested. In vessels from adult subjects, acute treatment with Dox in clinically relevant doses caused significant impairment of coronary arteriolar function, whereas vessels from pediatric subjects showed only marginal impairment to the same stressor. This interesting finding might explain the delayed onset of future adverse CV events in children compared with adults after anthracycline therapy. NEW & NOTEWORTHY We have characterized, for the first time, human microvascular responses to acute ex vivo exposure to doxorubicin in coronary vessels from patients without cancer. Our data show an augmented impairment of endothelial function in vessels from adult subjects compared with pediatric samples.
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Zhang, Dingguo, Liansheng Wang, and Zhijian Yang. "Recurrent Syncope Associated with Lung Cancer." Case Reports in Medicine 2015 (2015): 1–4. http://dx.doi.org/10.1155/2015/309784.
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Syncope is an important problem in clinical practice with many possible causes that might be misdiagnosed. We present an unusual case of syncope, which has a normal chest X-ray. Exercise EKG and coronary angioplasty results confirmed the existence of serious coronary heart disease. The patient was treated with coronary stent transplantation. However, scope occurred again and the elevated tumor makers cytokeratin-19-fragment and neuron-specific enolase revealed the bronchogenic carcinoma, which was confirmed by enhanced CT examination. The treatment of carcinoma by chemotherapy was indeed sufficient for prompt elimination of the syncope symptoms.
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Daher, Iyad N., Jose Banchs, Syed Wamique Yusuf, Elie Mouhayar, Jean-Bernard Durand, and Gregory Gladish. "Impact of Cardiac Computed Tomographic Angiography Findings on Planning of Cancer Therapy in Patients with Concomitant Structural Heart Disease." Cardiology Research and Practice 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/268058.
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Background. Exclusion of underlying coronary artery disease (CAD) is essential in the diagnosis of chemotherapy-induced cardiomyopathy. Presence and severity of CAD can also impact the choice of therapy in cancer patients. The value of cardiac computed tomographic angiography (CCTA) in this setting has not been reported.Methods. We collected data on the clinical presentation and indications for CCTA performed from January to December 2008 at the University of Texas MD Anderson Cancer Center (MDACC). All examinations were performed using a 64-detector scanner. CCTA results and subsequent treatment decisions were examined.Results. A total of 80 patients underwent CCTA during the study period for the following indications (not mutually exclusive): cardiomyopathy of unknown etiology in 33 pts (41.3%), chest pain in 32 (40.0%), abnormal stress test in 16 (20.0%), abnormal cardiac markers in 8 (10.0%), suspected cardiac mass or thrombus in 7 (8.8%). Chemotherapy-induced cardiomyopathy was diagnosed in 18 pts (22.5%). Severe CAD was detected in 22 pts (27.5%); due to concomitant advanced cancer or patient refusal, only 12 underwent coronary angiogram. Of these, 4 pts (5% of total) underwent coronary artery bypass grafting. A total of 41 pts (51.3%) had their cancer management altered based on CCTA findings.Conclusion. CCTA is useful in evaluating cancer pts with structural heart disease and can have an impact on the management of cancer and cardiac disease.
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van Leeuwen, Flora E., and Andrea K. Ng. "Long-term risk of second malignancy and cardiovascular disease after Hodgkin lymphoma treatment." Hematology 2016, no. 1 (December 2, 2016): 323–30. http://dx.doi.org/10.1182/asheducation-2016.1.323.
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Abstract Long-term survivors of Hodgkin lymphoma (HL) experience several late adverse effects of treatment, with second malignant neoplasms (SMNs) and cardiovascular diseases (CVDs) being the leading causes of death in these patients. Other late effects have also been identified, such as pulmonary dysfunction, endocrinopathies (thyroid dysfunction, infertility), neck muscle atrophy, and persistent fatigue. HL survivors have two- to fourfold increased risks to develop SMNs and CVD compared with the general population. With respect to SMNs, radiotherapy is associated with 1.5- to 15-fold increased risk of solid malignancies. The relative risk (RR) of solid tumors increases steadily with increasing follow-up time from 5 to 15 years since radiotherapy, and remains elevated for at least 40 years. The RR of solid SMNs increases strongly with younger age at first treatment. Risks of lung, breast, and gastrointestinal (GI) cancers increase with higher radiation dose. Alkylating agent chemotherapy, especially procarbazine, does not only increase risk of leukemia but also of solid malignancies, in particular, cancers of the lung and GI tract. In contrast, gonadotoxic chemotherapy decreases the risk of radiation-associated breast cancer, through induction of premature menopause. Smoking appears to multiply the radiation- and chemotherapy-associated risks of lung cancer. Both radiotherapy and chemotherapy for HL may cause cardiovascular toxicity. Radiotherapy increases the risk of coronary heart disease, valvular heart disease, congestive heart failure (HF), and pericarditis, whereas anthracycline-containing chemotherapy increases the risks of HF and valvular heart disease. Cardiovascular toxicity following radiotherapy is usually observed from 5 to at least 35 years after therapy, whereas anthracycline-related toxicity is already observed during treatment, up to at least 25 years. The joint effects of anthracyclines, radiotherapy, and conventional cardiovascular risk factors (eg, hypertension, smoking, and physical inactivity) appear to be additive rather than multiplicative. HL survivors need lifelong risk-based screening for selected SMNs and CVDs. Furthermore, preventive strategies should include lifestyle and drug-based interventions to minimize exposure to conventional risk factors for cancer and CVD.
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Chaulin, A. M., and D. V. Duplyakov. "Increased natriuretic peptides not associated with heart failure." Russian Journal of Cardiology 25 (January 11, 2021): 4140. http://dx.doi.org/10.15829/1560-4071-2020-4140.
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Natriuretic peptides (NPs) are key diagnostic and prognostic biomarkers for patients with heart failure (HF). The main mechanism for increasing serum NP levels, which is characteristic of heart failure, is secretion in response to myocardial wall distention. At the same time, according to Russian and foreign literature, an increase in NPs is reported in a number of many other conditions that are not associated with HF. The study of these causes and mechanisms is necessary to improve the differential diagnosis of HF.This article discusses the mechanisms of increasing NPs and their diagnostic value in heart failure, as well as a number of other conditions, such as acute coronary syndrome and coronary artery disease, atrial fibrillation, exercise, kidney failure, taking cardiotoxic drugs (chemotherapy) and sacubitril/valsartan. The article also provides data on identifying NPs in non-invasively obtained biological fluids (urine and oral fluid).
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Karev, E. A., S. L. Verbilo, E. G. Malev, M. N. Prokudina, P. A. Mochalov, E. A. Bobrova, N. P. Malinina, and A. V. Kozlenok. "Myocardial strain echocardiographic assessment: from theory to practice." Translational Medicine 7, no. 6 (December 18, 2020): 16–28. http://dx.doi.org/10.18705/2311-4495-2020-7-6-16-28.
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Assessment of systolic and diastolic ventricular function is one of the main goals of echocardiography. Nevertheless, some patients require data beyond standard echocardiographic protocol for making more precise clinical decision and prognosis determination. The spectrum of novel parameters, including myocardial strain and strain rate, provides more comprehensive evaluation of the initial changes in myocardium in a variety of clinical conditions. New methods of quantifying the systolic function of left and right ventricles can be applied in patients with arterial hypertension, coronary heart disease, hypertrophic and dilated cardiomyopathies, also in patients with valvular heart disease such as aortic stenosis, aortic and mitral insufficiency. Besides strain analysis in patients with myocardial storage diseases, patients on cardiotoxic chemotherapy and patients with heart transplant turned out to be a specific niche for the method. Here, we provide the possibilities of strain analysis in variable heart pathologies in clinical practice.
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Prasad, Megha, Michel T. Corban, Timothy D. Henry, Allan B. Dietz, Lilach O. Lerman, and Amir Lerman. "Promise of autologous CD34+ stem/progenitor cell therapy for treatment of cardiovascular disease." Cardiovascular Research 116, no. 8 (February 5, 2020): 1424–33. http://dx.doi.org/10.1093/cvr/cvaa027.
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Abstract CD34+ cells are haematopoietic stem cells used therapeutically in patients undergoing radiation or chemotherapy due to their regenerative potential and ability to restore the haematopoietic system. In animal models, CD34+ cells have been associated with therapeutic angiogenesis in response to ischaemia. Several trials have shown the potential safety and efficacy of CD34+ cell delivery in various cardiovascular diseases. Moreover, Phase III trials have now begun to explore the potential role of CD34+ cells in treatment of both myocardial and peripheral ischaemia. CD34+ cells have been shown to be safe and well-tolerated in the acute myocardial infarction (AMI), heart failure, and angina models. Several studies have suggested potential benefit of CD34+ cell therapy in patients with coronary microvascular disease as well. In this review, we will discuss the therapeutic potential of CD34+ cells, and describe the pertinent trials that have used autologous CD34+ cells in no-options refractory angina, AMI, and heart failure. Lastly, we will review the potential utility of autologous CD34+ cells in coronary endothelial and microvascular dysfunction.
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Champeaux, Anne L., Jason L. Blaser, Jerome B. Myers, and David T. Schachter. "Multiple Myeloma Involving the Myocardium and Coronary Vessels." Archives of Pathology & Laboratory Medicine 124, no. 6 (June 1, 2000): 910–12. http://dx.doi.org/10.5858/2000-124-0910-mmitma.
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Abstract We report a case of metastatic plasmacytoma to the myocardium and coronary vessels in a 57-year-old man with multiple myeloma. Originally, the patient had a large plasmacytoma in his left chest wall and lung. He received local radiation and chemotherapy. Subsequently, the patient presented with symptoms of congestive heart failure. He had no prior history of cardiac disease. The patient was treated medically and later died from respiratory failure. At autopsy, a metastatic plamacytoma was indentified within the myocardium and externally compressing the coronary arteries. The tumor infiltrated into the coronary sinus. It is difficult to speculate whether the patient's symptoms were due to cardiac involvement since the tumor burden in his chest was also considerable. To our knowledge, coronary vessel involvement with plasmacytoma has not been previously described.
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Gangaraju, Radhika, Yanjun Chen, Lindsey Hageman, Jessica Wu, Liton F. Francisco, Michelle Kung, Daniel J. Weisdorf, et al. "Coronary Heart Disease Risk in Blood or Marrow Transplant Survivors." Blood 136, Supplement 1 (November 5, 2020): 17–18. http://dx.doi.org/10.1182/blood-2020-137731.
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INTRODUCTION: Exposure to total body irradiation (TBI) increases the risk for cardiovascular risk factors (CVRFs) such as diabetes, hypertension and dyslipidemia in Blood or Marrow Transplant (BMT) survivors with the potential to increase the risk of post-BMT Coronary Heart Disease (CHD). Chest radiation is associated with accelerated atherosclerosis in conventionally treated patients. These factors, with or without additional factors such as smoking likely place BMT survivors at a high risk for CHD. Yet, a comprehensive evaluation of the risk of late-occurring CHD in BMT survivors is lacking. We addressed this gap using the resources offered by the BMT survivor study (BMTSS). METHODS: BMTSS includes patients transplanted between 1974 and 2014 at 3 US sites, and who had survived ≥2 years after BMT, and were alive and ≥18 years at BMTSS survey completion. The BMTSS survey asked participants to report chronic health conditions diagnosed by their healthcare provider (including CHD, diabetes, hypertension and dyslipidemia), along with age at diagnosis. The participants self-reported sociodemographics and health behaviors. Information regarding primary cancer diagnosis, therapeutic exposures, donor type, stem cell source, and history of chronic graft vs. host disease (GvHD; for allogeneic BMT recipients) was abstracted from medical records. A cohort of 1,131 siblings completed the BMTSS survey and served as a comparison group. We obtained informed consent from all participants. RESULTS: The study included 3,479 BMT survivors; 50.3% had received an allogeneic BMT, 54.8% were males, and 71.4% were non-Hispanic whites. Median age at study participation was 59 years (interquartile range [IQR]: 48-66 years) for BMT survivors and 57 years (IQR: 46-64 years) for siblings. BMT survivors were followed for a median of 9 years (range: 2-41 years) from BMT. CHD developed after BMT in 122 BMT survivors (52 allogeneic, 70 autologous). BMT recipients compared with siblings: After adjusting for sociodemographics and comorbidities, allogeneic BMT survivors were at a 7.2-fold higher odds (95%CI: 4.0-13.0, p<0.0001) and autologous BMT recipients at a 11.7-fold higher odds (95%CI: 6.8-20.2, p<0.0001) of reporting CHD as compared to siblings. Allogeneic BMT survivors: The 20 year cumulative incidence of CHD was 4.7% for allogeneic BMT recipients. Increasing age at BMT (HR=1.05/year, 95%CI: 1.02-1.07, p<0.0001), male sex (HR=2.09, 95%CI: 1.14-3.82, p=0.017), history of CVRFs (HR=3.6, 95%CI: 1.72-7.41, p=0.0006), and pre-BMT targeted chemotherapy such as tyrosine kinase inhibitors (HR=2.7, 95%CI: 1.10-6.77, p=0.030) were associated with increased CHD risk. The 20 year cumulative incidence of CHD among patients with CVRFs was 6.6% vs. 1.9% (p=0.005) among those who did not have CVRFs (Fig 1). Autologous BMT survivors: The 20 year cumulative incidence of CHD was 9.1% for autologous BMT recipients. The risk factors for CHD in autologous BMT survivors included: increasing age at BMT (HR=1.06/year, 95%CI: 1.03-1.09, p<0.0001), male sex (HR=2.3, 95%CI: 1.30-3.90, p=0.004), history of smoking (HR=1.66, 95%CI: 1.03-2.67, p=0.038), CVRFs (HR=1.77, 95%CI: 1.04-3.01, p=0.036), arrhythmia (HR=1.85, 95%CI: 1.01-3.42, p=0.048) and history of pre-BMT chest radiation (HR=4.56, 95%CI: 2.1-9.88, p=0.0001). For every 1 Gray increase in the dose of chest radiation, there was a 4% increase in the risk of CHD, p=0.0002. The 20 year cumulative incidence of CHD among patients with CVRFs was 10.2% vs. 7.4% among those who did not have CVRFs (p=0.04) (Fig 2). CONCLUSION: BMT survivors are at a 7-fold to 12-fold higher risk of CHD compared with a sibling comparison group. CVRFs are independent risk factors for CHD both among allogeneic and autologous BMT recipients. Pre-BMT chest radiation further increases this risk in autologous BMT recipients. These findings suggest a need for aggressive management of CVRFs in BMT recipients to prevent CHD-related morbidity. Disclosures Gangaraju: Sanofi Genzyme, Consultant for Cold Agglutinin Disease: Consultancy. Weisdorf:FATE Therapeutics: Consultancy; Incyte: Research Funding. Arora:Pharmacyclics: Research Funding; Kadmon: Research Funding; Syndax: Research Funding; Fate Therapeutics: Consultancy.
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Picano, Eugenio, Quirino Ciampi, Lauro Cortigiani, Adelaide M. Arruda-Olson, Clarissa Borguezan-Daros, José Luis de Castro e Silva Pretto, Rosangela Cocchia, et al. "Stress Echo 2030: The Novel ABCDE-(FGLPR) Protocol to Define the Future of Imaging." Journal of Clinical Medicine 10, no. 16 (August 17, 2021): 3641. http://dx.doi.org/10.3390/jcm10163641.
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With stress echo (SE) 2020 study, a new standard of practice in stress imaging was developed and disseminated: the ABCDE protocol for functional testing within and beyond CAD. ABCDE protocol was the fruit of SE 2020, and is the seed of SE 2030, which is articulated in 12 projects: 1-SE in coronary artery disease (SECAD); 2-SE in diastolic heart failure (SEDIA); 3-SE in hypertrophic cardiomyopathy (SEHCA); 4-SE post-chest radiotherapy and chemotherapy (SERA); 5-Artificial intelligence SE evaluation (AI-SEE); 6-Environmental stress echocardiography and air pollution (ESTER); 7-SE in repaired Tetralogy of Fallot (SETOF); 8-SE in post-COVID-19 (SECOV); 9: Recovery by stress echo of conventionally unfit donor good hearts (RESURGE); 10-SE for mitral ischemic regurgitation (SEMIR); 11-SE in valvular heart disease (SEVA); 12-SE for coronary vasospasm (SESPASM). The study aims to recruit in the next 5 years (2021–2025) ≥10,000 patients followed for ≥5 years (up to 2030) from ≥20 quality-controlled laboratories from ≥10 countries. In this COVID-19 era of sustainable health care delivery, SE2030 will provide the evidence to finally recommend SE as the optimal and versatile imaging modality for functional testing anywhere, any time, and in any patient.
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Gros, Rosine, Vincent Hugon, Jean-Marc Thouret, and Vincent Peigne. "Coronary Spasm after an Injection of Vincristine." Chemotherapy 62, no. 3 (2017): 169–71. http://dx.doi.org/10.1159/000455224.
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Cardiotoxicity, including heart failure, thromboembolic events, and myocardial ischemia, is a concern for cardiologists and oncologists. The most frequently involved drugs are anthracyclines. We report an episode of coronary spasm due to vincristine, a vinca alkaloid, in a 49-year-old man treated for a diffuse undifferentiated carcinoma. The patient suffered recurrent episodes of typical chest pain with ST-elevation in the inferior area. Coronary spasm was confirmed by an angiogram, which showed normal coronary arteries. No recurrence occurred with the medical management. Coronary spasm induced by vincristine is a newly described facet of chemotherapy-related cardiotoxicity.
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Alsara, Osama, Ahmad Alsarah, Jagadeesh K. Kalavakunta, Heather Laird-Fick, and George S. Abela. "Isolated Left Main Coronary Artery Stenosis after Thoracic Radiation Therapy: To Operate or Not to Operate." Case Reports in Medicine 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/834164.
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Radiation therapy of neoplasms involving the chest or mediastinum results in a wide spectrum of cardiac complications including coronary artery disease, which can present in patients with few or no traditional cardiac risk factors. We report a case of radiation induced coronary artery disease in a 60-year-old female with a history of stage IIIA nonsmall cell lung carcinoma which was diagnosed eight years earlier and treated with chemotherapy and radiotherapy. She presented to the hospital with atypical chest pain that had occurred intermittently over the preceding week. Her initial electrocardiogram and cardiac enzymes were within normal limits. However, following an indeterminate exercise nuclear stress test, she developed chest pain and elevated cardiac enzymes. Coronary angiography demonstrated 90% stenosis of the left main coronary artery ostium, without any evidence of atherosclerotic disease or stenosis in other coronary arteries. She underwent surgical revascularization, which revealed dense adhesions surrounding the heart. During surgery, she developed severe bleeding and died. Coronary artery disease can present within years of radiation exposure, and ostial lesions are typical. Treatment is often challenging because of the effects of radiation on other tissues and the risks of revascularization procedures. Therefore, a multidisciplinary team approach should be considered.
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Tew, Yong Yong, and Anne Scott. "Cardiac amyloidosis masquerading as acute coronary syndrome." BMJ Case Reports 14, no. 2 (February 2021): e238499. http://dx.doi.org/10.1136/bcr-2020-238499.
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A 53-year-old man presented to a district general hospital with chest pain, ECG changes and a small high-sensitivity cardiac troponin I rise. There were no symptoms of heart failure. CT coronary angiography revealed moderate calcific disease and conventional angiography confirmed no flow limitation. Echocardiography showed left ventricular hypertrophy (LVH). His blood pressure remained normal throughout his admission. The tertiary centre labelled this as a ‘plaque rupture’ event but the LVH remained unexplained. Cardiac MRI displayed an unusual pattern of late gadolinium enhancement, which was not classical of amyloid. However, a raised serum free kappa light chain along with the deposition of amyloid on his bone marrow aspirate confirmed the diagnosis of primary AL amyloidosis with cardiac involvement. The patient went on to have chemotherapy and remained stable at 1-year follow-up.
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Lindsey, Merry L., Richard A. Lange, Helen Parsons, Thomas Andrews, and Gregory J. Aune. "The tell-tale heart: molecular and cellular responses to childhood anthracycline exposure." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 10 (November 15, 2014): H1379—H1389. http://dx.doi.org/10.1152/ajpheart.00099.2014.
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Since the modern era of cancer chemotherapy that began in the mid-1940s, survival rates for children afflicted with cancer have steadily improved from 10% to current rates that approach 80% ( 60 ). Unfortunately, many long-term survivors of pediatric cancer develop chemotherapy-related health effects; 25% are afflicted with a severe or life-threatening medical condition, with cardiovascular disease being a primary risk ( 96 ). Childhood cancer survivors have markedly elevated incidences of stroke, congestive heart failure (CHF), coronary artery disease, and valvular disease ( 96 ). Their cardiac mortality is 8.2 times higher than expected ( 93 ). Anthracyclines are a key component of most curative chemotherapeutic regimens used in pediatric cancer, and approximately half of all childhood cancer patients are exposed to them ( 78 ). Numerous epidemiologic and observational studies have linked childhood anthracycline exposure to an increased risk of developing cardiomyopathy and CHF, often decades after treatment. The acute toxic effects of anthracyclines on cardiomyocytes are well described; however, myocardial tissue is comprised of additional resident cell types, and events occurring in the cardiomyocyte do not fully explain the pathological processes leading to late cardiomyopathy and CHF. This review will summarize the current literature regarding the cellular and molecular responses to anthracyclines, with an important emphasis on nonmyocyte cardiac cell types as well as those that mediate the myocardial injury response.
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van Nimwegen, Frederika A., Michael Schaapveld, David J. Cutter, Cècile P. M. Janus, Augustinus D. G. Krol, Michael Hauptmann, Karen Kooijman, et al. "Radiation Dose-Response Relationship for Risk of Coronary Heart Disease in Survivors of Hodgkin Lymphoma." Journal of Clinical Oncology 34, no. 3 (January 20, 2016): 235–43. http://dx.doi.org/10.1200/jco.2015.63.4444.
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Purpose Cardiovascular diseases are increasingly recognized as late effects of Hodgkin lymphoma (HL) treatment. The purpose of this study was to identify the risk factors for coronary heart disease (CHD) and to quantify the effects of radiation dose to the heart, chemotherapy, and other cardiovascular risk factors. Patients and Methods We conducted a nested case-control study in a cohort of 2,617 5-year HL survivors, treated between 1965 and 1995. Cases were patients diagnosed with CHD as their first cardiovascular event after HL. Detailed treatment information was collected from medical records of 325 cases and 1,204 matched controls. Radiation charts and simulation radiographs were used to estimate in-field heart volume and mean heart dose (MHD). A risk factor questionnaire was sent to patients still alive. Results The median interval between HL and CHD was 19.0 years. Risk of CHD increased linearly with increasing MHD (excess relative risk [ERR]) per Gray, 7.4%; 95% CI, 3.3% to 14.8%). This results in a 2.5-fold increased risk of CHD for patients receiving a MHD of 20 Gy from mediastinal radiotherapy, compared with patients not treated with mediastinal radiotherapy. ERRs seemed to decrease with each tertile of age at treatment (ERR/Gy<27.5years, 20.0%; ERR/Gy27.5-36.4years, 8.8%; ERR/Gy36.5-50.9years, 4.2%; Pinteraction = .149). Having ≥ 1 classic CHD risk factor (diabetes mellitus, hypertension, or hypercholesterolemia) independently increased CHD risk (rate ratio, 1.5; 95% CI, 1.1 to 2.1). A high level of physical activity was associated with decreased CHD risk (rate ratio, 0.5; 95% CI, 0.3 to 0.8). Conclusion The linear radiation dose-response relationship identified can be used to predict CHD risk for future HL patients and survivors. Appropriate early management of CHD risk factors and stimulation of physical activity may reduce CHD risk in HL survivors.
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Drapkina, O. M., A. A. Zeynapur, A. S. Klevina, and O. B. Vasileva. "Thoracalgia in a Patient with Determined Coronary Heart Disease. Is there Always a Relapse of Angina Pectoris?" Rational Pharmacotherapy in Cardiology 16, no. 1 (March 2, 2020): 46–50. http://dx.doi.org/10.20996/1819-6446-2020-02-05.
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This article presents a clinical case of a 62-year-old man with a long history of coronary heart disease and smoking, whose main complaint upon admission to the hospital was voice hoarseness and atypical pain syndrome in the chest. During a preliminary medical examination, attention was paid to the clinical picture, atypical for a coronary heart disease – voice hoarseness was identified as a manifestation of the recurrent nerve compression, or cardio-vocal syndrome. Given the lack of connection between the chest pain and physical exertion, a high index of a smoking person as well as signs of the recurrent nerve compression syndrome, a multi-spiral computer tomography with contrasting of the chest organs was performed (in line with official recommendations of the Russian Associations of Oncologists and Otolaryngologists). The results revealed a proliferative lesion of the mediastinum and multiple focal lesions of both lungs. A subsequent thoracoscopy and biopsy confirmed the mediastinal form of a lung cancer. Promptly initiated poly-chemotherapy allowed stabilizing the patient’s condition and significantly improving his prospects. In this context, the article discusses the complexity of a timely diagnosis of a primary lung cancer and emphasizes the need to focus on specific and unique features of the disease course as well as on a broader clinical picture. Tactics of a multidisciplinary approach allows making a diagnosis in a timely manner, significantly improving the effectiveness of therapy and patient’s survival prognosis.
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Pinder, Mary C., Zhigang Duan, James S. Goodwin, Gabriel N. Hortobagyi, and Sharon H. Giordano. "Congestive Heart Failure in Older Women Treated With Adjuvant Anthracycline Chemotherapy for Breast Cancer." Journal of Clinical Oncology 25, no. 25 (September 1, 2007): 3808–15. http://dx.doi.org/10.1200/jco.2006.10.4976.
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Purpose Limited data are available on long-term cardiac safety of adjuvant anthracycline chemotherapy in breast cancer patients over age 65 years. We evaluated rates and predictors of congestive heart failure (CHF) in this population. Patients and Methods We used the Surveillance, Epidemiology, and End Results Medicare database and included women with no history of CHF who were age 66 to 80 years and diagnosed with stage I to III breast cancer from 1992 to 2002. Cumulative rates of CHF were estimated, and multivariable Cox regression analysis was used to determine factors associated with the development of CHF. Results A total of 43,338 women were included. Anthracycline-treated women were younger, with fewer comorbidities and more advanced disease than women who received nonanthracycline or no chemotherapy (P < .001 for each). The adjusted hazard ratio (HR) for CHF was 1.26 (95% CI, 1.12 to 1.42) for women aged 66 to 70 treated with anthracycline compared with other chemotherapy. For women aged 71 to 80, adjuvant chemotherapy type was not associated with CHF. The following baseline characteristics were significant predictors of CHF: age (HR, 1.79 per 10 years; 95% CI, 1.66 to 1.93), black race (HR, 1.40; 95% CI, 1.30 to 1.50), trastuzumab treatment (HR, 1.46; 95% CI, 1.21 to 1.77), hypertension (HR, 1.45; 95% CI, 1.39 to 1.52), diabetes (HR, 1.74; 95% CI, 1.66 to 1.83), and coronary artery disease (HR, 1.58; 95% CI, 1.39 to 1.79). Left-sided radiotherapy did not confer an elevated risk of CHF (HR, 1.04; 95% CI, 0.98 to 1.11). Conclusion Women aged 66 to 70 years who received adjuvant anthracyclines had significantly higher rates of CHF. The difference in rates of CHF continued to increase through more than 10 years of follow-up.
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Baker, Laurence H., Venkatesh Locharla Murthy, Richard Lawrence Weinberg, Jose Jalife, and Todd Herron. "Evaluation of cardiovascular health in sarcoma survivors." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): e21579-e21579. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e21579.
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e21579 Background: Heart disease is the most common and serious chronic illness observed in sarcoma survivors treated with doxorubicin. Now the commonest heart disease in theses survivors is coronary artery disease (CAD). We established a Sarcoma Survivorship Program to include patients at high risk of chronic illness including exposure to doxorubicin who are at least 2 years free of disease post treatment. Methods: Every 6 months patients electronically complete NIH’s PROMIS (Patient-Reported Outcomes Measurement Information System) questionnaires (on Anxiety, Depression, Mobility, Pain Interference, Sleep Disturbance, and Physical Function). Detailed family history is documented. Chemotherapy doses are abstracted from original medical records. Data collected includes: blood pressure, lipid profile, high-sensitivity C-reactive protein (hs-CRP), basic metabolic panel, chemistries, renal and pulmonary function, expert echocardiography. All patients signed an IRB approved informed consent. Results: All patients had normal left ventricular ejection fractions (median = 60%) yet 8 (N = 24) patients had an elevated hs-CRP suggesting increased risk of early CAD. 10 patients had untreated hypertension. More than half of our patients have a BMI > 25 and self-declare that they do not exercise. Our high rate of family history of heart disease (58%) raises the issue of genetic predisposition both to heart disease and sarcoma. We compared standardized cardiac risk assessments with mediastinal calcification and epicardial fat on serial chest CT scans. A 39 y.o. man had a coronary calcium score > 400 Agatston units and scattered calcifications were found in 4 additional patients under the age of 40. Conclusions: This survivorship phase of oncologic care represents a unique opportunity to improve the health and quality of life for sarcoma survivors as well as a new focus for translational research to understand mechanisms driving premature aging and chronic heart disease. We assess cardiomyocyte function (cell viability, organization, fibrosis, electrical coupling and contractility) for survivors and matched sibling controls with cells from skin biopsy using 3D bioengineering techniques to culture and mature the phenotype from human stem cells.
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Kritz, H., C. Zielinski, and H. Sinzinger. "Low cholesterol and cancer." Journal of Clinical Oncology 14, no. 11 (November 1996): 3043–48. http://dx.doi.org/10.1200/jco.1996.14.11.3043.
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PURPOSE The relation between plasma cholesterol (CH) concentration and mortality is complex. The plasma CH concentration correlates positively with mortality from coronary heart disease, but some studies have shown a negative relation with death from cancer. If these two relations reflect causal mechanisms that are reversible by changing the plasma CH concentration, the benefits of lipid reduction for heart disease might be offset by an increased mortality from cancer. Different aspects between lipid metabolism and cancer, as well as new insights into this interesting field, are discussed. METHODS The literature was searched using MedLine through 1966 and January 1996. RESULTS There is no evidence from the data available at present that the association between low CH and a higher risk of cancer is causal. CONCLUSION This issue should not affect the advice on health matters offered by doctors, especially to patients with other risk factors for cardiovascular disease. The possibility that hypercholesterolemia (HC) drugs can induce a reduction of tumor-cell growth makes them potentially useful as an adjuvant to chemotherapy and ultimately increases the probabilities in the prevention and treatment of cancer.
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Paulenka, Yuliya, Maritza Cotto, Christine Rickette, and Krystal Hunter. "Latent atherosclerosis as a risk factor in chemotherapy-induced cardiomyopathy." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): e12525-e12525. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e12525.
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e12525 Background: Anthracyclines and monoclonal antibodies targeting HER2/neu receptors are widely used antineoplastic agents in breast cancer treatment. Both therapies have been known to cause cardiovascular adverse effects, notably chemotherapy-induced congestive heart failure, especially if used in combination. Multiple factors have been postulated to increase the risk of doxorubicin and trastuzumab-associated cardiotoxicity, including a pre-existing coronary artery disease, but the role of latent atherosclerosis has not been widely studied. Methods: We retrospectively reviewed health records of female breast cancer patients at our institution treated with doxorubicin or trastuzumab between 2012 and 2017. Using echocardiography, we identified patients with underlying atherosclerotic lesions at the start of the treatment and those who subsequently developed cardiotoxicity. Chemotherapy-induced cardiomyopathy was defined as a drop in the ejection fraction (EF) to < 50% from the normal EF of > 53% pre-therapy. We used a χ2 test to search for the relationship between atherosclerosis and subsequent cardiotoxicity. Results: A total of 518 patient records were reviewed. Of 518 patients with breast cancer, 93 (18%) received doxorubicin or trastuzumab-based chemotherapy. The median age for breast cancer diagnosis was 58. Sixty-one patients (66%) were identified to have atherosclerosis on echocardiography at the time of the first chemotherapy cycle. The most common location for atherosclerotic lesions was in the aortic arch and proximal upper abdominal aorta. Of 61 patients with atherosclerosis, ten (16.4%) subsequently developed chemotherapy-induced cardiomyopathy (p = 0.77). A post hoc analysis was performed to compare the two cohorts aged 40 to 50 (p = 0.49) and 51 to 75 (p = 1.00) as they represented the majority of breast cancer cases. Conclusions: The role of atherosclerosis in doxorubicin and trastuzumab-induced toxicity remains unclear. We did not observe any statistical correlation between atherosclerosis at the start of chemotherapy and increased rates of cardiac injury. A younger population may be more susceptible to cardiotoxicity, but further research is needed as the study has limitations. Although we identified patients with latent atherosclerosis, additional evaluation via carotid artery intima-media thickness measurements would yield more precision. Other methods such as the use of computed tomography and coronary artery calcium scores would also allow for assessing atherosclerotic plaque burden. Still, not all patients were subjected to these techniques. Furthermore, the study was challenged by the small sample size and its retrospective nature. Larger prospective studies are essential to explore this area further. Identifying the means of reducing cardiovascular complications remains a priority as heart disease is currently the leading cause of death among breast cancer survivors.
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Jain, Angita, Nadine Norton, Katelyn A. Bruno, Leslie T. Cooper, Paldeep S. Atwal, and DeLisa Fairweather. "Sex Differences, Genetic and Environmental Influences on Dilated Cardiomyopathy." Journal of Clinical Medicine 10, no. 11 (May 25, 2021): 2289. http://dx.doi.org/10.3390/jcm10112289.
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Dilated cardiomyopathy (DCM) is characterized by dilatation of the left ventricle and impaired systolic function and is the second most common cause of heart failure after coronary heart disease. The etiology of DCM is diverse including genetic pathogenic variants, infection, inflammation, autoimmune diseases, exposure to chemicals/toxins as well as endocrine and neuromuscular causes. DCM is inherited in 20–50% of cases where more than 30 genes have been implicated in the development of DCM with pathogenic variants in TTN (Titin) most frequently associated with disease. Even though male sex is a risk factor for heart failure, few studies have examined sex differences in the pathogenesis of DCM. We searched the literature for studies examining idiopathic or familial/genetic DCM that reported data by sex in order to determine the sex ratio of disease. We found 31 studies that reported data by sex for non-genetic DCM with an average overall sex ratio of 2.5:1 male to female and 7 studies for familial/genetic DCM with an overall average sex ratio of 1.7:1 male to female. No manuscripts that we found had more females than males in their studies. We describe basic and clinical research findings that may explain the increase in DCM in males over females based on sex differences in basic physiology and the immune and fibrotic response to damage caused by mutations, infections, chemotherapy agents and autoimmune responses.
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Chitu, Monica, Theodora Benedek, S. Condrea, C. Blendea, and I. Benedek. "An unusual case of cardiac syncope and acute coronary syndrome – a case report." Acta Medica Marisiensis 60, no. 6 (December 1, 2014): 285–87. http://dx.doi.org/10.1515/amma-2015-0011.
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Abstract Introduction: We aimed to present a case of acute coronary syndrome with unexpected etiology complicated by syncope and arrhythmias, confirmed by imagistic examinations as cardiac parasitosis. Cardiac parasitic diseases are rare diseases, whose diagnosis and therapy should be adapted to each case. Imaging techniques allow precise diagnosis of cardiac echinococcosis, providing essential structural details on the damage degree of heart structures, allowing optimization of complex treatment in these cases. Case presentation: A 67-year old, obese and diabetic woman presented with cardiac syncope, arrhythmias and acute chest pain. Imagistic examinations excluded intracoronary thrombosis and confirmed a severe structural damage of myocardial tissue, consisting in replacement of the myocardial structure by many cysts caused by parasitic infestation with echinococcus multilocularis and echinoccocus granulosus originating from the liver. CT scan confirmed severe distruction of the left ventricular myocardium by policysts, that led to thinning of inferior and apical left ventricle wall without any possibility of surgical excision. Therefore a specific chemotherapy with albendazole was initiated. Follow up at 2 months indicated a favorable evolution, with serological decrease of echinococcal antibodies and reduction of cysts volume. Conclusion: In cases of angina and arrhythmias with non-atherosclerotic etiology, imaging techniques can diagnose the anatomopathological substrate of the disease and represent a valuable tool for the follow up.
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Watson, G. J., M. R. Kugel, H. Shih, C. Tak Piech, and R. S. McKenzie. "Cardiac cormorbidities in women with metastatic breast cancer treated with doxorubicin-based and non-doxorubicin-based chemotherapy." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 1052. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.1052.
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1052 Background: Observational data are sparse regarding cardiac comorbidities in patients with metastatic breast cancer (MBC) newly initiated on chemotherapy. As some MBC treatments are associated with cardiac toxicity, such information would be useful in guiding treatment decisions. The objective of this analysis was to understand the frequency of cardiac comorbidities in MBC patients prior to chemotherapy initiation based on the Medicare 5% standard analytical file (SAF). Methods: The Medicare 5% SAF was used to investigate claims for women with breast neoplasm and > 1 distant metastatic site (based on ICD-9 diagnosis codes) that subsequently received chemotherapy (based on claims with a chemotherapy J code). Cardiac comorbidities [hypertension (HTN), coronary artery disease (CAD), myocardial function (MI), and congestive heart failure (CHF)] prior to initial chemotherapy were reported as non-mutually exclusive categories. The index quarter was based on chemotherapy initiation that occurred between 7/2001 and 12/2006. Patients were categorized based on receipt of non doxorubicin-based chemotherapy (non-DOX) vs DOX-based chemotherapy. Results: The study included 2,587 women with MBC that received cytotoxic chemotherapy subsequent to the diagnosis of MBC. The mean age was higher in the non-DOX group. Both groups reported a significant proportion of patients with cardiac comorbidities prior to chemotherapy, with greater proportions reported in the non-DOX group (table). Conclusions: Cardiac comorbidities were commonly reported in women with MBC prior to chemotherapy. Such information is useful to health care professionals when considering potential interventions for patients with MBC. [Table: see text] [Table: see text]
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Steuter, John Allen, Philip Bierman, R. Gregory Bociek, and Martin Bast. "Utility Of Pre-Chemotherapy Echocardiograms." Blood 122, no. 21 (November 15, 2013): 2950. http://dx.doi.org/10.1182/blood.v122.21.2950.2950.
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Abstract Anthracycline-based chemotherapy is widely used in a variety of regimens for Hodgkin’s Lymphoma (HL) and Non-Hodgkin’s Lymphoma (NHL). Unfortunately this agent is associated with cardiotoxicity, especially in larger cumulative doses. Doxorubicin cardiotoxicity is characterized by a dose-dependent decline in mitochondrial oxidative phosphorylation. Reactive oxygen species, generated by the interaction of doxorubicin with iron, can then damage the myocytes causing myofibrillar loss, cytoplasmic vacuolization, and apoptosis. Current NCCN guidelines for HL and NHL state that left ventricle function is recommended in patients who will receive such chemotherapy. Subsequent evaluations are recommended at a cumulative dose of doxorubicin of at least 300 mg/m² and periodically thereafter during the course of therapy. Despite these recommendations, there is little literature about the usefulness of this approach, the rate of abnormal findings, and whether routine testing changes management. A list of patients with HL or NHL treated with anthracycline-based chemotherapy from the University of Nebraska Medical Center from August 2004-May 2012 was obtained from our Lymphoma Registry. Baseline characteristics of age, disease diagnosis, gender, and prior history of cardiac diagnosis were collected. Prior cardiac diagnosis specified as patients with a past history of atrial fibrillation/flutter, supraventricular tachycardia, heart block requiring pacemaker implantation, coronary artery disease, valvular disease, pulmonary hypertension, or cardiomyopathy. Charts were reviewed for pre-chemotherapy evaluation of left ventricular function and the method of evaluation (echocardiogram, nuclear, cardiac MRI were included). Additionally, post treatment evaluation of cardiac function was evaluated for any change. The individual therapy for each patient was reviewed to determine if findings from the cardiac evaluation modified treatment regimens. A left ventricular function less than 50% was considered abnormal. Echocardiogram findings of moderate to severe valvular disease, diastolic dysfunction (grade 1-3), and moderate or severe pulmonary hypertension (moderate = pulmonary artery systolic pressure of 45-60, severe = pulmonary artery systolic pressure of > 60) were collected. We identified 309 patients from the UNMC lymphoma database. Of these 219 (71%) had an echocardiogram performed prior to therapy and documented in the patient record. Their mean age was 54.2 years of age with 53% of them being male and 47% female. 188 of the 219 (86%) had no prior cardiac diagnosis as defined previously. From this group 22 of the 188 (10%) had a pre-chemotherapy echocardiogram that demonstrated one of the following: moderate-severe valvular disease, diastolic dysfunction, moderate-severe pulmonary hypertension or abnormal EF (<50%). However, none of these findings altered the chemotherapy regimen for the 22 patients. 31 of the 219 patients with echocardiograms carried a prior cardiac diagnosis. 4 of the 31 had an alteration in their chemotherapy regimen as a result. Post therapy echocardiograms showed no change in cardiac function. 5 of the 219 patients were diagnosed with adriamycin induced cardiomyopathy following treatment. All 5 patients had no prior cardiac history and pre-chemotherapy echocardiograms were normal. These finding suggest that current methods of evaluating cardiac function prior to chemotherapy and risk stratifying patients are inadequate and do not alter patient outcomes. Disclosures: No relevant conflicts of interest to declare.
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Armenian, Saro H., Gregory T. Armstrong, Gregory Aune, Eric J. Chow, Matthew J. Ehrhardt, Bonnie Ky, Javid Moslehi, et al. "Cardiovascular Disease in Survivors of Childhood Cancer: Insights Into Epidemiology, Pathophysiology, and Prevention." Journal of Clinical Oncology 36, no. 21 (July 20, 2018): 2135–44. http://dx.doi.org/10.1200/jco.2017.76.3920.
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Cardiovascular disease (CVD), which includes cardiomyopathy/heart failure, coronary artery disease, stroke, pericardial disease, arrhythmias, and valvular and vascular dysfunction, is a major concern for long-term survivors of childhood cancer. There is clear evidence of increased risk of CVD largely attributable to treatment exposures at a young age, most notably anthracycline chemotherapy and chest-directed radiation therapy, and compounded by traditional cardiovascular risk factors accrued during decades after treatment exposure. Preclinical studies are limited; thus, it is a high priority to understand the pathophysiology of CVD as a result of anticancer treatments, taking into consideration the growing and developing heart. Recently developed personalized risk prediction models can provide decision support before initiation of anticancer therapy or facilitate implementation of screening strategies in at-risk survivors of cancer. Although consensus-based screening guidelines exist for the application of blood and imaging biomarkers of CVD, the most appropriate timing and frequency of these measures in survivors of childhood cancer are not yet fully elucidated. Longitudinal studies are needed to characterize the prognostic importance of subclinical markers of cardiovascular injury on long-term CVD risk. A number of prevention trials across the survivorship spectrum are under way, which include primary prevention (before or during cancer treatment), secondary prevention (after completion of treatment), and integrated approaches to manage modifiable cardiovascular risk factors. Ongoing multidisciplinary collaborations between the oncology, cardiology, primary care, and other subspecialty communities are essential to reduce therapeutic exposures and improve surveillance, prevention, and treatment of CVD in this high-risk population.
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Hancock, S. L., S. S. Donaldson, and R. T. Hoppe. "Cardiac disease following treatment of Hodgkin's disease in children and adolescents." Journal of Clinical Oncology 11, no. 7 (July 1993): 1208–15. http://dx.doi.org/10.1200/jco.1993.11.7.1208.
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PURPOSE Cardiac disease is second only to neoplastic disease as a cause of death after treatment for Hodgkin's disease. This study evaluates the risks of cardiac disease following treatment of Hodgkin's disease during childhood and adolescence. PATIENTS AND METHODS We reviewed records of 635 patients treated for Hodgkin's disease before 21 years of age at Stanford University between 1961 and 1991. Mean age was 15.4 years; mean follow-up duration was 10.3 years, representing 6,564 person-years of observation. Relative risks (RRs) of death from cardiac diseases were calculated by comparison with age-, sex-, and race-matched general population rates from United States decennial life-tables. RESULTS Twelve patients have died of cardiac disease (RR, 29.6; 95% confidence interval [CI], 16.0 to 49.3), including seven deaths from acute myocardial infarction ([AMI] RR, 41.5; 95% CI, 18.1 to 82.1), three from valvular heart disease, and two from radiation pericarditis/pancarditis. Thus far, the risk of AMI death was comparable after radiation alone (RO) or after chemotherapy and radiation (CM) (RO-AMI RR, 52.2; 95% CI, 21.1 to 108.7; CM-AMI RR, 21.1; 95% CI, 0.0 to 104.4; P = .6). The risk for other cardiac death (CD) tended to be higher after combined treatment (RO-non-AMI RR, 7.4; 95% CI, 0.0 to 36.5; CM-non-AMI RR, 45.8; 95% CI, 14.4 to 110.6; P = .1). Deaths occurred 3 to 22 years after patients received 42 to 45 Gy to the mediastinum between 9 and 20 years of age. There have been no deaths among patients treated to lower mediastinal radiation doses or without mediastinal radiation. There are no clear trends in the latency of risk. One hundred six nonfatal abnormalities have also been diagnosed. CONCLUSION Mediastinal radiation of 40 to 45 Gy increases the risk of death from coronary artery and other cardiac diseases. The risk increases within 5 years of irradiation. These observations support combined-modality, low-dose irradiation regimens in children and adolescents and suggest the need for careful cardiac screening of treated patients.
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Loria, Valentina, Christian Colizzi, Marcello Vaccarella, Francesco Franceschi, and Nadia Aspromonte. "Left Ventricular Noncompaction: Cause or Consequence of Myocardial Disease? A Case Report and Literature Review." Cardiology 143, no. 3-4 (2019): 100–104. http://dx.doi.org/10.1159/000500904.
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A 57-year-old woman presented to the Emergency Department with symptoms of worsening heart failure (HF). She had a past medical history of breast cancer treated with surgery and chemotherapy with anthracyclines and no family history of cardiomyopathy (CMP). In the last year, she received a diagnosis of HF with normal coronary arteries, during hospitalization for acute onset of dyspnea and was treated with medical therapy. After several months, few days before admission to our hospital, an echocardiography (ECHO) showed features of left ventricular noncompaction (LVNC), not described in previous ECHO and further confirmed by cardiac magnetic resonance. This case highlights the current uncertainties regarding the pathogenesis of LVNC and the clinical challenge of cardiologists facing LVNC morphology to decide if they are observing a genetic CMP, a phenotype overlapping with dilated or hypertrophic CMP, or a variant of the left ventricular (LV) wall anatomy. No consensus exists among scientific communities regarding diagnostic criteria of LVNC and in most cases; the key element in the diagnostic decision is not the LVNC by itself, but the associated LV dilation and/or dysfunction, hypertrophy, arrhythmias, and embolic events.
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Zaborowska-Szmit, Magdalena, Maciej Krzakowski, Dariusz M. Kowalski, and Sebastian Szmit. "Cardiovascular Complications of Systemic Therapy in Non-Small-Cell Lung Cancer." Journal of Clinical Medicine 9, no. 5 (April 27, 2020): 1268. http://dx.doi.org/10.3390/jcm9051268.
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Cardiovascular diseases may determine therapy outcomes of non-small-cell lung cancer (NSCLC). The evidence for how iatrogenic cardiovascular complications contribute to ceasing anticancer treatment, decreasing the quality of life or even premature death, is unclear. Older patients and smokers are at risk of atherosclerosis and arterial thromboembolic events (TE), such as myocardial infarction or stroke. Venous TE can be observed in up to 15% of NSCLC patients, but the risk increases three to five times in ALK (anaplastic lymphoma kinase)-rearranged NSCLC. ALK inhibitors are associated with electrophysiological disorders. Cytotoxic agents and anti-VEGF inhibitors mainly cause vascular complications, including venous or arterial TE. Cardiac dysfunction and arrhythmias seem to be less frequent. Chemotherapy is often administered in two-drug regimens. Clinical events can be triggered by different mechanisms. Among epidermal growth factor inhibitors, erlotinib and gefitinib can lead to coronary artery events; however, afatinib and osimertinib can be associated with the development of heart failure. During anti-PD1/anti-PDL1 therapy, myocarditis is possible, which must be differentiated from acute coronary syndrome and heart failure. Awareness of all possible cardiovascular complications in NSCLC encourages vigilance in early diagnostics and treatment.
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Charkviani, Mariam, Natia Murvelashvili, Francisco Barrera, Alisha Sharma, Randa Sharag Eldin, and Nur Un Nisa Nabil. "Rare Presentation of Cardiotoxicity Related to 5-Fluorouracil." Case Reports in Oncological Medicine 2020 (July 21, 2020): 1–4. http://dx.doi.org/10.1155/2020/4151474.
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5-Fluorouracil (5-FU) is a chemotherapeutic agent frequently used for the treatment of solid tumors. In a few cases, 5-FU can be associated with coronary vasospasm, cardiac ischemia, or life-threatening arrhythmias. Recognition of 5-FU cardiotoxicity is clinically important as after the rapid sensation of therapy, cardiotoxicity can be completely reversible, and on the other hand, readministration may lead to serious damage of the heart and even death. A 70-year-old male came to the emergency department (ED) with chest pain which started while receiving an infusion of 5-FU. The patient did not have a personal history or risk factors of coronary artery disease and his electrocardiogram (ECG) before starting chemotherapy was completely normal. In the ED, his ECG had ischemic changes, troponin was elevated, and echocardiogram showed anterior wall hypokinesis. However, emergent coronary angiogram did not reveal any acute coronary occlusion. 5-FU-induced cardiotoxicity was suspected; the patient was admitted to a progressive care unit for close monitoring and infusion of calcium channel blockers was initiated. The patient’s symptoms and ECG findings gradually resolved, and two days later on discharge, patient was chest pain free and ECG was normal. This case supports the vasospastic hypothesis of 5-FU cardiac toxicity, describes its clinical course, and emphasizes the importance of better awareness and early recognition of the rare side effect as it may allow physicians to reduce the risk of life-threatening complications.
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Hinduja, Archana, Kaustubh Limaye, Rahul Ravilla, Appalanaidu Sasapu, Xenofon Papanikolaou, and Sarah Waheed. "Spectrum of Cerebrovascular Disease in Multiple Myeloma Patients Undergoing Chemotherapy." Blood 126, no. 23 (December 3, 2015): 5498. http://dx.doi.org/10.1182/blood.v126.23.5498.5498.
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Abstract Introduction: The objective of study was to determine the risk factors, stroke mechanisms and outcome following a stroke in Multiple myeloma (MM) patients. Materials and Methods: We conducted a matched cohort study from a prospective database of MM patients enrolled in TT2, TT3A, TT3B protocols who developed a vascular event (transient ischemic attack, ischemic stroke and intracerebral hemorrhage) from 1998 to 2014 with age, sex and treatment matched controls. Comparison of baseline demographics, risk factors, myeloma characteristics, laboratory values and mortality between both groups was performed using Pearson's Chi-square test for categorical variables and student T test for continuous variables. Multivariate logistic regression analysis was performed to identify risk factors associated with stroke. For statistical analysis SAS 9.4 software was used and p value of ≤ 0.05 was considered significant. Strokes were classified using the modified Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria. Results: Of 1148 patients, 46 developed a vascular event (Ischemic stroke (TIA)-33, Transient ischemic attack-11, Hypertensive intracerebral hemorrhage-2). On univariate analysis, predictors of stroke were a positive smoking history (26.1% vs 13% p=0.0381), renal insufficiency (23.9% vs 8.0% p=0.0039), hemodialysis (10.9 vs 0.7% p=0.004) and MM Stage I and II as opposed to Stage III (Stage I - 23.9% vs 9.4%, Stage II - 17.4% vs 12.3, Stage III - 58.7% vs 78.3% p=0.025). Despite the lack of significant difference in the baseline laboratory values between both groups, among the cases, there was a significant decrease in the platelet count (112.6 vs 255.2, p<0.0001) and elevation in INR (1.25 vs 1.08, p=0.0096) during the vascular insult when compared to their baseline values. On multivariate analysis, independent predictors of stroke were renal insufficiency (Odds Ratio, 3.528, 95% CI, 1.36-9.14; p=0.0094) and MM Stage I and II (Odds Ratio, 2.770, 95% CI, 1.31-5.81; p=0.0073). The ischemic strokes subtypes were: Large vessel disease 6%, cardioembolic 18%, small vessel disease 21%, other known etiologies 49% (hypercoaguable state; watershed; others) and cryptogenic in 6%. Following ischemic event, antiplatelet agents were used in 16 patients, anticoagulation in 7 patients but 23 patients were ineligible for both due to thrombocytopenia. In our cohort, 78% were discharged home or rehabilitation facility, 4% were transferred to long-term nursing facility and in hospital mortality was 15%. Conclusion: In MMpatient'srenal insufficiency andMM Stage I and II were associated with increased stroke risk. Besides hypercoagulability other mechanisms like atrial fibrillation, watershed strokes and small vessel disease played major role. Table 1.Demographic and disease characteristics of multiple myeloma patients experiencing a stroke compared to controlsVariableStroke (N=46)No Stroke (N=138)p-valueAge [mean (sd)]60.6 (7.7)60.7 (7.8)0.8960Female50.0 (23)41.6 (57)0.3023Race Caucasian95.7 (44)90.6 (125)0.3635#Hypertension54.4 (25)43.5 (60)0.2003HPL33.3 (15/45)26.1 (36)0.3464Diabetes17.4 (8)9.4 (13)0.1409CAD10.9 (5)10.9 (15)>0.99CHF4.4 (2)8.7 (12)0.5237AFIB17.4 (8)9.4 (13)0.1409Smoking26.1 (12)13.0 (18)0.0381ETOH2.2 (1)1.5 (2)>0.99Malignancy8.7 (4)16.1 (22/137)0.2159Nephropathy23.9 (11)8.0 (11)0.0039Hemodialysis10.9 (5)0.7 (1)0.0040Protocol TT2 TT3A TT3B54.4 (25) 32.6 (15) 13.0 (6)57.2 (79) 21.0 (29) 21.7 (30)0.3036MM Stage I II III23.9 (11) 17.4 (8) 58.7 (27)9.4 (13) 12.3 (17) 78.3 (108)0.0182MM Isotype IgG IgA FLC-κ FLC-λ Other58.7 (27) 21.7 (10) 8.7 (4) 10.9 (5) 049.3 (68) 24.6 (34) 10.1 (14) 10.9 (15) 5.1 (7)0.6128MM Risk [mean (sd)] Death-0.13 (0.61; N=37) 65.2(30)0.09 (0.67; N=88) 51.5(71)0.0941 0.19OSA: Obstructive sleep apnea, CAD: coronary artery disease, CHF: Congestive heart failure, AFIB: Atrial fibrillation, HPL hyperlipidemia. Table 1. Results on multivariable logistic model Variable Odds Ratio 95% CI p-value Nephropathy 3.528 1.36 to 9.14 0.0094 MM Stage I or II 2.770 1.31 to 5.81 0.0073 Disclosures Hinduja: University of Arkansas for Medical Sciences: Employment. Limaye:University of Arkansas for Medical Sciences: Employment. Ravilla:University of Arkansas for Medical Sciences: Employment. Sasapu:University of Arkansas for Medical Sciences: Employment. Waheed:University of Arkansas for Medical Sciences: Employment.
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Huang, Sheng-Miauh, Li-Yin Chien, Cheng-Jeng Tai, Ling-Ming Tseng, Ping-Ho Chen, and Chen-Jei Tai. "Increases in Xu Zheng and Yu Zheng among Patients with Breast Cancer Receiving Different Anticancer Drug Therapies." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/392024.
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Aim. The objectives of this study were to compare yang-xu, yin-xu, and yu among patients with breast cancer right before, one month after, and three months after receiving target, chemo, or combined therapy.Method. After recruiting 126 patients from 4 hospitals in northern Taiwan, a longitudinal study was carried out with 61 patients receiving chemotherapy, 30 receiving target therapy, and 35 receiving combined therapy. Yang-xu, yin-xu, and yu were assessed using the Traditional Chinese Medical Constitutional Scale (TCMCS), with higher scores indicating more xu and yu.Results. There were significant increases in yang-xu, yin-xu, and yu at 1 month and 3 months after than before the start of the chemotherapy, target, or combined therapy. Patients receiving combined therapy had significantly higher scores in yang-xu and yin-xu than patients receiving chemo or target therapy. A history of coronary heart disease was associated with more yin-xu. Those patients who had undergone a mastectomy were associated with less yu zheng than those patients who had not.Conclusion and Implications. TCM doctors should focus their treatment on dealing with xu and yu in order to support their patients, as they complete their modern anticancer treatments.
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Chavez-Mac Gregor, Mariana, Ning Zhang, Jiangong Niu, Yufeng Zhang, Thomas A. Buchholz, Linda S. Elting, Gabriel N. Hortobagyi, and Sharon Hermes Giordano. "Trastuzumab-related cardiotoxicity among older breast cancer patients." Journal of Clinical Oncology 30, no. 27_suppl (September 20, 2012): 135. http://dx.doi.org/10.1200/jco.2012.30.27_suppl.135.
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135 Background: The use of trastuzumab in the adjuvant setting is associated with reduction in mortality and recurrence. Trastuzumab is extremely well tolerated, but its use is associated with congestive heart failure (CHF). The incidence of this complication in the general population remains largely unknown, especially in older patients. In this study we evaluated the rates and risk factors associated with trastuzumab-related CHF in a large cohort of older breast cancer patients. Methods: Breast cancer patients > 66 years with full Medicare coverage, diagnosed with stage I-III breast cancer between 2005-2007, and treated with chemotherapy were identified in the SEER-Medicare database. Chemotherapy and trastuzumab use, comorbidities and CHF were identified using ICD-9 and HCPCS codes. Analyses included descriptive statistics and Cox proportional hazard model using trastuzumab as a time-dependent variable and logistic regression. Results: From 3,983 patients included, 847 (21.7%) received trastuzumab. Median age of the entire cohort was 71 years old. Among trastuzumab users the rate of CHF was 28.6% compared to 18.1% in non-trastuzumab users (p<.0001). After adjusting for demographic and clinical characteristics, comorbidities, and type of chemotherapy used, trastuzumab users were more likely to develop CHF than non-trastuzumab users (HR 1.74; 95% CI 1.47-2.06). Among trastuzumab users, older age did not further increase the risk, however history of coronary artery disease (OR 2.23; 95%CI 1.56-3.19), heart valve disease (OR 1.41; 95%CI 1.41-2.88) and emphysema -as a proxy for smoking- (OR 2.03; 95% CI 1.13-3.63) significantly increased the risk of CHF. There was a trend for increased risk of CHF associated with anthracycline use (OR 1.36; 95% CI 0.93-2.00). Conclusions: In this large cohort of older breast cancer patients, the risk of CHF among trastuzumab users was 1.74 times higher than non-trastuzumab users, which is higher than what has been reported in younger clinical trial participants. Among older breast cancer patients treated with trastuzumab, cardiac comorbidities, and emphysema may identify high-risk patients.
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Chavez-Mac Gregor, Mariana, Ning Zhang, Thomas A. Buchholz, Yufeng Zhang, Jiangong Niu, Linda S. Elting, Gabriel N. Hortobagyi, and Sharon Hermes Giordano. "Trastuzumab-related cardiotoxicity among older breast cancer patients." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): 600. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.600.
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600 Background: The use of trastuzumab in the adjuvant setting is associated with reduction in mortality and recurrence. Although trastuzumab is extremely well tolerated, its use is associated with congestive heart failure (CHF). The incidence of this complication in the general population remains largely unknown, especially in older patients. In this study we evaluated the rates and risk factors associated with trastuzumab-related CHF in a large cohort of older breast cancer patients. Methods: Breast cancer patients ≥ 66 years with full Medicare coverage, diagnosed with stage I-III breast cancer between 2005-2007, and treated with chemotherapy were identified in the Surveillance, Epidemiology and End Results-Medicare (SEER-Medicare) database. Chemotherapy and trastuzumab use, comorbidities and CHF were identified using ICD-9 and HCPCS codes. Analyses included descriptive statistics, Cox proportional hazard model using trastuzumab as a time-dependent variable and logistic regression. Results: A total of 3,983 patients were included, 847 (21.7%) of them received trastuzumab, median age of the entire cohort was 71 years old. Among trastuzumab users the rate of CHF was 28.6% compared to 18.1% in non-trastuzumab users (p<.0001). After adjusting for demographic and clinical characteristics, comorbidities, and type of chemotherapy used, trastuzumab users were more likely to develop CHF than non-trastuzumab users (HR 1.74; 95% CI 1.47-2.06). Among trastuzumab users, older age did not further increase the risk, however history of coronary artery disease (OR 2.23; 95%CI 1.56-3.19), heart valve disease (OR 1.41; 95%CI 1.41-2.88) and emphysema -as a proxy for smoking- (OR 2.03; 95% CI 1.13-3.63) significantly increased the risk of CHF. There was a trend for increased risk of CHF associated with anthracycline use (OR 1.36; 95% CI 0.93-2.00). Conclusions: In this large cohort of older breast cancer patients, the risk of CHF among trastuzumab users was 1.74 times higher than non-trastuzumab users, which is higher than what has been reported in younger clinical trial participants. Among older breast cancer patients treated with trastuzumab, cardiac comorbidities and emphysema may identify high risk patients.
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Peippo, Maija Helena, Samu Kurki, Riitta Lassila, and Olli Mikael Carpén. "Real-world features associated with cancer-related venous thromboembolic events." ESMO Open 3, no. 5 (July 2018): e000363. http://dx.doi.org/10.1136/esmoopen-2018-000363.
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BackgroundThe incidence of venous thromboembolism (VTE) is 1–2/1000 individuals. Patients with cancer, especially during chemotherapy, are at enhanced risk, but real-world data on factors associated with VTE events are still scarce.AimThe aim of this retrospective study was to survey the incidence of VTE based on a large hospital database, and to identify comorbidities and features associated with VTE events. We focused on cancer-related VTE events and on factors indicating increased VTE risk during chemotherapy.MethodsThe cohort included patients treated at Turku University Hospital during years 2005–2013. Health information was derived and analysed from multiple electronic databases. The diagnoses of VTE and all comorbidities, including type of cancer, were based on International Classification of Diseases 10th Revision coding. For further analysis, we focused on 16 common types of cancers treated with chemotherapy. Age, gender, surgery, radiotherapy, distant metastasis, available laboratory values and platinum-based chemotherapy were evaluated for VTE group, and associations were estimated by Cox regression analyses.ResultsThe entire database contained information from 495 089 patients, of whom 5452 (1.1%) had a VTE diagnosis. Among individuals with VTE, 1437 (26.4%) had diagnosis of coronary heart disease and 1467 (26.9%) had cancer diagnosis. Among 7778 patients with cancer treated with chemotherapy, 282 (3.6%) had a VTE, platinum-based chemotherapy being a major risk factor (HR 1.77, 95% CI 1.40 to 2.24, p<0.001). In multivariate analysis, elevated blood neutrophil counts (>3.25×109 cells/L, HR 1.96, 95% CI 1.33 to 2.89, p<0.001) and plasma creatinine (>62.5 μmol/L; HR 1.60, 95% CI 1.21 to 2.13, p=0.001) values were independent indicators of increased VTE risk during chemotherapy.ConclusionsLongitudinal electronic health record analysis provides a powerful tool to gather meaningful real-world information to study clinical associations, like comorbidities, and to identify markers associated with VTE. The combination of various clinical and laboratory variables could be used for VTE risk evaluation and targeted prevention.
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Ivovic, Miomira, Biljana Radojkovic, Zorana Penezic, Mirjana Stojkovic, Milina Tancic, Svetlana Vujovic, Andrija Bogdanovic, and Milka Drezgic. "Agranulocytosis and acute coronary syndrom in apathetic hyperthyreoidism." Srpski arhiv za celokupno lekarstvo 131, no. 5-6 (2003): 249–53. http://dx.doi.org/10.2298/sarh0306249i.
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INTRODUCTION Tissue expose to excessive levels of circulating thyroid hormones results in thyrotoxicosis. In most cases, thyrotoxicosis is due to hyper-activity of the thyroid gland. Cardiovascular and myopathic manifestations are predominant clinical features in most hyperthyroid patients, aged 60 years and older. Some of patients have apathetic hyperthyreoidism which presents with weight loss, small goiter, severe depression and without clinical features of increased sympathetic activity [3, 6]. About 50% of patients with cardiovascular manifestations have no evidence of underlying heart disease. Cardiac problems resolve when euthyreoid state is established [3]. Three treatment modalities are available in hyperthyreodism, namely medicament therapy, surgery and radioactive iodine. Antithyroid drug therapy complications, can be mild such as rash, which is managed without cessation of therapy by antihistamines administration. On the other hand, very serious complications such as agranulocytosis, necessitate immediate discontinuation of the medication and appropriate treatment. Although extremely rear, it is life-threatening with highly variable recovery time. CASE REPORT A 62-year-old woman with recurrent hyperthyroidism was admitted after treatment of agranu locytosis due to antithyroid drugs in another institution with G-CSF. The patient presented with clinical features of apathetic hyperthyroidism with extremely elevated thyroid hormone levels (total and free T4) and suppressed TSH. Radioactive iodine (5 mCi) was administered after increased thyroid uptake was confirmed. Echocardiography on admission was normal. ECG revealed moderately inverted T waves in standard and V1, V2 precordial leads. Laboratory analysis revealed mild normocytic anemia with normal white blood cell count, hypokaliemia and normal concentration of creatine phosphokinase lactic dehidrogenase and mildly elevated aspartate transaminase in sera. Chest X-ray was consistent with pulmonary emphysema. Because the worsening of ECG changes she was transferred to Coronary unit. The diagnosis of non-Q myocardial infarction was confirmed and treatment with nitrates and beta-adrenergic antagonists was instituted. Four weeks later she became euthyroid and coronarography was performed. Subepicardial coronary arteries were normal (Figure 1). She was dismissed, and still euthyroid three months later. DISCUSSION Agranulocytosis is very rare but very serious complication of antithyroid drug therapy. It can be detected in about 0.1 -1 % patients during the first three months of treatment. Sudden appearance, heralded by sore throat and fever, prompt physicians to seek white blood cell and differential count [1-3]. Confirmation of diagnosis urges cessation of drug therapy and appropriate antibiotic treatment. Recently, it was reported that recombinant human granulocyte colony-stimulating factor (rhG-CSF) is to be effective in shortening the recovery time in the neutropenic patients undergoing chemotherapy and also in patients with other types of neutropenia [5]. Tamai at al. [7] confirmed positive outcome in 34 patients treated with rhG-CSF compared to corticosteroid treatment. Hematologic laboratory abnormalities disappear 7-10 days after secession of therapy. Patients completely recover two to three weeks later. Fatal outcome was also described [1 -5]. Thyroid hormones have profound effects on cardiovascular physiology, especially on heart rate, cardiac output and systemic vascular resistance. In patients with hyperthyroidism, cardiac output is much higher than in normal persons. This is the result of direct effect of thyroid hormones on cardiac muscle contractility, heart rate and decrease in systemic vascular resistance. Excessive thyroid hormone secretion increases cardiac Na-K-activated plasma membrane ATP-ase and sarcoplasmic reticulum Ca-activated ATP-ase with resultant in increase myocardial contractility [6 9]. Sinus tachycardia is the most common rhythm disorder in hyperthyroidism but paroxysmal tachycardia and atrial fibrillation are not rare. This can be explained by increased heart rate, cardiac output, blood volume, coronary artery flow and peripheral oxygen consumption in thyreotoxicosis [9]. Patients with coronary arteriosclerosis can develop angina pectoris during thyreotoxic stage, which can be explained by imbalance between cardiac demand and supply. Myocardial damage is often in thyrotoxic patients with chronic hart failure, together with myocardial infarction in patients without coronary disease [2,6]. Congestive heart failure and atrial fibrillation are relatively resistant to digitalis treatment because of high metabolic turn over of medication and excessive myocardial irritability in hyperthyro-idism [6]. Cardiovascular and myopathic manifestations predominate in older hyperthyroid patients (over 60 years) and some of them can have only few symptoms of hyperthyroidism [1-3]. Thyrotoxic state characterized by fatigue, apathy, extreme weakness, low-grade fever and sometimes congestive heart failure are designated as apathetic hyperthyroidism. Such patients have small goiters, mild tachycardia and often cool and dry skin with few eye signs [6]. Patients with subclinical hyperthyroidism are at increased risk for atrial fibrillation [9]. Unstable angina and non-Q myocardial infarction (non ST elevation) are acute manifestation of coronary artery disease. The acute coronary syndrome of unstable angina, non-Q myocardial infarction and Q-wave myocardial infarction have atherosclerotic lesions of the coronary arteries as a common pathogenic substrate. Errosions or ruptures of unstable atherosclerotic plaque triggered pathophysiologic processes, resulted in thrombus formation at the site of arterial injury. This leads to abrupt reduction or cessation through the affected vessel. Clinical manifestations of unstable angina and non-Q myocardial infarction are similar and diagnosis of non-Q myocardial infarction is made on the basis of elevated serum markers indicative of cardiac necrosis, detected in peripheral circulation. Acute coronary syndrome ranging from unstable angina to myocardial infarction an non-Q myocardial infarction represents increasingly severe manifestations of the same pathophysiologic processes [10,11]. In conclusion, these 62-year-old woman presented with apathetic form of recurrent hyperthyroidism associated with two serious complications life-threatening agranulocytosis and acute coronary syndrome.
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Peters, Christopher A., Andrew Kaleda, Anthony Manfredo, Elizabeth Tapen, and Lawrence Koutcher. "Cardiac dose evaluation in patients undergoing breast radiotherapy in the modern era." Journal of Clinical Oncology 32, no. 26_suppl (September 10, 2014): 78. http://dx.doi.org/10.1200/jco.2014.32.26_suppl.78.
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78 Background: Breast radiotherapy (RT) after conservative surgery improves overall survival and minimizes locoregional recurrence. The therapeutic ratio of adjuvant RT continues to improve with time. Cardiac toxicity from breast cancer treatment remains a concern, and can result from chemotherapy, biologic therapy, or RT in a dose-dependent fashion. Dose to avoidance structures can be minimized as technological improvements in radiotherapy evolve. We sought to investigate heart and coronary artery dose using modern RT techniques. Methods: We reviewed 164 consecutive non-metastatic breast cancer patients treated with adjuvant breast RT, from 3/2011 to 12/2013. 8 patients were excluded because they did not complete the prescribed dose. Patients were treated on 3 different machines, at 2 centers. Data was extracted using both the treatment planning system and electronic medical records. Univariate analysis was done using t-test and one way ANOVA for variables predicting higher mean heart dose (MHD). Multivariate analysis was performed using multiple linear regression. p values ≤0.05 were considered significant. Results: The median age of our cohort was 63 (range 33-85), and 90% had ≤ stage 2 disease. 53% had left sided RT, 45% right, and 2% had bilateral RT. 18% had breast/chest wall and nodal RT, with 2% dedicated IMN targeting. 22% of patients were treated prone. The median dose, including boost, was 60.4 Gy (range 42.4-66.4). 35% received cytotoxic chemotherapy and 10% received trastuzumab. Mean heart dose was 1.4Gy (SD 2.2), and mean LAD dose was 4.9Gy (SD 4.4). MHD were lower in the prone position compared to supine, but did not reach statistical significance p=0.3. Advanced AJCC stage grouping, left sided or bilateral treatment, breast/nodal target volume, and helical treatment were associated with significantly higher MHD on univariate analysis. On multivariate analysis, only breast/nodal volume and helical technique remained significant, both p<0.001. Conclusions: Modern techniques result in low heart and LAD doses in our series. Because adjuvant breast RT plays a critical role in the definitive management of breast cancer, these data are reassuring to patients, physicians, and payers.
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Dreyling, Martin, Sebastian Fetscher, P. Kornek, Arnd Nusch, Martin Kornacker, Ralf Angermund, Harold Pliskat, Lenka Kellermann, and Thomas Kegel. "Treatment of Indolent Non-Hodgkin’s Lymphoma in Germany - Results of a Representative Population-Based Survey." Blood 110, no. 11 (November 16, 2007): 1353. http://dx.doi.org/10.1182/blood.v110.11.1353.1353.
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Abstract In advanced stage indolent lymphoma, therapeutic approaches may vary from watch and wait, antibody monotherapy, conventional chemotherapy or dose-intensified consolidation up to allogeneic strategies. In this nation-wide survey, representative hematological/oncological centers monitored current treatment strategies under routine conditions. 495 centers involved in the treatment of indolent lymphoma including university hospitals (UH), community hospitals (CH), and office-based hematologists (OBH) were contacted. 13% of identified centers provided information on 741 patients corresponding to 10% of the expected national prevalence. Detailed data on 576 unselected patients (median age 67 years, range 17 to 95) with treatment decision in the second and third quarter of 2006 (start, change or end of therapy) of 46 representative centers (2 UH, 25 CH, and 19 OBH) were included in this analysis. Data were verified by monitoring anonymized patients source data. Median age was 67 with hypertension (28%), coronary heart disease (14%), diabetes (11%), heart failure (8%), cardiac arrhythmia (7%) and renal impairment (7%) being the most frequent concomitant diseases at time of diagnosis. Histology included 39% follicular lymphoma, 26% chronic lymphocytic leukemia (CLL), 10% marginal zone, 9% mantle cell lymphoma, and 16% other histologies. Aim of initial therapy was curative in 35%, aiming at improved survival in 62% and palliation in 54% of patients. Radiation (10%), antibody monotherapy (4%), chemotherapy (33%) and combined immuno-chemotherapy (31%) were the most frequent approaches. Applied chemotherapies included CHOP (46%), fludarabine combinations (F/FC/FCM: 15%), chlorambucil (14%), CVP/COP (9%), Bendamustin (4%), with maintenance (12%) and autologous/allogeneic stem cell consolidation both in 3% of patients. In first relapse, complex regimen including immuno-chemotherapy (49%), maintenance therapy (16%), and autologous/allogeneic transplantation (14%/4%) were more frequently planned. As expected, significant differences were observed between follicular, mantle cell lymphoma and CLL. Interestingly, supportive measures including antibiotics (34%), erythrocyte transfusions (32%), G-CSF (22%), immunoglobulins (19%), antifungal drugs (13%), and erythropoietin (10%) were frequently applied already in first line therapy. Overall response was 83% (FL: 97%, MCL: 95%, CLL: 74%) with a 39% CR rate. Only 10% of first line patients were treated within studies (UH: 19%, CH: 5%, OBH: 13%). In this population-based survey, patient characteristics differed significantly from published study cohorts as did clinical strategies and therapeutic approaches. Thus, clinical studies more relevant to the treatment of medically compromised patients are urgently warranted.
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Blann, Andrew D., and Simon Dunmore. "Arterial and Venous Thrombosis in Cancer Patients." Cardiology Research and Practice 2011 (2011): 1–11. http://dx.doi.org/10.4061/2011/394740.
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The most frequent ultimate cause of death is myocardial arrest. In many cases this is due to myocardial hypoxia, generally arising from failure of the coronary macro- and microcirculation to deliver enough oxygenated red cells to the cardiomyocytes. The principle reason for this is occlusive thrombosis, either by isolated circulating thrombi, or by rupture of upstream plaque. However, an additionally serious pathology causing potentially fatal stress to the heart is extra-cardiac disease, such as pulmonary hypertension. A primary cause of the latter is pulmonary embolus, considered to be a venous thromboembolism. Whilst the thrombotic scenario has for decades been the dominating paradigm in cardiovascular disease, these issues have, until recently, been infrequently considered in cancer. However, there is now a developing view that cancer is also a thrombotic disease, and notably a disease predominantly of the venous circulation, manifesting as deep vein thrombosis and pulmonary embolism. Indeed, for many, a venous thromboembolism is one of the first symptoms of a developing cancer. Furthermore, many of the standard chemotherapies in cancer are prothrombotic. Accordingly, thromboprophylaxis in cancer with heparins or oral anticoagulation (such as Warfarin), especially in high risk groups (such as those who are immobile and on high dose chemotherapy), may be an important therapy. The objective of this communication is to summarise current views on the epidemiology and pathophysiology of arterial and venous thrombosis in cancer.
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Cramer, Paula, Valentin Goede, Petra Jenke, Raymonde Busch, Michael Hallek, and Barbara Eichhorst. "Impact of Different Chemotherapy Regimen in Comorbid Patients with Advanced Chronic Lymphocytic Leukemia: Metaanalysis of Two Phase-III-Trials of the German CLL Study Group." Blood 108, no. 11 (November 16, 2006): 2840. http://dx.doi.org/10.1182/blood.v108.11.2840.2840.
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Abstract Introduction: Since chronic lymphocytic leukemia (CLL) is a disease of elderly patients (pts) comorbidity is a frequent feature which has already been shown to be associated with survival-shortening in lymphoma patients. It has been hypothesized that intensity of chemotherapy may interfere with treatment outcome, but the precise mechanisms underlying the impact of comorbidity are still not understood. Consequently, comorbitity currently keeps away oncologists from administering intense combined (immuno−)chemotherapy to pts with CLL and concomitant diseases. Patients & methods: 554 pts treated in two different phase-III-trials of the GCLLSG were eligible for this analysis: 362 pts (65%) younger than 65 years were treated on the CLL4-protocol with Fludarabine (F) or Fludarabine-Cyclophosphamide (FC) and 192 pts (35%) aged 65 years and older on the CLL5-protocol with F or Chlorambucile (Clb). The mean age for all pts was 61 years; 68% of the pts were male. Results: Comorbidity was present in 53% of the pts, 25% had at least two comorbidities. The most common comorbidities were: hypertension (19%), lipometabolic disorders (16%), diabetes mellitus (10%) and coronary heart disease (7%). Progression free survival (PFS) and overall survival (OS) were significantly shorter in comorbid pts (median OS: 43,5 vs. 51,6 months, p=0,01; median PFS: 20,3 vs. 23,5 months, p=0,03). Survival was also impaired if pts had a higher number of comorbidities (PFS & OS: p=0,0001) or more severe concomitant diseases (PFS: p=0,007, OS: p=0,0000). Whereas this impact of comorbidity on OS was not significant in the FC- and Clb-arm, comorbid pts treated with F had a significantly shorter survival (median OS: 38,29 vs. 51,58 months, p=0,0452). Notably only the younger F-treated comorbid pts were affected by this disadvantage (CLL4: p=0,0221). Although myelotoxicity, infections and all grade III–IV adverse effects were not influenced by comorbidity, pts with concomitant disease had a higher rate of treatment terminations (38% vs. 25%, p=0,002). The higher percentage of dose reductions and treatment terminations for comorbid pts were only significant in the subgroup of F-treated pts (dose reduction: 31% vs. 19,1%, p=0,029; treatment termination in the younger CLL4-pts: 28,2% vs. 18,0%, p=0,023). Administration of more intense chemotherapy-regimen improved the survival of pts with concomitant disease (median OS: FC: not reached, F: 38,29 and Clb: 33,72 months, p=0,0248; median PFS: FC: not reached, F: 18,8 and Clb: 14,1 months, p=0,0000). A multivariate analysis on the prognostic impact of comorbidity and different chemotherapy regimen will be presented. Conclusions: Due to the here presented results the wide impact of comorbidity in CLL pts is apparent. It should be considered when it comes to treatment decisions eventhough this population was selected due to the strict criteria of the clinical trial. The mechanism of survival shortening in comorbid pts with CLL is not yet understood, but seems to be related with dose reductions and treatment terminations. Additional harm to these pts by an insufficient treatment and a poor control of the CLL ought to be avoided. As more intense chemotherapy-regimen, like FC are feasible for pts with comorbidity, more trials surveying these therapies in pts with more severe concomitant disease are needed.
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Kattih, Badder, Amir Shirvani, Piroska Klement, Abel Martin Garrido, Razif Gabdoulline, Alessandro Liebich, Maximilian Brandes, et al. "IDH Mutations Are Associated with an Increased Risk of Coronary Artery Disease and Cardiotoxicity in Patients with Established AML." Blood 136, Supplement 1 (November 5, 2020): 32–33. http://dx.doi.org/10.1182/blood-2020-143026.
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Introduction: Clonal hematopoiesis initiated by acquired somatic mutations in hematopoietic cells has been identified as an independent driver of increased all-cause mortality, risk of coronary artery disease and heart failure. Oncogenic mutations in isocitrate dehydrogenases 1 and 2 (IDH1 and IDH2) lead to conversion of αKG to R-2-hydroxyglutarate (R-2HG), which is a competitive inhibitor of TET2 and a known oncometabolite. Oncometabolite R-2HG (produced by IDH mutant cells) has been implicated in pathological cardiac remodeling and dysfunction in preclinical studies. Whether IDH mutant leukemic cells in patients with established AML are also associated with the development of cardiovascular diseases or exacerbate cardiotoxicity during anthracycline containing chemotherapy is still unknown. Methods: In this observational study, a propensity score-based analysis was performed in 363 adult AML patients being stratified by mutation status in the IDH gene. To analyze whether the IDH mutation status in AML patients was associated with increased cardiotoxicity, we analyzed echocardiographic left ventricular ejection fraction (LVEF) in the control group (AML patients without IDH mutation) and the exposed group (AML patients with IDH mutation) at baseline and at different time points during AML therapy. Results: IDH 1 and IDH2 mutations occurred in 26 (7.2%) and 39 adult AML patients (10.7%), respectively. The median age of the total population was 60 years. The estimated 2-year relapse-free survival and overall survival rates in the overall study cohort were 49.4% (5-year RFS 38.9%) and 59.2% (5-year OS 43.1%) during a median follow-up of 7.6 years. IDH1 mutant AML patients exhibited a significantly higher prevalence of coronary artery disease (26.1% vs. 6.4%, p=0.002). A propensity score analysis by inverse probability-weighting was performed based on the 295 patients who received intensive cytarabine and anthracycline-containing chemotherapy. This analysis revealed an increased risk for a declining cardiac function during AML treatment in IDH1/2 mutated compared to IDH1/2 wild type patients [LVEF pretreatment compared to 10 months after diagnosis: 59.2% to 41.9% (P<0.001) vs 58.5% to 55.4% (P=0.27), respectively], suggesting that the IDH mutations in AML patients were associated with a declining cardiac function during AML therapy, which was independent of measured baseline characteristics. To validate whether the oncometabolite R-2HG drives vulnerability of cardiac cells in patients with IDH mutant AML, human iPS-derived cardiomyocytes were exposed to R-2HG (or control) during anthracycline treatment. Indeed, an exaggerated sarcomere disarray when R-2HG was added to anthracycline treatment was identified by immunostaining in human induced pluripotent stem cell (hIPS) derived cardiomyocytes. By RNA sequencing of R-2HG exposed hiPS-derived cardiomyocytes during anthracycline treatment, we demonstrate the transcriptomic basis for putative biological processes mediating the increased cardiotoxicity. Conclusion: The presence of an IDH mutation in adult AML was associated with a higher prevalence of coronary artery disease and an exacerbated cardiotoxicity during anthracycline treatment, which was at least in part mediated by the oncometabolite R-2HG. Disclosures Thol: Daiichi Sankyo: Membership on an entity's Board of Directors or advisory committees; Astellas: Membership on an entity's Board of Directors or advisory committees; Abbvie: Membership on an entity's Board of Directors or advisory committees; Celgene: Membership on an entity's Board of Directors or advisory committees; Pfizer: Membership on an entity's Board of Directors or advisory committees. Ganser:Novartis: Consultancy; Celgene: Consultancy. Heuser:BerGenBio ASA: Research Funding; Roche: Research Funding; Astellas: Research Funding; Janssen: Consultancy; Abbvie: Consultancy; Pfizer: Consultancy, Honoraria, Research Funding; Novartis: Consultancy, Honoraria, Research Funding; Amgen: Research Funding; PriME Oncology: Honoraria; Daiichi Sankyo: Consultancy, Research Funding; Stemline Therapeutics: Consultancy; Bayer: Consultancy, Research Funding; Karyopharm: Research Funding.
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Chen, John H., Daniel J. Lenihan, Sharon E. Phillips, Madan H. Jagasia, Stacey A. Goodman, Adetola A. Kassim, Shelton L. Lacy, et al. "Risk Factors for Cardiac Toxicities Associated with Proteasome Inhibitor Chemotherapy during Treatment of Multiple Myeloma." Blood 126, no. 23 (December 3, 2015): 5363. http://dx.doi.org/10.1182/blood.v126.23.5363.5363.
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Abstract Introduction Proteasome inhibitors (PI) bortezomib (B) and carfilzomib (C) are cornerstone therapies for multiple myeloma (MM). An increased incidence of PI-induced cardiac adverse events (CAEs) has been reported in patients receiving C. However, risk factors for cardiac toxicity in this population remain unclear. Our objective is to evaluate the incidence of CAEs associated with C compared with B and identify risk factors for developing events. Patients and Method This was a retrospective analysis of 96 consecutive patients treated for MM at Vanderbilt University from 2011 to 2014 who received B (n=44) and/or C (n=52). Patients in the C group had been previously treated with B, whereas patients in the B group did not have exposure to C. No patients studied were included in both cohorts. We evaluated the clinical features and frequency of CAEs (grade II-IV heart failure, acute coronary syndrome, left ventricular dysfunction, atrial fibrillation/flutter, thromboembolism, systemic hypertension, pulmonary hypertension, orthostatic hypotension, or sudden cardiac death). To identify factors that predisposed patients to CAEs, we analyzed duration of PI therapy, 10-year atherosclerotic cardiovascular disease (ASCVD) risk (calculated risk of myocardial infarction or stroke), gender, use of antithrombotic (antiplatelet/anticoagulant) and antihypertensive medications, prior history of cardiac events, and disease cytogenetic profile. Patients with a prior history of cardiac events were followed by a cardio-oncologist during the course of treatment. Results Table 1 shows patient characteristics. Twenty-five patients experienced CAEs (B, 13% (n=12); C, 25% (n=13)). Cumulative incidence (CI) of CAEs was not significantly different in patients on C compared with B (log-rank test P = 0.41) (Figure 1). Heart failure was the most common type of CAE (Table 2). CAEs occurred after a median of 90 days (range, 4-456) with C and 63.5 days (range, 5-336) with B. By univariate analysis, more patients in the C group were prior smokers, underwent stem cell transplantation and had more prior lines of therapy. More patients in the B group used antithrombotic and ACE inhibitor agents. There were no other significant differences in the use of antihypertensive, antiarrhythmic, and lipid-lowering medications between cohorts. Multivariate analysis showed that male gender (HR 5.3, 95% CI 1.5-18.0, P = 0.007) was an independent risk factor for developing CAEs. Patients taking antithrombotic agents had a lower risk of CAE compared with those not on these therapies (HR 0.1, 95% CI 0.04-0.54, P = 0.004). While ASCVD risk was not predictive of CAEs, patients with a prior history of cardiac events who were followed by a cardio-oncologist experienced fewer CAEs (HR 0.2, 95% CI 0.05-0.72, P = 0.014). Longer duration of PI use resulted in decreasing risk of CAE (HR 0.8, 95% CI 0.7-0.9, P = 0.010). There were no interactions between these outcomes. Conclusions In this series, the incidence of CAEs associated with C did not differ significantly from that of B. We found that events occurred early in therapy. Male gender was an independent risk factor for CAEs. Use of antithrombotic therapy was associated with significantly reduced risk of CAEs. These data suggest that patients may benefit from antithrombotic therapy and follow-up by a cardio-oncologist while on PI therapy, particularly if there is a prior history of cardiac events. Table 1. Bortezomib % (n=44) Carfilzomib % (n=52) P-value ASCVD Risk 0.43 0-10% 46 50 10-20% 29 36 >20% 26 14 Male Gender 57 71 0.82 Median Age, y 61 (38-91) 60 (36-86) 0.20 Past Smoker 26 51 0.02 Type II Diabetes 11 17 0.41 Hyperlipidemia 27 27 0.97 Kidney Disease 9 12 0.70 Prior History of Cardiac Event 59 60 0.96 Median Duration on Bortezomib, d 229 203 0.67 Median Duration on Carfilzomib, d 87.5 ACE Inhibitor Use 32 13 0.03 Antithrombotic Use 48 23 0.01 ISS Stage 0.72 III 34 25 FISH Risk 0.13 Standard/Intermediate 93 85 High 7 15 Median Prior Lines of Therapy 0 (0-4) 2 (0-8) <0.001 Stem Cell Transplant 45 65 0.05 Table 2. Cardiac adverse events Bortezomib Carfilzomib P-value Total Cardiac Adverse Events* 19 17 0.08 Heart Failure 9 6 Acute Coronary Syndrome 1 2 Left Ventricular Dysfunction 0 1 Atrial Fibrillation/Flutter 2 2 Thromboembolism 2 2 Systemic Hypertension 3 3 Pulmonary Hypertension 0 1 Orthostatic Hypotension 2 0 Sudden Cardiac Death 0 0 *Some patients had multiple events Figure 1. Cumulative incidence of cardiac adverse events Figure 1. Cumulative incidence of cardiac adverse events Disclosures No relevant conflicts of interest to declare.
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Hu, Min, Tianyu Li, Zixiang Bo, and Feixiang Xiang. "The protective role of carnosic acid in ischemic/reperfusion injury through regulation of autophagy under T2DM." Experimental Biology and Medicine 244, no. 7 (April 4, 2019): 602–11. http://dx.doi.org/10.1177/1535370219840987.
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Ischemic heart disease (IHD) is the most common cardiovascular disease and is the main cause of death and disability worldwide. Myocardial ischemia/reperfusion (MI/R) injury has been linked to IHD-induced cardiomyocytes apoptosis and tissue damage. Recently, it has been reported that carnosic acid (CA) may function as a potent antioxidant in liver ischemia/reperfusion (I/R). However, whether it regulates I/R in the heart remains unclear. Here, we elucidated the emerging role of CA in MI/R under diabetic myocardial conditions. Diabetes mellitus (DM) was induced in mice by consumption of a high-fat diet for 16 weeks. To create the I/R in mice, the left anterior descending coronary artery was occluded for 30 min, and then occlusion was released to reperfuse the heart for 3 or 24 h. In diabetic myocardial ischemia/reperfusion (DMI/R) mice, pre-treatment with CA suppressed the overgeneration of reactive oxygen species (ROS) and production of cytokine. Importantly, the activation of autophagy was significantly increased by CA treatment, as assessed by p62 degradation and LC3-II/LC3-I conversion, as well as by phosphorylation of AMPKα, Akt, and mTOR. Interestingly, all of the protective effects of CA were impeded by the treatment with chloroquine, which is an autophagy inhibitor. These studies suggest that CA prevents DMI/R injury via regulation of autophagy. In conclusion, our findings indicate that CA has potential as a novel therapeutic to prevent DMI/R injury. Impact statement We have provided, for the first time, evidence that carnosic acid (CA) attenuates ischemia–reperfusion injury of diabetic myocardium, i.e. diabetic myocardial ischemia/reperfusion (DMI/R) injury, via enhancement of autophagy. A greater understanding of the target molecule in CA-enhanced autophagy is necessary for the development of potential chemotherapy for DMI/R injury.
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de Haas, E. C., N. Zwart, C. Meijer, H. M. Boezen, A. J. Suurmeijer, J. van der Meer, H. J. Hoekstra, F. E. van Leeuwen, D. T. Sleijffer, and J. A. Gietema. "Association of plasminogen-activator inhibitor 1 (PAI-1) 4G/5G gene polymorphism with survival and chemotherapy-related vascular toxicity in non-seminomatous testicular cancer (TC)." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 5083. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.5083.
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5083 Background: High PAI-1 expression by tumor has been associated with poor prognosis in different cancer types, while high systemic PAI-1 levels may increase the risk of vascular thrombosis. We investigated whether the 4G/5G del/ins polymorphism in the PAI-1 promoter (rs1799889; 4G might lead to higher transcription), is associated with differences in survival and prevalence of cardiovascular events in TC. Methods: Data were collected on survival and cardiovascular events (venous thromboembolism [VTE] and coronary heart disease [CHD]) of TC patients treated with standard platinum based chemotherapy from 1977–2004. PAI-1 genotype was determined from non-tumor genomic DNA by a Taqman SNP assay. Genotypes were compared for survival (Kaplan-Meier curves + log-rank and Cox-regression analysis), disease outcome (logistic regression) and prevalence of VTE and CHD (χ2-test). Results: Data are available for 324 patients with median follow-up of 10 yrs (range 0–28). The 3 genotypes 4G/4G (n = 84), 4G/5G (n = 164), and 5G/5G (n = 76) do not differ in age and initial chemotherapy regime. However, the 4G/4G variant shows a higher prevalence of International Germ Cell Cancer Classification (IGCCC) poor prognosis compared to 4G/5G + 5G/5G (24% vs 10%; p = 0.003), as well as a decreased TC related survival compared to 4G/5G + 5G/5G (83% vs 94%; p = 0.001) with a hazard ratio of 2.68 for TC related death (95%CI 1.26–5.72; adjusted for IGCCC p = 0.011). In addition, the 4G/4G variant shows an odds ratio of 3.35 for refractory TC and early relapses (<2 yrs) (95% CI 1.48–7.58; p = 0.004). The 3 genotypes do not differ significantly in prevalence of VTE (4G/4G 11.9%, 4G/5G 8.5%, 5G/5G 7.9%; p = 0.616) and CHD during/after chemotherapy (4G/4G 6.0%; 4G/5G 4.9%; 5G/5G 2.6%; p = 0.594). Conclusions: The 4G/4G variant of the PAI-1 4G/5G gene polymorphism is associated with IGCCC poor prognosis, reduced survival and higher prevalence of refractory disease and early relapses. No effect on vascular toxicity was found. The 4G/4G variant of the PAI-1 gene may be an unfavorable prognostic factor as well as an unfavorable predictive factor for response to chemotherapy in patients with TC. No significant financial relationships to disclose.
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Glimelius, Ingrid, Karin Ekstroem Smedby, Mats Jerkeman, Sandra Eloranta, and Caroline Weibull. "Prognostic Implications of Specific Comorbidities in Mantle Cell Lymphoma Patients, a Swedish Lymphoma Registry Study." Blood 132, Supplement 1 (November 29, 2018): 2891. http://dx.doi.org/10.1182/blood-2018-99-111471.
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Abstract Purpose The prognosis for patients with mantle cell lymphoma (MCL) is rather dismal where particularly elderly patients, often with comorbidities, have difficulties tolerating the intensive treatments needed for long-term remission. Our aim was to describe the frequency and spectrum of comorbidities among patients with MCL in a population-based setting, and assess the impact of comorbidities on treatment choice, lymphoma-specific and overall survival as well as causes of death in MCL patients by age and sex. Methods In the nationwide Swedish Lymphoma Register, we identified 1,385 MCL patients (1,009 males and 376 females) diagnosed 2000-2015 at all ages. Comorbid diseases within 10 years prior to diagnosis were identified from the national Swedish In- and Outpatient registers and included somatic diseases defined according to the Charlson comorbidity index (CCI; 0, 1 and 2+), with the addition of psychiatric disorders. Comorbidities were both categorized and presented individually. Hazard ratios (HR) with 95% confidence intervals (CIs) comparing lymphoma-specific and all-cause mortality among patients with different levels of CCI were estimated from flexible parametric survival models, adjusted for calendar year of diagnosis, age at diagnosis, sex, educational level, and MCL international prognostic index (MIPI). Model-based predictions were used to obtain cumulative probabilities of death due to lymphoma and other causes. Results In the cohort, 24% were <59 years of age, 32% between 60-69, 30% between 70-79 and 14% >80 years. In total, 606 out of 1,385 patients (44%) had a history of one or more comorbidities at the time of diagnosis, among which 388 (28%) had a CCI=2+. The most common specific comorbidities were prior malignancy (17%), (prostate cancer was most frequent), and prior coronary heart disease (14%). Moreover, 9% of the patients had diabetes, 7% had pulmonary disease, 3% renal disease, 3% connective tissue disease and 1% had dementia. In addition, 2% had a psychiatric disorder. With a mean follow-up of 3.7 years (range: 0.0-15.6), 633 (46%) patients died from lymphoma. Lymphoma was the major cause of death among males, irrespective of CCI (Figure 1A). Lymphoma was also the major cause of death among females with CCI=0 whereas among females with comorbidities (CCI≥1), approximately half of the patients died due to other causes (Figure 1B). A CCI=2+ was associated with worse overall and lymphoma-specific survival (adjusted lymphoma-specific HR=1.31; 95% CI: 1.04-1.65). Specific comorbidities associated with significantly worse lymphoma-specific survival were history of coronary heart disease, connective tissue disease, renal disease, dementia and psychiatric disorders (Figure 1C). Patients aged below 70 years at diagnosis who presented with no comorbidities were primarily treated according to the NLG-MCL2/3 protocol* (177 out of 437, 41%). However, this was not the case among patients in the same age range but with CCI=1 (24 out of 177, 34%) or CCI=2+ (13 out of 112, 12%). Primary treatment concepts for comorbid patients were CHOP, bendamustine, or chlorambucil with the addition of rituximab. *NLG-MCL2/3= R-maxi-CHOP alternating with high dose cytarabine, rituximab, and consolidation with high-dose therapy and autologous stem-cell transplantation Conclusions A large fraction of MCL patients are elderly and comorbidity was present in almost half of the patients overall. A CCI of 2+ was an independent negative prognostic factor. Lymphoma-death was the major cause of death among males, motivating the need for MCL-specific treatment irrespectively of a high burden of comorbidities, while approximately 50% of comorbid-females died due to other reasons. Patients with comorbidities were less often treated according to intensive first-line chemotherapy protocols. In the introduction and development of new treatment regimens, consideration of toxicity and tolerability specifically in patients with comorbidities is warranted, particularly in patients with coronary heart disease, connective tissue disease and renal disorders. . Disclosures Ekstroem Smedby: Janssen Pharmaceuticals: Other: The Department have recieved partial funding from Janssen Pharmaceuticals. Eloranta:Janssen Pharmaceuticals: Other: S Eloranta is currently employed as a project coordinator and her salary is funded via a public-private real world evidence collaboration between Karolinska Institutet and Janssen Pharmaceuticals.
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Gaddh, Manila, Bernice Fokum, Hamid Bouiri, Augustin Haidau, and Margaret Telfer. "Prologed Use of Pegylated Liposomal Doxorubicin In An HIV-Infected Population with Kaposi's Sarcoma at An Inner-City Safety Net Hospital." Blood 116, no. 21 (November 19, 2010): 4873. http://dx.doi.org/10.1182/blood.v116.21.4873.4873.
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Abstract Abstract 4873 Introduction: Kaposi's sarcoma (KS) is a low-grade HHV-8 associated vascular tumor that is particularly prevalent in patients infected with HIV. The mainstay of treatment is HAART, which has decreased the aggressiveness, and possibly the prevalence of this disease. Cytotoxic chemotherapy is generally added for moderate to severe symptomatic disease, with Pegylated Liposomal Doxorubicin (Doxil) being the treatment of choice. Studies have shown that unlike regular anthracyclines, Doxil can be safely administered over long periods at low doses without inducing cardio toxicity. The present study was done to evaluate cardiac toxicity associated with prolonged administration of Doxil in patients with KS. Methods: Seven-year retrospective chart review of 55 KS patients treated with 20mg/m2 of Doxil every 3 weeks until disappearance of lesions, withdrawal or change of treatment, or discovery of cardiac damage by annual MUGA scans. All patients received HAART concomitantly. In general, compliance was good. All presenting patients were male with one genetic male transsexual. Results: The median age of patients was 40 years; range between 25 – 56 years. 5 patients died during the study; 3 due to infectious complications and 2 due to heart disease. 7 patients had to discontinue Doxil when LVEF decreased to < 50%. Of the 16 patients who received >500mg/m2 Doxil, 1 died of cancer and 3 were switched to other drugs due to low LVEF. 1 of these 3 patients with decreased LVEF had a severely abnormal MUGA which then led to the diagnosis of coronary artery disease. The other 12 in this subgroup remain alive with no evidence of heart disease. Conclusion: In concordance with prior studies, our study shows that patients can tolerate greater than 500mg/m2 of cumulative Doxil dose, while being monitored closely with physical examination and MUGA scans. Obtaining MUGA scans every 6 months, instead of annually as was done in our study, may lead to earlier recognition of cardiotoxicity. Disclosures: No relevant conflicts of interest to declare.
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Chavez-MacGregor, Mariana, Ning Zhang, Thomas A. Buchholz, Yufeng Zhang, Jiangong Niu, Linda Elting, Benjamin D. Smith, Gabriel N. Hortobagyi, and Sharon H. Giordano. "Trastuzumab-Related Cardiotoxicity Among Older Patients With Breast Cancer." Journal of Clinical Oncology 31, no. 33 (November 20, 2013): 4222–28. http://dx.doi.org/10.1200/jco.2013.48.7884.
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Purpose The use of trastuzumab in the adjuvant setting improves outcomes but is associated with cardiotoxicity manifested as congestive heart failure (CHF). The rates and risk factors associated with trastuzumab-related CHF among older patients are unknown. Patients and Methods Breast cancer patients at least 66 years old with full Medicare coverage, diagnosed with stage I-III breast cancer between 2005 and 2009, and treated with chemotherapy were identified in the SEER-Medicare and in the Texas Cancer Registry–Medicare databases. The rates and risk factors associated with CHF were evaluated. Chemotherapy, trastuzumab use, comorbidities, and CHF were identified using International Classification of Diseases, version 9, and Healthcare Common Procedure Coding System codes. Analyses included descriptive statistics and Cox proportional hazards models. Results In total, 9,535 patients were included, of whom 2,203 (23.1%) received trastuzumab. Median age of the entire cohort was 71 years old. Among trastuzumab users, the rate of CHF was 29.4% compared with 18.9% in nontrastuzumab users (P < .001). Trastuzumab users were more likely to develop CHF than nontrastuzumab users (hazard ratio [HR], 1.95; 95% CI, 1.75 to 2.17). Among trastuzumab-treated patients, older age (age > 80 years; HR, 1.53; 95% CI, 1.16 to 2.10), coronary artery disease (HR, 1.82; 95% CI, 1.34 to 2.48), hypertension (HR, 1.24; 95% CI, 1.02 to 1.50), and weekly trastuzumab administration (HR, 1.33; 95% CI, 1.05 to 1.68) increased the risk of CHF. Conclusion In this large cohort of older breast cancer patients, the rates of trastuzumb-related CHF are higher than those reported in clinical trials. Among patients treated with trastuzumab, those with cardiac comorbidities and older age may be at higher risk. Further studies need to confirm the role that the frequency of administration plays in the development of trastuzumab-related CHF.