Pub Date : 2024-02-29DOI: 10.1186/s40959-024-00204-6
Anna Talty, Roseanne Morris, Carolyn Deighan
Background: Due to advancements in methods of cancer treatment, the population of people living with and beyond cancer is dramatically growing. The number of cancer survivors developing cardiovascular diseases and heart failure is also rising, due in part to the cardiotoxic nature of many cancer treatments. Guidelines are being increasingly released, emphasising the need for interdisciplinary action to address this gap in survivorship care. However, the extent to which interventions exist, incorporating the recommendations of cardio-oncology research, remains undetermined.
Objective: The aim of this scoping review is to assess the nature, extent and remit of existing cancer care interventions and their integration of cardio-oncology principles.
Methods: The review was conducted in accordance with the PRISMA Extension for Scoping Reviews Guidelines. Databases were independently searched for articles from 2010 to 2022, by two members of the research team. Data were charted and synthesised using the following criteria: (a) the focus of the intervention (b) the medium of delivery (c) the duration (d) the modalities included in the interventions (e) the research articles associated with each intervention (f) the type of studies conducted (g) key measures used (h) outcomes reported.
Results: Interventions encompassed six key modalities: Psychological Support, Physical Activity, Nutrition, Patient Education, Lifestyle and Caregiver Support. The focus, medium of delivery and duration of interventions varied significantly. While a considerable number of study protocols and pilot studies exist documenting HSMIs, only 25% appear to have progressed beyond this stage of development. Of those that have, the present review did not identify any 'feasible' interventions that covered each of the six modalities, while being generalisable to all cancer survivors and incorporating the recommendations from cardio-oncology research.
Conclusion: Despite the substantial volume of research and evidence from the field of cardio-oncology, the findings of this scoping review suggest that the recommendations from guidelines have yet to be successfully translated from theory to practice. There is an opportunity, if not necessity, for cardiac rehabilitation to expand to meet the needs of those living with and beyond cancer.
{"title":"Home-based self-management multimodal cancer interventions & cardiotoxicity: a scoping review.","authors":"Anna Talty, Roseanne Morris, Carolyn Deighan","doi":"10.1186/s40959-024-00204-6","DOIUrl":"10.1186/s40959-024-00204-6","url":null,"abstract":"<p><strong>Background: </strong>Due to advancements in methods of cancer treatment, the population of people living with and beyond cancer is dramatically growing. The number of cancer survivors developing cardiovascular diseases and heart failure is also rising, due in part to the cardiotoxic nature of many cancer treatments. Guidelines are being increasingly released, emphasising the need for interdisciplinary action to address this gap in survivorship care. However, the extent to which interventions exist, incorporating the recommendations of cardio-oncology research, remains undetermined.</p><p><strong>Objective: </strong>The aim of this scoping review is to assess the nature, extent and remit of existing cancer care interventions and their integration of cardio-oncology principles.</p><p><strong>Methods: </strong>The review was conducted in accordance with the PRISMA Extension for Scoping Reviews Guidelines. Databases were independently searched for articles from 2010 to 2022, by two members of the research team. Data were charted and synthesised using the following criteria: (a) the focus of the intervention (b) the medium of delivery (c) the duration (d) the modalities included in the interventions (e) the research articles associated with each intervention (f) the type of studies conducted (g) key measures used (h) outcomes reported.</p><p><strong>Results: </strong>Interventions encompassed six key modalities: Psychological Support, Physical Activity, Nutrition, Patient Education, Lifestyle and Caregiver Support. The focus, medium of delivery and duration of interventions varied significantly. While a considerable number of study protocols and pilot studies exist documenting HSMIs, only 25% appear to have progressed beyond this stage of development. Of those that have, the present review did not identify any 'feasible' interventions that covered each of the six modalities, while being generalisable to all cancer survivors and incorporating the recommendations from cardio-oncology research.</p><p><strong>Conclusion: </strong>Despite the substantial volume of research and evidence from the field of cardio-oncology, the findings of this scoping review suggest that the recommendations from guidelines have yet to be successfully translated from theory to practice. There is an opportunity, if not necessity, for cardiac rehabilitation to expand to meet the needs of those living with and beyond cancer.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10903028/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139995714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-27DOI: 10.1186/s40959-024-00214-4
Maciej Kabat, Roma Padalkar, Sara Hazaveh, Vladimir Joseph, David Feigenblum, Sean Sadikot
Capecitabine, a pro-drug of 5-fluorouracil, is commonly used in the treatment of breast and colorectal cancer. Its side effects, including nausea, vomiting, diarrhea, fatigue, loss of appetite, and bone marrow suppression, are well recognized. However, coronary vasospasm represents a less commonly recognized but significant complication of fluoropyrimidine-based therapies such as capecitabine. Proposed mechanisms for this adverse effect complication include direct endothelium-independent vasoconstriction, activation of protein kinase C, and activation of the cyclooxygenase pathway. In this report, we present a case of capecitabine-induced coronary vasospasm leading to progressive, focal ST-elevations, myocardial ischemia, and subsequently polymorphic ventricular tachycardia. These events were captured on telemetry, in a male in his early 40s, diagnosed with stage IIIB sigmoid colon cancer. Notably, the patient had no pre-existing coronary artery disease or other cardiovascular risk factors. Upon diagnosis, the patient was initiated on a calcium channel blocker, verapamil, to mitigate further coronary vasospasm events. After thorough discussions that prioritized the patient's input and values, an implantable cardioverter-defibrillator was placed subcutaneously. Following discharge, the patient restarted capecitabine therapy along with verapamil prophylaxis and did not experience any subsequent shocks from his ICD as assessed during his outpatient follow-up visits. This case emphasizes the need to involve patients in decision-making processes, especially when managing unexpected and serious complications, to ensure treatments align with their quality of life and personal preferences.
卡培他滨是 5-氟尿嘧啶的原研药,常用于治疗乳腺癌和结直肠癌。其副作用包括恶心、呕吐、腹泻、乏力、食欲不振和骨髓抑制,这些副作用已得到广泛认可。然而,冠状动脉血管痉挛是以氟嘧啶为基础的疗法(如卡培他滨)的一种不太常见但却很重要的并发症。这种不良反应并发症的拟议机制包括直接的内皮依赖性血管收缩、激活蛋白激酶 C 和激活环氧化酶途径。在本报告中,我们介绍了一例卡培他滨诱导的冠状动脉血管痉挛导致进行性、局灶性 ST 抬高、心肌缺血以及随后的多形性室性心动过速的病例。这些事件是通过遥测技术捕捉到的,患者是一名 40 岁出头的男性,被诊断为乙状结肠癌 IIIB 期。值得注意的是,患者之前没有冠状动脉疾病或其他心血管风险因素。确诊后,患者开始服用钙通道阻滞剂维拉帕米,以减轻进一步的冠状动脉血管痉挛事件。经过充分讨论并优先考虑患者的意见和价值观后,皮下植入了植入式心律转复除颤器。出院后,患者重新开始了卡培他滨治疗和维拉帕米预防治疗,根据门诊随访评估,ICD 没有再发生电击。本病例强调了让患者参与决策过程的必要性,尤其是在处理意外和严重并发症时,以确保治疗符合患者的生活质量和个人偏好。
{"title":"Capecitabine-induced-coronary-vasospasm leading to polymorphic ventricular tachycardia and cardiac arrest.","authors":"Maciej Kabat, Roma Padalkar, Sara Hazaveh, Vladimir Joseph, David Feigenblum, Sean Sadikot","doi":"10.1186/s40959-024-00214-4","DOIUrl":"10.1186/s40959-024-00214-4","url":null,"abstract":"<p><p>Capecitabine, a pro-drug of 5-fluorouracil, is commonly used in the treatment of breast and colorectal cancer. Its side effects, including nausea, vomiting, diarrhea, fatigue, loss of appetite, and bone marrow suppression, are well recognized. However, coronary vasospasm represents a less commonly recognized but significant complication of fluoropyrimidine-based therapies such as capecitabine. Proposed mechanisms for this adverse effect complication include direct endothelium-independent vasoconstriction, activation of protein kinase C, and activation of the cyclooxygenase pathway. In this report, we present a case of capecitabine-induced coronary vasospasm leading to progressive, focal ST-elevations, myocardial ischemia, and subsequently polymorphic ventricular tachycardia. These events were captured on telemetry, in a male in his early 40s, diagnosed with stage IIIB sigmoid colon cancer. Notably, the patient had no pre-existing coronary artery disease or other cardiovascular risk factors. Upon diagnosis, the patient was initiated on a calcium channel blocker, verapamil, to mitigate further coronary vasospasm events. After thorough discussions that prioritized the patient's input and values, an implantable cardioverter-defibrillator was placed subcutaneously. Following discharge, the patient restarted capecitabine therapy along with verapamil prophylaxis and did not experience any subsequent shocks from his ICD as assessed during his outpatient follow-up visits. This case emphasizes the need to involve patients in decision-making processes, especially when managing unexpected and serious complications, to ensure treatments align with their quality of life and personal preferences.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10898064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139982445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-23DOI: 10.1186/s40959-024-00208-2
Ahmed Mazen Amin, Yehya Khlidj, Mohamed Abuelazm, Ahmed A Ibrahim, Mohammad Tanashat, Muhammad Imran, Abubakar Nazir, Hosam Shaikhkhalil, Basel Abdelazeem
Background: Cardiotoxicity is one of the most common adverse events of the chemotherapy. Physical exercise was shown to be cardioprotective. We aim to estimate the efficacy and safety of exercise in cancer patients receiving cardiotoxic chemotherapy.
Methods: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs), which were retrieved by systematically searching PubMed, Web of Science, SCOPUS, Cochrane, Clinical Trials.gov, and MedRxiv through July 17th, 2023. We used RevMan V. 5.4 to pool dichotomous data using risk ratio (RR) and continuous data using mean difference (MD), with a 95% confidence interval (CI).
Prospero id: CRD42023460902.
Results: We included thirteen RCTs with a total of 952 patients. Exercise significantly increased VO2 peak (MD: 1.95 with 95% CI [0.59, 3.32], P = 0.005). However, there was no significant effect regarding left ventricular ejection fraction, global longitudinal strain, cardiac output, stroke volume, left ventricular end-diastolic volume, left ventricular end-systolic volume, E/A ratio, resting heart rate, peak heart rate, resting systolic blood pressure, and resting diastolic blood pressure. Also, there was no significant difference regarding any adverse events (AEs) (RR: 4.44 with 95% CI [0.47, 41.56], P = 0.19), AEs leading to withdrawal (RR: 2.87 with 95% CI [0.79, 10.43], P = 0.11), serious AEs (RR: 3.00 with 95% CI [0.14, 65.90], P = 0.49), or all-cause mortality (RR: 0.25 with 95% CI [0.03, 2.22], P = 0.21).
Conclusion: Exercise is associated with increased VO2 peak in cancer patients receiving cardiotoxic chemotherapy. However, there was no significant difference between exercise and usual care regarding the echocardiographic and safety outcomes.
背景:心脏毒性是化疗最常见的不良反应之一:心脏毒性是化疗最常见的不良反应之一。体育锻炼对心脏有保护作用。我们旨在评估运动对接受心脏毒性化疗的癌症患者的有效性和安全性:我们对随机对照试验(RCT)进行了系统综述和荟萃分析,这些试验是通过系统检索 PubMed、Web of Science、SCOPUS、Cochrane、Clinical Trials.gov 和 MedRxiv(截至 2023 年 7 月 17 日)获得的。我们使用 RevMan V. 5.4 使用风险比 (RR) 汇集二分数据,使用平均差 (MD) 汇集连续数据,并得出 95% 的置信区间 (CI):CRD42023460902.Results:结果:我们纳入了 13 项 RCT,共有 952 名患者。运动明显增加了 VO2 峰值(MD:1.95,95% CI [0.59,3.32],P = 0.005)。然而,运动对左心室射血分数、整体纵向应变、心输出量、每搏量、左心室舒张末期容积、左心室收缩末期容积、E/A 比值、静息心率、峰值心率、静息收缩压和静息舒张压均无明显影响。此外,任何不良事件(AEs)(RR:4.44,95% CI [0.47,41.56],P = 0.19)、导致停药的不良事件(AEs)(RR:2.87,95% CI [0.79,10.43],P = 0.19)均无明显差异。79,10.43],P = 0.11)、严重 AE(RR:3.00,95% CI [0.14,65.90],P = 0.49)或全因死亡率(RR:0.25,95% CI [0.03,2.22],P = 0.21):结论:在接受心脏毒性化疗的癌症患者中,运动可增加 VO2 峰值。结论:运动可提高接受心脏毒性化疗的癌症患者的 VO2 峰值,但在超声心动图和安全性结果方面,运动和常规护理没有明显差异。
{"title":"The efficacy and safety of exercise regimens to mitigate chemotherapy cardiotoxicity: a systematic review and meta-analysis of randomized controlled trials.","authors":"Ahmed Mazen Amin, Yehya Khlidj, Mohamed Abuelazm, Ahmed A Ibrahim, Mohammad Tanashat, Muhammad Imran, Abubakar Nazir, Hosam Shaikhkhalil, Basel Abdelazeem","doi":"10.1186/s40959-024-00208-2","DOIUrl":"10.1186/s40959-024-00208-2","url":null,"abstract":"<p><strong>Background: </strong>Cardiotoxicity is one of the most common adverse events of the chemotherapy. Physical exercise was shown to be cardioprotective. We aim to estimate the efficacy and safety of exercise in cancer patients receiving cardiotoxic chemotherapy.</p><p><strong>Methods: </strong>We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs), which were retrieved by systematically searching PubMed, Web of Science, SCOPUS, Cochrane, Clinical Trials.gov, and MedRxiv through July 17th, 2023. We used RevMan V. 5.4 to pool dichotomous data using risk ratio (RR) and continuous data using mean difference (MD), with a 95% confidence interval (CI).</p><p><strong>Prospero id: </strong>CRD42023460902.</p><p><strong>Results: </strong>We included thirteen RCTs with a total of 952 patients. Exercise significantly increased VO<sub>2</sub> peak (MD: 1.95 with 95% CI [0.59, 3.32], P = 0.005). However, there was no significant effect regarding left ventricular ejection fraction, global longitudinal strain, cardiac output, stroke volume, left ventricular end-diastolic volume, left ventricular end-systolic volume, E/A ratio, resting heart rate, peak heart rate, resting systolic blood pressure, and resting diastolic blood pressure. Also, there was no significant difference regarding any adverse events (AEs) (RR: 4.44 with 95% CI [0.47, 41.56], P = 0.19), AEs leading to withdrawal (RR: 2.87 with 95% CI [0.79, 10.43], P = 0.11), serious AEs (RR: 3.00 with 95% CI [0.14, 65.90], P = 0.49), or all-cause mortality (RR: 0.25 with 95% CI [0.03, 2.22], P = 0.21).</p><p><strong>Conclusion: </strong>Exercise is associated with increased VO<sub>2</sub> peak in cancer patients receiving cardiotoxic chemotherapy. However, there was no significant difference between exercise and usual care regarding the echocardiographic and safety outcomes.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10885653/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139939792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-17DOI: 10.1186/s40959-024-00210-8
Bartosz Puła, Jarosław Kępski, Irena Misiewicz-Krzemińska, Sebastian Szmit
The hematopoietic stem cell transplantation (HSCT) procedure is considered a cardiovascular burden. This is due to the potentially cardiotoxic cytostatic agents used before and the risks associated with peri-transplant procedures. We designed a pilot study to determine the clinical utility of the new ST2 marker; furthermore, we routinely assessed cardiac parameters in HSCT recipients. Based on previous cardio-oncology experience in lung and prostate cancer, we can confirm the prognostic and predictive value of classic cardiac biomarkers and modern echocardiography parameters such as global longitudinal strain of the left and right ventricle. After conducting this pilot study we can create a predictive and prognostic model for patients undergoing HSCT. This will greatly enrich our clinical practice, especially in treating older people.
{"title":"Left and right ventricular global longitudinal strain assessment together with biomarker evaluation may have a predictive and prognostic role in patients qualified for hematopoietic stem cell transplantation due to hematopoietic and lymphoid malignancies - a pilot study description.","authors":"Bartosz Puła, Jarosław Kępski, Irena Misiewicz-Krzemińska, Sebastian Szmit","doi":"10.1186/s40959-024-00210-8","DOIUrl":"10.1186/s40959-024-00210-8","url":null,"abstract":"<p><p>The hematopoietic stem cell transplantation (HSCT) procedure is considered a cardiovascular burden. This is due to the potentially cardiotoxic cytostatic agents used before and the risks associated with peri-transplant procedures. We designed a pilot study to determine the clinical utility of the new ST2 marker; furthermore, we routinely assessed cardiac parameters in HSCT recipients. Based on previous cardio-oncology experience in lung and prostate cancer, we can confirm the prognostic and predictive value of classic cardiac biomarkers and modern echocardiography parameters such as global longitudinal strain of the left and right ventricle. After conducting this pilot study we can create a predictive and prognostic model for patients undergoing HSCT. This will greatly enrich our clinical practice, especially in treating older people.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10873966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139897883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-16DOI: 10.1186/s40959-024-00207-3
S Mori, M Bertamino, L Guerisoli, S Stratoti, C Canale, P Spallarossa, I Porto, P Ameri
Background: This article provides an up-to-date overview of pericardial effusion in oncological practice and a guidance on its management. Furthermore, it addresses the question of when malignancy should be suspected in case of newly diagnosed pericardial effusion.
Main body: Cancer-related pericardial effusion is commonly the result of localization of lung and breast cancer, melanoma, or lymphoma to the pericardium via direct invasion, lymphatic dissemination, or hematogenous spread. Several cancer therapies may also cause pericardial effusion, most often during or shortly after administration. Pericardial effusion following radiation therapy may instead develop after years. Other diseases, such as infections, and, rarely, primary tumors of the pericardium complete the spectrum of the possible etiologies of pericardial effusion in oncological patients. The diagnosis of cancer-related pericardial effusion is usually incidental, but cancer accounts for approximately one third of all cardiac tamponades. Drainage, which is mainly attained by pericardiocentesis, is needed when cancer or cancer treatment-related pericardial effusion leads to hemodynamic impairment. Placement of a pericardial catheter for 2-5 days is advised after pericardial fluid removal. In contrast, even a large pericardial effusion should be conservatively managed when the patient is stable, although the best frequency and timing of monitoring by echocardiography in this context are yet to be established. Pericardial effusion secondary to immune checkpoint inhibitors typically responds to corticosteroid therapy. Pericardiocentesis may also be considered to confirm the presence of neoplastic cells in the pericardial fluid, but the yield of cytological examination is low. In case of newly found pericardial effusion in individuals without active cancer and/or recent cancer treatment, a history of malignancy, unremitting or recurrent course, large effusion or presentation with cardiac tamponade, incomplete response to empirical therapy with nonsteroidal anti-inflammatory, and hemorrhagic fluid at pericardiocentesis suggest a neoplastic etiology.
{"title":"Pericardial effusion in oncological patients: current knowledge and principles of management.","authors":"S Mori, M Bertamino, L Guerisoli, S Stratoti, C Canale, P Spallarossa, I Porto, P Ameri","doi":"10.1186/s40959-024-00207-3","DOIUrl":"10.1186/s40959-024-00207-3","url":null,"abstract":"<p><strong>Background: </strong>This article provides an up-to-date overview of pericardial effusion in oncological practice and a guidance on its management. Furthermore, it addresses the question of when malignancy should be suspected in case of newly diagnosed pericardial effusion.</p><p><strong>Main body: </strong>Cancer-related pericardial effusion is commonly the result of localization of lung and breast cancer, melanoma, or lymphoma to the pericardium via direct invasion, lymphatic dissemination, or hematogenous spread. Several cancer therapies may also cause pericardial effusion, most often during or shortly after administration. Pericardial effusion following radiation therapy may instead develop after years. Other diseases, such as infections, and, rarely, primary tumors of the pericardium complete the spectrum of the possible etiologies of pericardial effusion in oncological patients. The diagnosis of cancer-related pericardial effusion is usually incidental, but cancer accounts for approximately one third of all cardiac tamponades. Drainage, which is mainly attained by pericardiocentesis, is needed when cancer or cancer treatment-related pericardial effusion leads to hemodynamic impairment. Placement of a pericardial catheter for 2-5 days is advised after pericardial fluid removal. In contrast, even a large pericardial effusion should be conservatively managed when the patient is stable, although the best frequency and timing of monitoring by echocardiography in this context are yet to be established. Pericardial effusion secondary to immune checkpoint inhibitors typically responds to corticosteroid therapy. Pericardiocentesis may also be considered to confirm the presence of neoplastic cells in the pericardial fluid, but the yield of cytological examination is low. In case of newly found pericardial effusion in individuals without active cancer and/or recent cancer treatment, a history of malignancy, unremitting or recurrent course, large effusion or presentation with cardiac tamponade, incomplete response to empirical therapy with nonsteroidal anti-inflammatory, and hemorrhagic fluid at pericardiocentesis suggest a neoplastic etiology.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10870633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139746198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-09DOI: 10.1186/s40959-024-00206-4
Yvonne Koop, Femke Atsma, Marilot C T Batenburg, Hanneke Meijer, Femke van der Leij, Roxanne Gal, Sanne G M van Velzen, Ivana Išgum, Hester Vermeulen, Angela H E M Maas, Saloua El Messaoudi, Helena M Verkooijen
Background: Thoracic radiotherapy may damage the myocardium and arteries, increasing cardiovascular disease (CVD) risk. Women with a high local breast cancer (BC) recurrence risk may receive an additional radiation boost to the tumor bed.
Objective: We aimed to evaluate the CVD risk and specifically ischemic heart disease (IHD) in BC patients treated with a radiation boost, and investigated whether this was modified by age.
Methods: We identified 5260 BC patients receiving radiotherapy between 2005 and 2016 without a history of CVD. Boost data were derived from hospital records and the national cancer registry. Follow-up data on CVD events were obtained from Statistics Netherlands until December 31, 2018. The relation between CVD and boost was evaluated with competing risk survival analysis.
Results: 1917 (36.4%) received a boost. Mean follow-up was 80.3 months (SD37.1) and the mean age 57.8 years (SD10.7). Interaction between boost and age was observed for IHD: a boost was significantly associated with IHD incidence in patients younger than 40 years but not in patients over 40 years. The subdistribution hazard ratio (sHR) was calculated for ages from 25 to 75 years, showing a sHR range from 5.1 (95%CI 1.2-22.6) for 25-year old patients to sHR 0.5 (95%CI 0.2-1.02) for 75-year old patients.
Conclusion: In patients younger than 40, a radiation boost is significantly associated with an increased risk of CVD. In absolute terms, the increased risk was low. In older patients, there was no association between boost and CVD risk, which is likely a reflection of appropriate patient selection.
{"title":"Competing risk analysis of cardiovascular disease risk in breast cancer patients receiving a radiation boost.","authors":"Yvonne Koop, Femke Atsma, Marilot C T Batenburg, Hanneke Meijer, Femke van der Leij, Roxanne Gal, Sanne G M van Velzen, Ivana Išgum, Hester Vermeulen, Angela H E M Maas, Saloua El Messaoudi, Helena M Verkooijen","doi":"10.1186/s40959-024-00206-4","DOIUrl":"10.1186/s40959-024-00206-4","url":null,"abstract":"<p><strong>Background: </strong>Thoracic radiotherapy may damage the myocardium and arteries, increasing cardiovascular disease (CVD) risk. Women with a high local breast cancer (BC) recurrence risk may receive an additional radiation boost to the tumor bed.</p><p><strong>Objective: </strong>We aimed to evaluate the CVD risk and specifically ischemic heart disease (IHD) in BC patients treated with a radiation boost, and investigated whether this was modified by age.</p><p><strong>Methods: </strong>We identified 5260 BC patients receiving radiotherapy between 2005 and 2016 without a history of CVD. Boost data were derived from hospital records and the national cancer registry. Follow-up data on CVD events were obtained from Statistics Netherlands until December 31, 2018. The relation between CVD and boost was evaluated with competing risk survival analysis.</p><p><strong>Results: </strong>1917 (36.4%) received a boost. Mean follow-up was 80.3 months (SD37.1) and the mean age 57.8 years (SD10.7). Interaction between boost and age was observed for IHD: a boost was significantly associated with IHD incidence in patients younger than 40 years but not in patients over 40 years. The subdistribution hazard ratio (sHR) was calculated for ages from 25 to 75 years, showing a sHR range from 5.1 (95%CI 1.2-22.6) for 25-year old patients to sHR 0.5 (95%CI 0.2-1.02) for 75-year old patients.</p><p><strong>Conclusion: </strong>In patients younger than 40, a radiation boost is significantly associated with an increased risk of CVD. In absolute terms, the increased risk was low. In older patients, there was no association between boost and CVD risk, which is likely a reflection of appropriate patient selection.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10854185/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139711733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-07DOI: 10.1186/s40959-024-00201-9
Arsalan Hamid, Gregg C Fonarow, Javed Butler, Michael E Hall
Background: Different breast cancer pharmacotherapy agents cause different forms of cardiovascular toxicity. We aim to assess if breast cancer pharmacotherapy trials approach cardiovascular safety in a targeted or generalized manner when administering different agents.
Methods: We searched Embase and Medline for phase 2 and 3 breast cancer pharmacotherapy trials. We examined exclusion criterion for cardiovascular conditions and cardiovascular safety assessment through cardiovascular imaging, electrocardiogram, troponin, or natriuretic peptides. Fisher's exact test was utilized to compare reporting.
Results: Fifty breast cancer clinical trials were included in this study. Trials administering microtubule inhibitors were most likely to exclude patients with any CV condition compared with trials administering other agents (93.5% vs. 68.4%; p < 0.05), particularly coronary artery disease (77.4% vs. 36.8%; p < 0.01) but reported performing an electrocardiogram in 13 (41.9%) trials. Trials administering anti-HER 2 agents excluded all patients with at least one CV condition, particularly patients with heart failure (100.0% vs. 62.9%) and were more likely to perform echocardiograms (80.0% vs. 22.9%, p < 0.001) compared with other agents. Other agents excluded participants in a generalized manner and do not frequently perform targeted safety assessments.
Conclusions: Only trials administering microtubule inhibitors or anti-HER 2 therapy exclude patients with cardiovascular disease in a targeted approach. However, anti-HER 2 therapy trials are the only breast cancer clinical trials that perform targeted safety assessments. Breast cancer clinical trials need to develop a targeted approach to cardiovascular safety assessments to permit inclusion of high-risk participants and generate clinical trial data generalizable to patients with cardiovascular disease undergoing cancer therapy.
背景:不同的乳腺癌药物疗法会导致不同形式的心血管毒性。我们旨在评估乳腺癌药物治疗试验在使用不同药物时是有针对性地还是普遍性地处理心血管安全问题:我们检索了 Embase 和 Medline 中的 2 期和 3 期乳腺癌药物治疗试验。我们研究了心血管疾病的排除标准以及通过心血管成像、心电图、肌钙蛋白或利钠肽进行的心血管安全性评估。采用费雪精确检验对报告进行比较:本研究共纳入了 50 项乳腺癌临床试验。与使用其他药物的试验相比,使用微管抑制剂的试验最有可能排除患有任何心血管疾病的患者(93.5% 对 68.4%;P 结论:只有使用微管抑制剂的试验排除了患有心血管疾病的患者:只有使用微管抑制剂或抗 HER 2 疗法的试验以靶向方法排除了心血管疾病患者。然而,抗 HER 2 治疗试验是唯一进行针对性安全性评估的乳腺癌临床试验。乳腺癌临床试验需要开发一种有针对性的心血管安全性评估方法,以便纳入高风险参与者,并生成适用于接受癌症治疗的心血管疾病患者的临床试验数据。
{"title":"How do breast cancer clinical trials approach cardiovascular safety: targeted or generalized?","authors":"Arsalan Hamid, Gregg C Fonarow, Javed Butler, Michael E Hall","doi":"10.1186/s40959-024-00201-9","DOIUrl":"10.1186/s40959-024-00201-9","url":null,"abstract":"<p><strong>Background: </strong>Different breast cancer pharmacotherapy agents cause different forms of cardiovascular toxicity. We aim to assess if breast cancer pharmacotherapy trials approach cardiovascular safety in a targeted or generalized manner when administering different agents.</p><p><strong>Methods: </strong>We searched Embase and Medline for phase 2 and 3 breast cancer pharmacotherapy trials. We examined exclusion criterion for cardiovascular conditions and cardiovascular safety assessment through cardiovascular imaging, electrocardiogram, troponin, or natriuretic peptides. Fisher's exact test was utilized to compare reporting.</p><p><strong>Results: </strong>Fifty breast cancer clinical trials were included in this study. Trials administering microtubule inhibitors were most likely to exclude patients with any CV condition compared with trials administering other agents (93.5% vs. 68.4%; p < 0.05), particularly coronary artery disease (77.4% vs. 36.8%; p < 0.01) but reported performing an electrocardiogram in 13 (41.9%) trials. Trials administering anti-HER 2 agents excluded all patients with at least one CV condition, particularly patients with heart failure (100.0% vs. 62.9%) and were more likely to perform echocardiograms (80.0% vs. 22.9%, p < 0.001) compared with other agents. Other agents excluded participants in a generalized manner and do not frequently perform targeted safety assessments.</p><p><strong>Conclusions: </strong>Only trials administering microtubule inhibitors or anti-HER 2 therapy exclude patients with cardiovascular disease in a targeted approach. However, anti-HER 2 therapy trials are the only breast cancer clinical trials that perform targeted safety assessments. Breast cancer clinical trials need to develop a targeted approach to cardiovascular safety assessments to permit inclusion of high-risk participants and generate clinical trial data generalizable to patients with cardiovascular disease undergoing cancer therapy.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10848621/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139697037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-15DOI: 10.1186/s40959-023-00191-0
Jian Chu, Lillian Tung, Issam Atallah, Changli Wei, Melody Cobleigh, Ruta Rao, Steven B Feinstein, Lydia Usha, Kathrin Banach, Jochen Reiser, Tochukwu M Okwuosa
Background: Soluble urokinase plasminogen activator receptor is an inflammatory biomarker that may prognosticate cardiovascular outcomes. We sought to determine the associations between soluble urokinase plasminogen activator receptor and established markers of cardiotoxicity in breast cancer patients receiving doxorubicin.
Methods: We conducted a prospective cohort study of women with newly diagnosed breast cancer receiving standard-dose doxorubicin (240 mg/m2) at Rush University Medical Center and Rush Oak Park Hospital (Chicago, IL) between January 2017 and May 2019. Left ventricular ejection fraction, global longitudinal strain, and cardiac biomarkers (N-terminal prohormone B-type natriuretic peptide, troponin-I, and high-sensitivity C-reactive protein) were measured at baseline and at intervals up to 12-month follow-up after end of treatment. The associations between soluble urokinase plasminogen activator receptor and these endpoints were evaluated using multivariable mixed effects linear regression.
Results: Our study included 37 women (mean age 47.0 ± 9.3 years, 60% white) with a median baseline soluble urokinase plasminogen activator receptor level of 2.83 ng/dL. No participant developed cardiomyopathy based on serial echocardiography by one-year follow-up. The median percent change in left ventricular strain was -4.3% at 6-month follow-up and absolute changes in cardiac biomarkers were clinically insignificant. There were no significant associations between soluble urokinase plasminogen activator receptor and these markers of cardiotoxicity (all p > 0.05).
Conclusions: In this breast cancer cohort, doxorubicin treatment was associated with a very low risk for cardiotoxicity. Across this narrow range of clinical endpoints, soluble urokinase plasminogen activator receptor was not associated with markers of subclinical cardiotoxicity. Further studies are needed to clarify the prognostic utility of soluble urokinase plasminogen activator receptor in doxorubicin-associated cardiomyopathy and should include a larger cohort of leukemia and lymphoma patients who receive higher doses of doxorubicin.
{"title":"Soluble urokinase plasminogen activator receptor and cardiotoxicity in doxorubicin-treated breast cancer patients: a prospective exploratory study.","authors":"Jian Chu, Lillian Tung, Issam Atallah, Changli Wei, Melody Cobleigh, Ruta Rao, Steven B Feinstein, Lydia Usha, Kathrin Banach, Jochen Reiser, Tochukwu M Okwuosa","doi":"10.1186/s40959-023-00191-0","DOIUrl":"10.1186/s40959-023-00191-0","url":null,"abstract":"<p><strong>Background: </strong>Soluble urokinase plasminogen activator receptor is an inflammatory biomarker that may prognosticate cardiovascular outcomes. We sought to determine the associations between soluble urokinase plasminogen activator receptor and established markers of cardiotoxicity in breast cancer patients receiving doxorubicin.</p><p><strong>Methods: </strong>We conducted a prospective cohort study of women with newly diagnosed breast cancer receiving standard-dose doxorubicin (240 mg/m<sup>2</sup>) at Rush University Medical Center and Rush Oak Park Hospital (Chicago, IL) between January 2017 and May 2019. Left ventricular ejection fraction, global longitudinal strain, and cardiac biomarkers (N-terminal prohormone B-type natriuretic peptide, troponin-I, and high-sensitivity C-reactive protein) were measured at baseline and at intervals up to 12-month follow-up after end of treatment. The associations between soluble urokinase plasminogen activator receptor and these endpoints were evaluated using multivariable mixed effects linear regression.</p><p><strong>Results: </strong>Our study included 37 women (mean age 47.0 ± 9.3 years, 60% white) with a median baseline soluble urokinase plasminogen activator receptor level of 2.83 ng/dL. No participant developed cardiomyopathy based on serial echocardiography by one-year follow-up. The median percent change in left ventricular strain was -4.3% at 6-month follow-up and absolute changes in cardiac biomarkers were clinically insignificant. There were no significant associations between soluble urokinase plasminogen activator receptor and these markers of cardiotoxicity (all p > 0.05).</p><p><strong>Conclusions: </strong>In this breast cancer cohort, doxorubicin treatment was associated with a very low risk for cardiotoxicity. Across this narrow range of clinical endpoints, soluble urokinase plasminogen activator receptor was not associated with markers of subclinical cardiotoxicity. Further studies are needed to clarify the prognostic utility of soluble urokinase plasminogen activator receptor in doxorubicin-associated cardiomyopathy and should include a larger cohort of leukemia and lymphoma patients who receive higher doses of doxorubicin.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10788987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139471909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}