Pub Date : 2023-04-05DOI: 10.1186/s40959-023-00171-4
Sarju Ganatra, Sonu Abraham, Ashish Kumar, Rohan Parikh, Rushin Patel, Sumanth Khadke, Amudha Kumar, Victor Liu, Andrea Nathalie Rosas Diaz, Tomas G Neilan, David Martin, Bruce Hook, Sourbha S Dani, Aarti Asnani, Anju Nohria
Background: Though the incidence of atrial fibrillation (AF) is increased in patients with cancer, the effectiveness of catheter ablation (CA) for AF in patients with cancer is not well studied.
Methods: We conducted a retrospective cohort study of patients who underwent CA for AF. Patients with a history of cancer within 5-years prior to, or those with an exposure to anthracyclines and/or thoracic radiation at any time prior to the index ablation were compared to patients without a history of cancer who underwent AF ablation. The primary outcome was freedom from AF [with or without anti-arrhythmic drugs (AADs), or need for repeat CA at 12-months post-ablation]. Secondary endpoints included freedom from AF at 12 months post-ablation with AADs and without AADs. Safety endpoints included bleeding, pulmonary vein stenosis, stroke, and cardiac tamponade. Multivariable regression analysis was performed to identify independent risk predictors of the primary outcome.
Results: Among 502 patients included in the study, 251 (50%) had a history of cancer. Freedom from AF at 12 months did not differ between patients with and without cancer (83.3% vs 72.5%, p 0.28). The need for repeat ablation was also similar between groups (20.7% vs 27.5%, p 0.29). Multivariable regression analysis did not identify a history of cancer or cancer-related therapy as independent predictors of recurrent AF after ablation. There was no difference in safety endpoints between groups.
Conclusion: CA is a safe and effective treatment for AF in patients with a history of cancer and those with exposure to potentially cardiotoxic therapy.
背景:虽然癌症患者心房颤动(AF)的发病率增加,但对癌症患者心房颤动导管消融术(CA)的疗效却没有很好的研究:我们对接受房颤导管消融术的患者进行了一项回顾性队列研究。我们将消融术前 5 年内有癌症病史或在消融术前任何时候接触过蒽环类药物和/或胸部放射线的患者与接受房颤消融术的无癌症病史患者进行了比较。主要结果是[使用或不使用抗心律失常药物 (AAD),或消融术后 12 个月时需要重复 CA]摆脱房颤。次要终点包括使用或不使用抗心律失常药物(AADs)消融术后 12 个月无房颤。安全性终点包括出血、肺静脉狭窄、中风和心脏填塞。研究人员进行了多变量回归分析,以确定主要结果的独立风险预测因素:在 502 名参与研究的患者中,251 人(50%)有癌症病史。有癌症和没有癌症的患者在12个月内免房颤的比例没有差异(83.3% vs 72.5%,P 0.28)。两组患者需要重复消融的比例也相似(20.7% vs 27.5%,P 0.29)。多变量回归分析并未发现癌症病史或癌症相关治疗是消融术后房颤复发的独立预测因素。各组间的安全性终点无差异:CA是一种安全有效的房颤治疗方法,适用于有癌症史和接受过潜在心脏毒性治疗的患者。
{"title":"Efficacy and safety of catheter ablation for atrial fibrillation in patients with history of cancer.","authors":"Sarju Ganatra, Sonu Abraham, Ashish Kumar, Rohan Parikh, Rushin Patel, Sumanth Khadke, Amudha Kumar, Victor Liu, Andrea Nathalie Rosas Diaz, Tomas G Neilan, David Martin, Bruce Hook, Sourbha S Dani, Aarti Asnani, Anju Nohria","doi":"10.1186/s40959-023-00171-4","DOIUrl":"10.1186/s40959-023-00171-4","url":null,"abstract":"<p><strong>Background: </strong>Though the incidence of atrial fibrillation (AF) is increased in patients with cancer, the effectiveness of catheter ablation (CA) for AF in patients with cancer is not well studied.</p><p><strong>Methods: </strong>We conducted a retrospective cohort study of patients who underwent CA for AF. Patients with a history of cancer within 5-years prior to, or those with an exposure to anthracyclines and/or thoracic radiation at any time prior to the index ablation were compared to patients without a history of cancer who underwent AF ablation. The primary outcome was freedom from AF [with or without anti-arrhythmic drugs (AADs), or need for repeat CA at 12-months post-ablation]. Secondary endpoints included freedom from AF at 12 months post-ablation with AADs and without AADs. Safety endpoints included bleeding, pulmonary vein stenosis, stroke, and cardiac tamponade. Multivariable regression analysis was performed to identify independent risk predictors of the primary outcome.</p><p><strong>Results: </strong>Among 502 patients included in the study, 251 (50%) had a history of cancer. Freedom from AF at 12 months did not differ between patients with and without cancer (83.3% vs 72.5%, p 0.28). The need for repeat ablation was also similar between groups (20.7% vs 27.5%, p 0.29). Multivariable regression analysis did not identify a history of cancer or cancer-related therapy as independent predictors of recurrent AF after ablation. There was no difference in safety endpoints between groups.</p><p><strong>Conclusion: </strong>CA is a safe and effective treatment for AF in patients with a history of cancer and those with exposure to potentially cardiotoxic therapy.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2023-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10074889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9639587","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 : 2023-04-01DOI: 10.1186/s40959-023-00170-5
Dae Hyun Lee, Sanjay Chandrasekhar, Michael D Jain, Rahul Mhaskar, Kayla Reid, Sae Bom Lee, Salvatore Corallo, Melanie J Hidalgo-Vargas, Abhishek Kumar, Julio Chavez, Bijal Shah, Aleksandr Lazaryan, Farhad Khimani, Taiga Nishihori, Christina Bachmeier, Rawan Faramand, Michael G Fradley, Daniel Jeong, Guilherme H Oliveira, Frederick L Locke, Marco L Davila, Mohammed Alomar
Background: Chimeric antigen receptor T- Cell (CAR-T) immunotherapy has been a breakthrough treatment for various hematological malignancies. However, cardiotoxicities such as new-onset heart failure, arrhythmia, acute coronary syndrome and cardiovascular death occur in 10-15% of patients treated with CAR-T. This study aims to investigate the changes in cardiac and inflammatory biomarkers in CAR-T therapy to determine the role of pro-inflammatory cytokines.
Methods: In this observational study, ninety consecutive patients treated with CAR-T underwent baseline cardiac investigation with electrocardiogram (ECG), transthoracic echocardiogram (TTE), troponin-I, and B-type natriuretic peptide (BNP). Follow-up ECG, troponin-I and BNP were obtained five days post- CAR-T. In a subset of patients (N = 53), serum inflammatory cytokines interleukin (IL)-2, IL-6, IL-15, interferon (IFN)-γ, tumor necrosis factor (TNF)-α, granulocyte-macrophage colony-stimulating factor (GM-CSF), and angiopoietin 1 & 2 were tested serially, including baseline and daily during hospitalization. Adverse cardiac events were defined as new-onset cardiomyopathy/heart failure, acute coronary syndrome, arrhythmia and cardiovascular death.
Results: Eleven patients (12%) had adverse cardiac events (one with new-onset cardiomyopathy and ten with new-onset atrial fibrillation). Adverse cardiac events appear to have occurred among patients with advanced age (77 vs. 66 years; p = 0.002), higher baseline creatinine (0.9 vs. 0.7 mg/dL; 0.007) and higher left atrial volume index (23.9 vs. 16.9mL/m2; p = 0.042). Day 5 BNP levels (125 vs. 63pg/mL; p = 0.019), but not troponin-I, were higher in patients with adverse cardiac events, compared to those without. The maximum levels of IL-6 (3855.0 vs. 254.0 pg/mL; p = 0.021), IFN-γ (474.0 vs. 48.8pg/mL; p = 0.006) and IL-15 (70.2 vs. 39.2pg/mL; p = 0.026) were also higher in the adverse cardiac events group. However, cardiac and inflammatory biomarker levels were not associated with cardiac events. Patients who developed cardiac events did not exhibit worse survival compared to patients without cardiac events (Log-rank p = 0.200).
Conclusion: Adverse cardiac events, predominantly atrial fibrillation, occur commonly after CAR-T (12%). The changes in serial inflammatory cytokine after CAR-T in the setting of adverse cardiac events suggests pro-inflammation as a pathophysiology and require further investigation for their role in adverse cardiac events.
Tweet brief handle: CAR-T related Cardiotoxicity has elevated cardiac and inflammatory biomarkers. #CARTCell #CardioOnc #CardioImmunology.
背景:嵌合抗原受体T细胞(CAR-T)免疫疗法已成为治疗多种血液系统恶性肿瘤的突破性疗法。然而,10-15%接受CAR-T治疗的患者会出现心脏毒性,如新发心力衰竭、心律失常、急性冠状动脉综合征和心血管死亡。本研究旨在研究CAR-T治疗中心脏和炎症生物标志物的变化,以确定促炎细胞因子的作用。方法:在这项观察性研究中,90例连续接受CAR-T治疗的患者接受了基线心脏检查,包括心电图(ECG)、经胸超声心动图(TTE)、肌钙蛋白- i和b型利钠肽(BNP)。CAR-T术后5天随访心电图、肌钙蛋白i和BNP。在一部分患者(N = 53)中,连续检测血清炎症因子白介素(IL)-2、IL-6、IL-15、干扰素(IFN)-γ、肿瘤坏死因子(TNF)-α、粒细胞-巨噬细胞集落刺激因子(GM-CSF)和血管生成素1和2,包括基线和住院期间的日常检测。不良心脏事件定义为新发心肌病/心力衰竭、急性冠状动脉综合征、心律失常和心血管性死亡。结果:11例(12%)患者发生心脏不良事件(1例新发心肌病,10例新发心房颤动)。不良心脏事件似乎发生在高龄患者中(77岁vs 66岁;p = 0.002),基线肌酐较高(0.9 vs. 0.7 mg/dL;0.007)和较高的左房容积指数(23.9 vs. 16.9mL/m2;p = 0.042)。第5天BNP水平(125 vs. 63pg/mL;p = 0.019),但与没有心脏不良事件的患者相比,肌钙蛋白- i在有心脏不良事件的患者中较高。IL-6最高水平(3855.0 vs. 254.0 pg/mL;p = 0.021), IFN-γ (474.0 vs. 48.8pg/mL;p = 0.006)和IL-15 (70.2 vs. 39.2pg/mL;P = 0.026),心脏不良事件组的发生率也更高。然而,心脏和炎症生物标志物水平与心脏事件无关。发生心脏事件的患者与没有心脏事件的患者相比,生存率并不差(Log-rank p = 0.200)。结论:CAR-T术后常见心脏不良事件,主要是房颤(12%)。CAR-T后一系列炎症细胞因子在心脏不良事件中的变化表明促炎症是一种病理生理学,需要进一步研究其在心脏不良事件中的作用。微博简介:CAR-T相关的心脏毒性升高了心脏和炎症生物标志物。#CARTCell #CardioOnc #CardioImmunology
{"title":"Cardiac and inflammatory biomarker differences in adverse cardiac events after chimeric antigen receptor T-Cell therapy: an exploratory study.","authors":"Dae Hyun Lee, Sanjay Chandrasekhar, Michael D Jain, Rahul Mhaskar, Kayla Reid, Sae Bom Lee, Salvatore Corallo, Melanie J Hidalgo-Vargas, Abhishek Kumar, Julio Chavez, Bijal Shah, Aleksandr Lazaryan, Farhad Khimani, Taiga Nishihori, Christina Bachmeier, Rawan Faramand, Michael G Fradley, Daniel Jeong, Guilherme H Oliveira, Frederick L Locke, Marco L Davila, Mohammed Alomar","doi":"10.1186/s40959-023-00170-5","DOIUrl":"https://doi.org/10.1186/s40959-023-00170-5","url":null,"abstract":"<p><strong>Background: </strong>Chimeric antigen receptor T- Cell (CAR-T) immunotherapy has been a breakthrough treatment for various hematological malignancies. However, cardiotoxicities such as new-onset heart failure, arrhythmia, acute coronary syndrome and cardiovascular death occur in 10-15% of patients treated with CAR-T. This study aims to investigate the changes in cardiac and inflammatory biomarkers in CAR-T therapy to determine the role of pro-inflammatory cytokines.</p><p><strong>Methods: </strong>In this observational study, ninety consecutive patients treated with CAR-T underwent baseline cardiac investigation with electrocardiogram (ECG), transthoracic echocardiogram (TTE), troponin-I, and B-type natriuretic peptide (BNP). Follow-up ECG, troponin-I and BNP were obtained five days post- CAR-T. In a subset of patients (N = 53), serum inflammatory cytokines interleukin (IL)-2, IL-6, IL-15, interferon (IFN)-γ, tumor necrosis factor (TNF)-α, granulocyte-macrophage colony-stimulating factor (GM-CSF), and angiopoietin 1 & 2 were tested serially, including baseline and daily during hospitalization. Adverse cardiac events were defined as new-onset cardiomyopathy/heart failure, acute coronary syndrome, arrhythmia and cardiovascular death.</p><p><strong>Results: </strong>Eleven patients (12%) had adverse cardiac events (one with new-onset cardiomyopathy and ten with new-onset atrial fibrillation). Adverse cardiac events appear to have occurred among patients with advanced age (77 vs. 66 years; p = 0.002), higher baseline creatinine (0.9 vs. 0.7 mg/dL; 0.007) and higher left atrial volume index (23.9 vs. 16.9mL/m<sup>2</sup>; p = 0.042). Day 5 BNP levels (125 vs. 63pg/mL; p = 0.019), but not troponin-I, were higher in patients with adverse cardiac events, compared to those without. The maximum levels of IL-6 (3855.0 vs. 254.0 pg/mL; p = 0.021), IFN-γ (474.0 vs. 48.8pg/mL; p = 0.006) and IL-15 (70.2 vs. 39.2pg/mL; p = 0.026) were also higher in the adverse cardiac events group. However, cardiac and inflammatory biomarker levels were not associated with cardiac events. Patients who developed cardiac events did not exhibit worse survival compared to patients without cardiac events (Log-rank p = 0.200).</p><p><strong>Conclusion: </strong>Adverse cardiac events, predominantly atrial fibrillation, occur commonly after CAR-T (12%). The changes in serial inflammatory cytokine after CAR-T in the setting of adverse cardiac events suggests pro-inflammation as a pathophysiology and require further investigation for their role in adverse cardiac events.</p><p><strong>Tweet brief handle: </strong>CAR-T related Cardiotoxicity has elevated cardiac and inflammatory biomarkers. #CARTCell #CardioOnc #CardioImmunology.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10067156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9253162","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 : 2023-03-27DOI: 10.1186/s40959-023-00161-6
Mônica M C Becker, Gustavo F A Arruda, Diego R F Berenguer, Roberto O Buril, Daniela Cardinale, Simone C S Brandão
Despite advances in chemotherapy, the drugs used in cancer treatment remain rather harmful to the cardiovascular system, causing structural and functional cardiotoxic changes. Positron-emission tomography associated with computed tomography (PET/CT) has emerged like a promising technique in the early diagnosis of these adverse drug effects as the myocardial tissue uptake of fluorodeoxyglucose labeled with fluorine-18 (18F-FDG), a glucose analog, is increased after their use. Among these drugs, anthracyclines are the most frequently associated with cardiotoxicity because they promote heart damage through DNA breaks, and induction of an oxidative, proinflammatory, and toxic environment. This review aimed to present the scientific evidence available so far regarding the use of 18F-FDG PET/CT as an early biomarker of anthracycline-related cardiotoxicity. Thus, it discusses the physiological basis for its uptake, hypotheses to justify its increase in the myocardium affected by anthracyclines, importance of 18F-FDG PET/CT findings for cardio-oncology, and primary challenges of incorporating this technique in standard clinical oncology practice.
{"title":"Anthracycline cardiotoxicity: current methods of diagnosis and possible role of <sup>18</sup>F-FDG PET/CT as a new biomarker.","authors":"Mônica M C Becker, Gustavo F A Arruda, Diego R F Berenguer, Roberto O Buril, Daniela Cardinale, Simone C S Brandão","doi":"10.1186/s40959-023-00161-6","DOIUrl":"https://doi.org/10.1186/s40959-023-00161-6","url":null,"abstract":"<p><p>Despite advances in chemotherapy, the drugs used in cancer treatment remain rather harmful to the cardiovascular system, causing structural and functional cardiotoxic changes. Positron-emission tomography associated with computed tomography (PET/CT) has emerged like a promising technique in the early diagnosis of these adverse drug effects as the myocardial tissue uptake of fluorodeoxyglucose labeled with fluorine-18 (<sup>18</sup>F-FDG), a glucose analog, is increased after their use. Among these drugs, anthracyclines are the most frequently associated with cardiotoxicity because they promote heart damage through DNA breaks, and induction of an oxidative, proinflammatory, and toxic environment. This review aimed to present the scientific evidence available so far regarding the use of <sup>18</sup>F-FDG PET/CT as an early biomarker of anthracycline-related cardiotoxicity. Thus, it discusses the physiological basis for its uptake, hypotheses to justify its increase in the myocardium affected by anthracyclines, importance of <sup>18</sup>F-FDG PET/CT findings for cardio-oncology, and primary challenges of incorporating this technique in standard clinical oncology practice.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2023-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10041777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9199948","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 : 2023-03-27DOI: 10.1186/s40959-023-00167-0
Yan Liu
Background: Despite the rapid growth of cardio-oncology as a subspecialty, cancer patients are still underserved from a cardiovascular perspective. A new care model is needed to integrate comprehensive cardio-oncology care with community-based facilities to improve care access, quality, and equity. Here, we present a cardio-oncology service line model for large, multi-hospital health systems to address this need.
Methods: An academic cardio-oncology program was first established using a multidisciplinary approach. Five infrastructure elements for a service line model were created, including strategic accountability, standardized care, dedicated resources, patient experience/education, and branding/identity. We then utilized these elements across our healthcare system to establish a quality-controlled and centrally governed cardio-oncology service line structure. Protocols were created to standardize care and ensure consistency and quality, including referral workflow, imaging, cardiotoxicity surveillance, and clinical management. An IRB-approved cardio-oncology registry was established for outcome tracking.
Results: The standardized cardio-oncology services were expanded to eight hospitals and ten outpatient care centers, including rural outreach offices, resulting in increased patient access and improved clinical quality measures. The service area expanded 17-fold, and an estimated rural population of 204,133 gained access to care. Cardio-oncology office visits increased by approximately 600% three years after implementation of the service line model.
Conclusions: A cardio-oncology service line with standardized care is a feasible and effective care model to improve cardio-oncology care quality, patient access, and health equity in large, multi-hospital health systems. It can be used in conjunction with academic cardio-oncology programs to improve the overall cardio-oncology healthcare efficacy in the US.
{"title":"A novel cardio-oncology service line model in optimizing care access, quality and equity for large, multi-hospital health systems.","authors":"Yan Liu","doi":"10.1186/s40959-023-00167-0","DOIUrl":"https://doi.org/10.1186/s40959-023-00167-0","url":null,"abstract":"<p><strong>Background: </strong>Despite the rapid growth of cardio-oncology as a subspecialty, cancer patients are still underserved from a cardiovascular perspective. A new care model is needed to integrate comprehensive cardio-oncology care with community-based facilities to improve care access, quality, and equity. Here, we present a cardio-oncology service line model for large, multi-hospital health systems to address this need.</p><p><strong>Methods: </strong>An academic cardio-oncology program was first established using a multidisciplinary approach. Five infrastructure elements for a service line model were created, including strategic accountability, standardized care, dedicated resources, patient experience/education, and branding/identity. We then utilized these elements across our healthcare system to establish a quality-controlled and centrally governed cardio-oncology service line structure. Protocols were created to standardize care and ensure consistency and quality, including referral workflow, imaging, cardiotoxicity surveillance, and clinical management. An IRB-approved cardio-oncology registry was established for outcome tracking.</p><p><strong>Results: </strong>The standardized cardio-oncology services were expanded to eight hospitals and ten outpatient care centers, including rural outreach offices, resulting in increased patient access and improved clinical quality measures. The service area expanded 17-fold, and an estimated rural population of 204,133 gained access to care. Cardio-oncology office visits increased by approximately 600% three years after implementation of the service line model.</p><p><strong>Conclusions: </strong>A cardio-oncology service line with standardized care is a feasible and effective care model to improve cardio-oncology care quality, patient access, and health equity in large, multi-hospital health systems. It can be used in conjunction with academic cardio-oncology programs to improve the overall cardio-oncology healthcare efficacy in the US.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2023-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10041762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9252746","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 : 2023-03-20DOI: 10.1186/s40959-023-00165-2
Khan O Mohammad, Hanna Fanous, Sneha Vakamudi, Yan Liu
Background: Immune checkpoint inhibitors (ICIs) are currently widely used for treatment of various types of cancers. ICI-induced myocarditis, though uncommon, accounts for high risk of major adverse cardiac events and mortality, which makes appropriate diagnosis important. We here present a unique, challenging case of ICI-induced, refractory and isolated right ventricular (RV) myocarditis.
Case presentation: A 32-year-old female with breast cancer presented with newly onset chest pain and dyspnea shortly after initiation of Pembrolizumab. Coronary angiography showed normal coronary arteries and a cardiac magnetic resonance (CMR) revealed myocarditis involving the right ventricle with chamber dilation and severe dysfunction. ICI therapy was stopped, and high dose steroid therapy was initiated and symptoms resolved. However, three months after initial presentation, the patient was hospitalized for DKA and decompensated right heart failure, and a repeat cardiac MRI at that time showed recurrent, isolated right ventricular myocardial inflammation/edema without LV involvement. High dose steroid therapy was started again and at 6-month follow up, surveillance CMR continued to show persistent right-sided myocarditis, patient was eventually treated with Abatacept with resolution of HF symptoms, RV dysfunction and biomarkers at 10-month follow up.
Conclusions: We describe a unique case of isolated ICI-induced right ventricular myocarditis leading to right ventricular failure, that was refractory despite ICI therapy cessation and immune suppression by repeated high dose steroids. Co-stimulatory pathway modulation with Abatacept eventually lead to the normalization of RV function and dilation ten months after initial myocarditis onset.
{"title":"Refractory right ventricular myocarditis induced by immune checkpoint inhibitor despite therapy cessation and immune suppression.","authors":"Khan O Mohammad, Hanna Fanous, Sneha Vakamudi, Yan Liu","doi":"10.1186/s40959-023-00165-2","DOIUrl":"https://doi.org/10.1186/s40959-023-00165-2","url":null,"abstract":"<p><strong>Background: </strong>Immune checkpoint inhibitors (ICIs) are currently widely used for treatment of various types of cancers. ICI-induced myocarditis, though uncommon, accounts for high risk of major adverse cardiac events and mortality, which makes appropriate diagnosis important. We here present a unique, challenging case of ICI-induced, refractory and isolated right ventricular (RV) myocarditis.</p><p><strong>Case presentation: </strong>A 32-year-old female with breast cancer presented with newly onset chest pain and dyspnea shortly after initiation of Pembrolizumab. Coronary angiography showed normal coronary arteries and a cardiac magnetic resonance (CMR) revealed myocarditis involving the right ventricle with chamber dilation and severe dysfunction. ICI therapy was stopped, and high dose steroid therapy was initiated and symptoms resolved. However, three months after initial presentation, the patient was hospitalized for DKA and decompensated right heart failure, and a repeat cardiac MRI at that time showed recurrent, isolated right ventricular myocardial inflammation/edema without LV involvement. High dose steroid therapy was started again and at 6-month follow up, surveillance CMR continued to show persistent right-sided myocarditis, patient was eventually treated with Abatacept with resolution of HF symptoms, RV dysfunction and biomarkers at 10-month follow up.</p><p><strong>Conclusions: </strong>We describe a unique case of isolated ICI-induced right ventricular myocarditis leading to right ventricular failure, that was refractory despite ICI therapy cessation and immune suppression by repeated high dose steroids. Co-stimulatory pathway modulation with Abatacept eventually lead to the normalization of RV function and dilation ten months after initial myocarditis onset.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2023-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10026228/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9529512","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 : 2023-03-13DOI: 10.1186/s40959-023-00166-1
Jesus Jimenez, Nicolas Kostelecky, Joshua D Mitchell, Kathleen W Zhang, Chieh-Yu Lin, Daniel J Lenihan, Kory J Lavine
Background: Immune checkpoint inhibitor (ICI) myocarditis is associated with high morbidity and mortality. While endomyocardial biopsy (EMB) is considered a gold standard for diagnosis, the sensitivity of EMB is not well defined. Additionally, the pathological features that correlate with the clinical diagnosis of ICI-associated myocarditis remain incompletely understood.
Methods: We retrospectively identified and reviewed the clinicopathological features of 26 patients with suspected ICI-associated myocarditis based on institutional major and minor criteria. Seventeen of these patients underwent EMB, and the histopathological features were assessed by routine hematoxylin and eosin (H&E) staining and immunohistochemical (IHC) staining for CD68, a macrophage marker.
Results: Only 2/17 EMBs obtained from patients with suspected ICI myocarditis satisfied the Dallas criteria. Supplemental IHC staining and quantification of CD68+ macrophages identified an additional 7 patients with pathological features of myocardial inflammation (> 50 CD68+ cells/HPF). Macrophage abundance positively correlated with serum Troponin I (P = 0.010) and NT-proBNP (N-terminal pro-brain natriuretic peptide, P = 0.047) concentration. Inclusion of CD68 IHC could have potentially changed the certainty of the diagnosis of ICI-associated myocarditis to definite in 6/17 cases.
Conclusions: While the Dallas criteria can identify a subset of ICI-associated myocarditis patients, quantification of macrophage abundance may expand the diagnostic role of EMB. Failure to meet the traditional Dallas Criteria should not exclude the diagnosis of myocarditis.
{"title":"Clinicopathological classification of immune checkpoint inhibitor-associated myocarditis: possible refinement by measuring macrophage abundance.","authors":"Jesus Jimenez, Nicolas Kostelecky, Joshua D Mitchell, Kathleen W Zhang, Chieh-Yu Lin, Daniel J Lenihan, Kory J Lavine","doi":"10.1186/s40959-023-00166-1","DOIUrl":"https://doi.org/10.1186/s40959-023-00166-1","url":null,"abstract":"<p><strong>Background: </strong>Immune checkpoint inhibitor (ICI) myocarditis is associated with high morbidity and mortality. While endomyocardial biopsy (EMB) is considered a gold standard for diagnosis, the sensitivity of EMB is not well defined. Additionally, the pathological features that correlate with the clinical diagnosis of ICI-associated myocarditis remain incompletely understood.</p><p><strong>Methods: </strong>We retrospectively identified and reviewed the clinicopathological features of 26 patients with suspected ICI-associated myocarditis based on institutional major and minor criteria. Seventeen of these patients underwent EMB, and the histopathological features were assessed by routine hematoxylin and eosin (H&E) staining and immunohistochemical (IHC) staining for CD68, a macrophage marker.</p><p><strong>Results: </strong>Only 2/17 EMBs obtained from patients with suspected ICI myocarditis satisfied the Dallas criteria. Supplemental IHC staining and quantification of CD68<sup>+</sup> macrophages identified an additional 7 patients with pathological features of myocardial inflammation (> 50 CD68<sup>+</sup> cells/HPF). Macrophage abundance positively correlated with serum Troponin I (P = 0.010) and NT-proBNP (N-terminal pro-brain natriuretic peptide, P = 0.047) concentration. Inclusion of CD68 IHC could have potentially changed the certainty of the diagnosis of ICI-associated myocarditis to definite in 6/17 cases.</p><p><strong>Conclusions: </strong>While the Dallas criteria can identify a subset of ICI-associated myocarditis patients, quantification of macrophage abundance may expand the diagnostic role of EMB. Failure to meet the traditional Dallas Criteria should not exclude the diagnosis of myocarditis.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2023-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10009938/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9287905","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 : 2023-03-09DOI: 10.1186/s40959-023-00163-4
Anthony F Yu, Chau T Dang, Justine Jorgensen, Chaya S Moskowitz, Patricia DeFusco, Eric Oligino, Kevin C Oeffinger, Jennifer E Liu, Richard M Steingart
Background: Echocardiograms are recommended every 3 months in patients receiving human epidermal growth factor 2 (HER2)-targeted therapy for surveillance of left ventricular ejection fraction (LVEF). Efforts to tailor treatment for HER2-positive breast cancer have led to greater use of non-anthracycline regimens that are associated with lower cardiotoxicity risk, raising into question the need for frequent cardiotoxicity surveillance for these patients. This study seeks to evaluate whether less frequent cardiotoxicity surveillance (every 6 months) is safe for patients receiving a non-anthracycline HER2-targeted treatment regimen.
Methods/design: We will enroll 190 women with histologically confirmed HER2-positive breast cancer scheduled to receive a non-anthracycline HER2-targeted treatment regimen for a minimum of 12 months. All participants will undergo echocardiograms before and 6-, 12-, and 18-months after initiation of HER2-targeted treatment. The primary composite outcome is symptomatic heart failure (New York Heart Association class III or IV) or death from cardiovascular causes. Secondary outcomes include: 1) echocardiographic indices of left ventricular systolic function; 2) incidence of cardiotoxicity, defined by a ≥ 10% absolute reduction in left ventricular ejection fraction (LVEF) from baseline to < 53%; and 3) incidence of early interruption of HER2-targeted therapy.
Conclusions: To our knowledge, this will be the first prospective study of a risk-based approach to cardiotoxicity surveillance. We expect findings from this study will inform the development of updated clinical practice guidelines to improve cardiotoxicity surveillance practices during HER2-positive breast cancer treatment.
Trial registration: The trial was registered in the ClinicalTrials.gov registry (identifier NCT03983382) on June 12, 2019.
{"title":"Rationale and design of a cardiac safety study for reduced cardiotoxicity surveillance during HER2-targeted therapy.","authors":"Anthony F Yu, Chau T Dang, Justine Jorgensen, Chaya S Moskowitz, Patricia DeFusco, Eric Oligino, Kevin C Oeffinger, Jennifer E Liu, Richard M Steingart","doi":"10.1186/s40959-023-00163-4","DOIUrl":"https://doi.org/10.1186/s40959-023-00163-4","url":null,"abstract":"<p><strong>Background: </strong>Echocardiograms are recommended every 3 months in patients receiving human epidermal growth factor 2 (HER2)-targeted therapy for surveillance of left ventricular ejection fraction (LVEF). Efforts to tailor treatment for HER2-positive breast cancer have led to greater use of non-anthracycline regimens that are associated with lower cardiotoxicity risk, raising into question the need for frequent cardiotoxicity surveillance for these patients. This study seeks to evaluate whether less frequent cardiotoxicity surveillance (every 6 months) is safe for patients receiving a non-anthracycline HER2-targeted treatment regimen.</p><p><strong>Methods/design: </strong>We will enroll 190 women with histologically confirmed HER2-positive breast cancer scheduled to receive a non-anthracycline HER2-targeted treatment regimen for a minimum of 12 months. All participants will undergo echocardiograms before and 6-, 12-, and 18-months after initiation of HER2-targeted treatment. The primary composite outcome is symptomatic heart failure (New York Heart Association class III or IV) or death from cardiovascular causes. Secondary outcomes include: 1) echocardiographic indices of left ventricular systolic function; 2) incidence of cardiotoxicity, defined by a ≥ 10% absolute reduction in left ventricular ejection fraction (LVEF) from baseline to < 53%; and 3) incidence of early interruption of HER2-targeted therapy.</p><p><strong>Conclusions: </strong>To our knowledge, this will be the first prospective study of a risk-based approach to cardiotoxicity surveillance. We expect findings from this study will inform the development of updated clinical practice guidelines to improve cardiotoxicity surveillance practices during HER2-positive breast cancer treatment.</p><p><strong>Trial registration: </strong>The trial was registered in the ClinicalTrials.gov registry (identifier NCT03983382) on June 12, 2019.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2023-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9996968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9390866","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}
Background: This study aimed to evaluate the association between preoperative hs-cTnI and long-term mortality and major adverse cardiovascular events (MACE) in colorectal cancer patients.
Methods: This single-center retrospective cohort study included 1105 consecutive colorectal cancer patients who received tumor resection surgery between January 2018 and June 2020. Inclusion criteria were an age ≥ 18 years and had been tested for hs-cTnI on admission within 7 days prior to tumor resection surgery. Exclusion criteria were emergent surgery, failure to received tumor resection surgery, hospital death, there was clinical evidence of unstable coronary artery disease or pulmonary embolism occurred before operation according to medical record. The primary endpoint was all-cause death. Secondary endpoint was major adverse cardiovascular events (MACE).
Results: A total of 1105 patients were enrolled: 1032 with normal hs-cTnI and 73 with elevated hs-cTnI. The mean follow-up was 24.4 ± 10.8 months, 176 patients died and 39 patients met MACE. In the elevated troponin group, 50%, 32.1% and 17.9% died from cancer, cardiovascular and other causes, while those in the normal troponin group were 75.7%, 2% and 22.3%, there was statistical difference between 2 groups (P < 0.001). Patients with elevated preoperative hs-cTnI had significantly higher mortality (P < 0.001) and more MACE (P < 0.001) compared with those with normal hs-cTnI. A propensity-matching analysis were performed, resulting in 151 patients with normal hs-cTnI and 60 patients with elevated hs-cTnI. The matched population had the similar results for all-cause death (P = 0.009) and MACE (P = 0.001). The results were consistent after further excluding 147 patients who had received chemoradiotherapy prior to surgery in subgroup analysis. The results of multivariate Cox regression analysis shown that hs-cTnI was one of the best predictors for all-cause death (hazard ratio [HR] 2.278; 95% confidence interval [CI] 1.19-4.361) and MACE (HR, 3.523; 95%CI, 1.477-8.403) in total populations, similar results were found in subgroup analysis.
Conclusions: Colorectal cancer patients without myocardial ischemia manifestation but with elevated hs-cTnI prior to tumor resection surgery were at increased risk for long-term all-cause death and MACE, irrespective of whether they have received chemoradiotherapy prior to surgery.
{"title":"The association of preoperative high-sensitivity cardiac troponin i and long-term outcomes in colorectal cancer patients received tumor resection surgery.","authors":"Yitao Zhang, Zicheng Huang, Sutian Hu, Jinhong Si, Shiyao Cheng, Zhichong Chen, Jiaojie Xue, Xue Lou, Huajing Peng, Zequan Li, Mao Ouyang, Xiang Gao, Weijie Zeng","doi":"10.1186/s40959-023-00162-5","DOIUrl":"https://doi.org/10.1186/s40959-023-00162-5","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to evaluate the association between preoperative hs-cTnI and long-term mortality and major adverse cardiovascular events (MACE) in colorectal cancer patients.</p><p><strong>Methods: </strong>This single-center retrospective cohort study included 1105 consecutive colorectal cancer patients who received tumor resection surgery between January 2018 and June 2020. Inclusion criteria were an age ≥ 18 years and had been tested for hs-cTnI on admission within 7 days prior to tumor resection surgery. Exclusion criteria were emergent surgery, failure to received tumor resection surgery, hospital death, there was clinical evidence of unstable coronary artery disease or pulmonary embolism occurred before operation according to medical record. The primary endpoint was all-cause death. Secondary endpoint was major adverse cardiovascular events (MACE).</p><p><strong>Results: </strong>A total of 1105 patients were enrolled: 1032 with normal hs-cTnI and 73 with elevated hs-cTnI. The mean follow-up was 24.4 ± 10.8 months, 176 patients died and 39 patients met MACE. In the elevated troponin group, 50%, 32.1% and 17.9% died from cancer, cardiovascular and other causes, while those in the normal troponin group were 75.7%, 2% and 22.3%, there was statistical difference between 2 groups (P < 0.001). Patients with elevated preoperative hs-cTnI had significantly higher mortality (P < 0.001) and more MACE (P < 0.001) compared with those with normal hs-cTnI. A propensity-matching analysis were performed, resulting in 151 patients with normal hs-cTnI and 60 patients with elevated hs-cTnI. The matched population had the similar results for all-cause death (P = 0.009) and MACE (P = 0.001). The results were consistent after further excluding 147 patients who had received chemoradiotherapy prior to surgery in subgroup analysis. The results of multivariate Cox regression analysis shown that hs-cTnI was one of the best predictors for all-cause death (hazard ratio [HR] 2.278; 95% confidence interval [CI] 1.19-4.361) and MACE (HR, 3.523; 95%CI, 1.477-8.403) in total populations, similar results were found in subgroup analysis.</p><p><strong>Conclusions: </strong>Colorectal cancer patients without myocardial ischemia manifestation but with elevated hs-cTnI prior to tumor resection surgery were at increased risk for long-term all-cause death and MACE, irrespective of whether they have received chemoradiotherapy prior to surgery.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2023-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9979437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10826649","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}
Background: Arterial occlusive events are an emerging problem in patients with chronic myeloid leukemia (CML) receiving tyrosine kinase inhibitor (TKI) therapy. Endothelial cell damage is thought to play an important role in the development of vascular events. Measurement of the peripheral vasodilator response by peripheral arterial tonometry (PAT) has reportedly been useful in the non-invasive assessment of endothelial dysfunction. To date, no studies have assessed endothelial function using PAT in patients with CML receiving TKIs.
Method: We measured the reactive hyperemia index (RHI) using PAT in young patients with CML (men aged ≤ 55 years and women aged ≤ 65 years) receiving TKIs.
Results: Thirty patients with CML were examined (mean age, 43.5 ± 9.8 years; men, 57%). The median RHI was 1.81. Among these patients, 16.7% and 83.3% were taking imatinib and second- or third-generation TKIs, respectively. There were no differences in the baseline characteristics between the low RHI (< 1.67, n = 10), borderline RHI (≥ 1.67 and < 2.10, n = 14), and normal RHI (≥ 2.10, n = 6) groups. Serum uric acid (UA) levels and the RHI were significantly negatively correlated (r = -0.40, p = 0.029).
Conclusion: One-third of young patients with CML receiving TKI therapy were classified as having a low RHI. The RHI was negatively correlated with serum UA level. Larger prospective studies are necessary to examine whether the RHI predicts cardiovascular events in such patients.
{"title":"Endothelial function measured by peripheral arterial tonometry in patients with chronic myeloid leukemia on tyrosine kinase inhibitor therapy: a pilot study.","authors":"Tomohiro Kaneko, Sakiko Miyazaki, Azusa Kurita, Ryoko Morimoto, Shun Tsuchiya, Naoki Watanabe, Tomoiku Takaku, Norio Komatsu, Tohru Minamino","doi":"10.1186/s40959-023-00164-3","DOIUrl":"https://doi.org/10.1186/s40959-023-00164-3","url":null,"abstract":"<p><strong>Background: </strong>Arterial occlusive events are an emerging problem in patients with chronic myeloid leukemia (CML) receiving tyrosine kinase inhibitor (TKI) therapy. Endothelial cell damage is thought to play an important role in the development of vascular events. Measurement of the peripheral vasodilator response by peripheral arterial tonometry (PAT) has reportedly been useful in the non-invasive assessment of endothelial dysfunction. To date, no studies have assessed endothelial function using PAT in patients with CML receiving TKIs.</p><p><strong>Method: </strong>We measured the reactive hyperemia index (RHI) using PAT in young patients with CML (men aged ≤ 55 years and women aged ≤ 65 years) receiving TKIs.</p><p><strong>Results: </strong>Thirty patients with CML were examined (mean age, 43.5 ± 9.8 years; men, 57%). The median RHI was 1.81. Among these patients, 16.7% and 83.3% were taking imatinib and second- or third-generation TKIs, respectively. There were no differences in the baseline characteristics between the low RHI (< 1.67, n = 10), borderline RHI (≥ 1.67 and < 2.10, n = 14), and normal RHI (≥ 2.10, n = 6) groups. Serum uric acid (UA) levels and the RHI were significantly negatively correlated (r = -0.40, p = 0.029).</p><p><strong>Conclusion: </strong>One-third of young patients with CML receiving TKI therapy were classified as having a low RHI. The RHI was negatively correlated with serum UA level. Larger prospective studies are necessary to examine whether the RHI predicts cardiovascular events in such patients.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2023-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9945366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10771717","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 : 2023-02-18DOI: 10.1186/s40959-023-00159-0
Ali Mir, Yasra Badi, Seif Bugazia, Anas Zakarya Nourelden, Ahmed Hashem Fathallah, Khaled Mohamed Ragab, Mohammed Alsillak, Sarah Makram Elsayed, Abdulrahman Ibrahim Hagrass, Sawyer Bawek, Mohamad Kalot, Zachary L Brumberger
Background: Cancer patients receiving chemotherapy have an increased risk of cardiovascular complications. This limits the widespread use of lifesaving therapies, often necessitating alternate lower efficacy regimens, or precluding chemotherapy entirely. Prior studies have suggested that using common cardioprotective agents may attenuate chemotherapy-induced cardiotoxicity. However, small sample sizes and conflicting outcomes have limited the clinical significance of these results.
Hypothesis: A comprehensive network meta-analysis using updated and high-quality data can provide more conclusive information to assess which drug or drug class has the most significant effect in the management of chemotherapy-induced cardiotoxicity.
Methods: We performed a literature search for randomized controlled trials (RCTs) investigating the effects of cardioprotective agents in patients with chemotherapy-induced cardiotoxicity. We used established analytical tools (netmeta package in RStudio) and data extraction formats to analyze the outcome data. To obviate systematic bias in the selection and interpretation of RCTs, we employed the validated Cochrane risk-of-bias tools. Agents included were statins, aldosterone receptor antagonists (MRAs), ACEIs, ARBs, and beta-blockers. Outcomes examined were improvement in clinical and laboratory parameters of cardiac function including a decreased reduction in left ventricular ejection fraction (LVEF), clinical HF, troponin-I, and B-natriuretic peptide levels.
Results: Our study included 33 RCTs including a total of 3,285 patients. Compared to control groups, spironolactone therapy was associated with the greatest LVEF improvement (Mean difference (MD) = 12.80, [7.90; 17.70]), followed by enalapril (MD = 7.62, [5.31; 9.94]), nebivolol (MD = 7.30, [2.39; 12.21]), and statins (MD = 6.72, [3.58; 9.85]). Spironolactone was also associated with a significant reduction in troponin elevation (MD = - 0.01, [- 0.02; - 0.01]). Enalapril demonstrated the greatest BNP reduction (MD = - 49.00, [- 68.89; - 29.11]), which was followed by spironolactone (MD = - 16.00, [- 23.9; - 8.10]). Additionally, patients on enalapril had the lowest risk of developing clinical HF compared to the control population (RR = 0.05, [0.00; 0.75]).
Conclusion: Our analysis reaffirmed that statins, MRAs, ACEIs, and beta-blockers can significantly attenuate chemotherapy-induced cardiotoxicity, while ARBs showed no significant effects. Spironolactone showed the most robust improvement of LVEF, which best supports its use among this population. Our analysis warrants future clinical studies examining the cardioprotective effects of cardiac remodeling therapy in cancer patients treated with chemotherapeutic agents.
{"title":"Efficacy and safety of cardioprotective drugs in chemotherapy-induced cardiotoxicity: an updated systematic review & network meta-analysis.","authors":"Ali Mir, Yasra Badi, Seif Bugazia, Anas Zakarya Nourelden, Ahmed Hashem Fathallah, Khaled Mohamed Ragab, Mohammed Alsillak, Sarah Makram Elsayed, Abdulrahman Ibrahim Hagrass, Sawyer Bawek, Mohamad Kalot, Zachary L Brumberger","doi":"10.1186/s40959-023-00159-0","DOIUrl":"https://doi.org/10.1186/s40959-023-00159-0","url":null,"abstract":"<p><strong>Background: </strong>Cancer patients receiving chemotherapy have an increased risk of cardiovascular complications. This limits the widespread use of lifesaving therapies, often necessitating alternate lower efficacy regimens, or precluding chemotherapy entirely. Prior studies have suggested that using common cardioprotective agents may attenuate chemotherapy-induced cardiotoxicity. However, small sample sizes and conflicting outcomes have limited the clinical significance of these results.</p><p><strong>Hypothesis: </strong>A comprehensive network meta-analysis using updated and high-quality data can provide more conclusive information to assess which drug or drug class has the most significant effect in the management of chemotherapy-induced cardiotoxicity.</p><p><strong>Methods: </strong>We performed a literature search for randomized controlled trials (RCTs) investigating the effects of cardioprotective agents in patients with chemotherapy-induced cardiotoxicity. We used established analytical tools (netmeta package in RStudio) and data extraction formats to analyze the outcome data. To obviate systematic bias in the selection and interpretation of RCTs, we employed the validated Cochrane risk-of-bias tools. Agents included were statins, aldosterone receptor antagonists (MRAs), ACEIs, ARBs, and beta-blockers. Outcomes examined were improvement in clinical and laboratory parameters of cardiac function including a decreased reduction in left ventricular ejection fraction (LVEF), clinical HF, troponin-I, and B-natriuretic peptide levels.</p><p><strong>Results: </strong>Our study included 33 RCTs including a total of 3,285 patients. Compared to control groups, spironolactone therapy was associated with the greatest LVEF improvement (Mean difference (MD) = 12.80, [7.90; 17.70]), followed by enalapril (MD = 7.62, [5.31; 9.94]), nebivolol (MD = 7.30, [2.39; 12.21]), and statins (MD = 6.72, [3.58; 9.85]). Spironolactone was also associated with a significant reduction in troponin elevation (MD = - 0.01, [- 0.02; - 0.01]). Enalapril demonstrated the greatest BNP reduction (MD = - 49.00, [- 68.89; - 29.11]), which was followed by spironolactone (MD = - 16.00, [- 23.9; - 8.10]). Additionally, patients on enalapril had the lowest risk of developing clinical HF compared to the control population (RR = 0.05, [0.00; 0.75]).</p><p><strong>Conclusion: </strong>Our analysis reaffirmed that statins, MRAs, ACEIs, and beta-blockers can significantly attenuate chemotherapy-induced cardiotoxicity, while ARBs showed no significant effects. Spironolactone showed the most robust improvement of LVEF, which best supports its use among this population. Our analysis warrants future clinical studies examining the cardioprotective effects of cardiac remodeling therapy in cancer patients treated with chemotherapeutic agents.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2023-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9938608/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10763554","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}