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Early Diagnosis, Monitoring, Prevention and Treatment of Cardiotoxicity

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Cardiology".

Deadline for manuscript submissions: closed (1 March 2021) | Viewed by 54140

Special Issue Editor


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Guest Editor
Cardioncology Unit, European Institute of Oncology, I.R.C.C.S, Milan, Italy
Interests: cardioncology; troponin; malignant pericardial effusion; cancer and heart disease

Special Issue Information

Dear Colleagues,

In recent years, advances in oncologic therapies have led to a considerable improvement in cancer patients’ prognosis and survival. However, these improvements may ultimately be blunted by the increase of cardiovascular side effects. The spectrum of the abnormalities that can impair the cardiovascular system includes acute coronary syndromes, hypertension, arrhythmias, valve impairment, pericarditis, and thromboembolic events. However, the most frequent and typical clinical manifestation of cardiotoxicity, feared both by cardiologists and oncologists, is the development of asymptomatic or symptomatic left ventricular dysfunction. This form of cardiomyopathy may be induced not only by conventional cancer therapy, but also by new anti-tumoral targeted therapies—including HER2 inhibitors, tyrosine kinase inhibitors, proteasome inhibitors, and immune checkpoint inhibitors—and remains a major deterrent that may compromise the clinical effectiveness of a cancer treatment, independently of the oncologic prognosis, and have a serious impact on the patient’s survival and quality of life. This Special Issue of the Journal of Clinical Medicine will focus on the strategies/approaches that have been demonstrated to be effective in preventing or limiting cancer-drug-induced cardiotoxicity, including early diagnosis, monitoring, prevention, and treatment.

Dr. Daniela Cardinale
Guest Editor

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Keywords

  • cardioncology
  • early diagnosis, prevention, and treatment of cardiotoxicity
  • troponin
  • malignant pericardial effusion
  • cancer and heart disease

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Published Papers (12 papers)

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Research

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9 pages, 221 KiB  
Article
Factors Associated with Adverse Cardiovascular Events in Cancer Patients Treated with Bevacizumab
by Doan T. M. Ngo, Trent Williams, Sophie Horder, Leonard Kritharides, Janette Vardy, Hiren Mandaliya, Ina I. C. Nordman, James Lynam, Tony Bonaventura and Aaron L. Sverdlov
J. Clin. Med. 2020, 9(8), 2664; https://doi.org/10.3390/jcm9082664 - 18 Aug 2020
Cited by 18 | Viewed by 3416
Abstract
Background: Bevacizumab, a vascular endothelial growth factor (VEGF) monoclonal antibody commonly used for the treatment of various cancers, is often associated with adverse cardiovascular effects such as hypertension, cardiac and cerebral ischemia, thrombosis, and bleeding events. Factors associated with increased risks of adverse [...] Read more.
Background: Bevacizumab, a vascular endothelial growth factor (VEGF) monoclonal antibody commonly used for the treatment of various cancers, is often associated with adverse cardiovascular effects such as hypertension, cardiac and cerebral ischemia, thrombosis, and bleeding events. Factors associated with increased risks of adverse cardiovascular effects with bevacizumab have not been intensively studied. In this study, we determined factors associated with hospital admissions due to cardiovascular complications in patients who received bevacizumab for cancer treatment. Methods and Results: We retrospectively collected data for all patients treated with bevacizumab between the 1st January 2016 and the 31st December 2017 at the Hunter New England Local Health District. Patients’ characteristics and their medical history were obtained from hospital electronic medical records. Outcome data were sourced from the Institutional Cardiac and Stroke Outcomes Unit database. A total of n = 230 patients (mean age 65, males n = 124 (53.9%)) were treated with bevacizumab during the study period. N = 28 patients were admitted to hospital for a major cardiovascular-related event. Higher total treatment dose (p < 0.05), concomitant hypertension (p = 0.005), diabetes (p = 0.04), atrial fibrillation (p = 0.03), and lack of use of statin therapy (p = 0.03) were key contributors to hospital admission. Conclusions: Results of our study highlight the fact that patients with concomitant baseline cardiovascular disease/risk factors are at an increased risk of cardiovascular hospitalization related to bevacizumab treatment. Careful baseline cardiovascular assessment may be an essential step to minimize cardiovascular complications. Full article
13 pages, 1716 KiB  
Article
Circulating MicroRNAs as Potential Predictors of Anthracycline-Induced Troponin Elevation in Breast Cancer Patients: Diverging Effects of Doxorubicin and Epirubicin
by Sonia Gioffré, Mattia Chiesa, Daniela Maria Cardinale, Veronica Ricci, Chiara Vavassori, Carlo Maria Cipolla, Serge Masson, Maria Teresa Sandri, Michela Salvatici, Fabio Ciceri, Roberto Latini, Lidia Irene Staszewsky, Giulio Pompilio, Gualtiero I. Colombo and Yuri D’Alessandra
J. Clin. Med. 2020, 9(5), 1418; https://doi.org/10.3390/jcm9051418 - 11 May 2020
Cited by 29 | Viewed by 3407
Abstract
Anthracyclines are anti-neoplastic drugs presenting cardiotoxicity as a side effect. Cardiac troponins (cTn) and echocardiography are currently used to assess cardiac damage and dysfunction, but early biomarkers identifying patients in need of preventive treatments remain a partially met need. Circulating microRNAs (miRNAs) represent [...] Read more.
Anthracyclines are anti-neoplastic drugs presenting cardiotoxicity as a side effect. Cardiac troponins (cTn) and echocardiography are currently used to assess cardiac damage and dysfunction, but early biomarkers identifying patients in need of preventive treatments remain a partially met need. Circulating microRNAs (miRNAs) represent good candidates, so we investigated their possible roles as predictors of troponin elevation upon anthracycline treatment. Eighty-eight female breast cancer patients administered with doxorubicin (DOX) or epirubicin (EPI) were divided into four groups basing on drug type and cTn positive (cTn+) or negative (cTn−) levels: DOX cTn−, DOX cTn+, EPI cTn− and EPI cTn+. Blood was collected at baseline, during treatment, and at follow-up. We identified plasma miRNAs of interest by OpenArray screening and single assay validation. Our results showed miR-122-5p, miR-499a-5p and miR-885-5p dysregulation in DOX patients at T0, identifying a signature separating, with good accuracy, DOX cTn− from DOX cTn+. No miRNAs showed differential expression in EPI subjects. Conversely, an anthracycline-mediated modulation (regardless of cTn) was observed for miR-34a-5p, -122-5p and -885-5p. Our study indicates specific circulating miRNAs as possible prediction markers for cardiac troponin perturbation upon anthracycline treatment. Indeed, our findings hint at the possible future use of plasma miRNAs to predict the cardiac responsiveness of patients to different anticancer agents. Full article
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9 pages, 3780 KiB  
Article
Metabolomic Analysis of Patients with Chronic Myeloid Leukemia and Cardiovascular Adverse Events after Treatment with Tyrosine Kinase Inhibitors
by Giovanni Caocci, Martino Deidda, Antonio Noto, Marianna Greco, Maria Pina Simula, Olga Mulas, Daniele Cocco, Claudia Fattuoni, Giuseppe Mercuro, Giorgio La Nasa and Christian Cadeddu Dessalvi
J. Clin. Med. 2020, 9(4), 1180; https://doi.org/10.3390/jcm9041180 - 20 Apr 2020
Cited by 9 | Viewed by 3920
Abstract
Background: Cardiovascular adverse events (CV-AEs) are considered critical complications in chronic myeloid leukemia (CML) patients treated with second- and third-generation tyrosine kinase inhibitors (TKIs). The aim of our study was to assess the correlation between metabolic profiles and CV-AEs in CML patients treated [...] Read more.
Background: Cardiovascular adverse events (CV-AEs) are considered critical complications in chronic myeloid leukemia (CML) patients treated with second- and third-generation tyrosine kinase inhibitors (TKIs). The aim of our study was to assess the correlation between metabolic profiles and CV-AEs in CML patients treated with TKIs. Methods: We investigated 39 adult CML patients in chronic-phase (mean age 49 years, range 24–70 years), with no comorbidities evidenced at baseline, who were consecutively identified with CML and treated with imatinib, nilotinib, dasatinib, and ponatinib. All patients performed Gas-Chromatography-Mass-Spectrometry-based metabolomic analysis and were divided into two groups (with and without CV-AEs). Results: Ten CV-AEs were documented. Seven CV-AEs were rated as 3 according to the Common Toxicity Criteria, and one patient died of a dissecting aneurysm of the aorta. The patients’ samples were clearly separated into two groups after analysis and the main discriminant metabolites were tyrosine, lysine, glutamic acid, ornithine, 2-piperdinecarboxylic acid, citric acid, proline, phenylalanine, threonine, mannitol, leucine, serine, creatine, alanine, and 4-hydroxyproline, which were more abundant in the CV-AE group. Conversely, myristic acid, oxalic acid, arabitol, 4-deoxy rithronic acid, ribose, and elaidic acid were less represented in the CV-AE group. Conclusions: CML patients with CV-AEs show a different metabolic profile, suggesting probable mechanisms of endothelial damage. Full article
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17 pages, 3005 KiB  
Article
Ponatinib Induces Vascular Toxicity through the Notch-1 Signaling Pathway
by Rosalinda Madonna, Damiana Pieragostino, Maria Concetta Cufaro, Vanessa Doria, Piero Del Boccio, Martino Deidda, Sante Donato Pierdomenico, Christian Cadeddu Dessalvi, Raffaele De Caterina and Giuseppe Mercuro
J. Clin. Med. 2020, 9(3), 820; https://doi.org/10.3390/jcm9030820 - 18 Mar 2020
Cited by 22 | Viewed by 3784
Abstract
Ponatinib, a third-generation tyrosine kinase inhibitor (TKI), is the only approved TKI that is effective against T315I mutations in patients with chronic myeloid leukemia (CML). Specific activation of Notch signaling in CML cells by ponatinib can be considered as the “on-target effect” on [...] Read more.
Ponatinib, a third-generation tyrosine kinase inhibitor (TKI), is the only approved TKI that is effective against T315I mutations in patients with chronic myeloid leukemia (CML). Specific activation of Notch signaling in CML cells by ponatinib can be considered as the “on-target effect” on the tumor and represents a therapeutic approach for CML. Nevertheless, ponatinib-induced vascular toxicity remains a serious concern, with underlying mechanisms being poorly understood. We aimed to determine the mechanisms of ponatinib-induced vascular toxicity, defining associated signaling pathways and identifying potential rescue strategies. We exposed human umbilical endothelial cells (HUVECs) to ponatinib or vehicle in the presence or absence of the neutralizing factor anti-Notch-1 antibody for exposure times of 0–72 h. Label-free proteomics and network analysis showed that protein cargo of HUVECs treated with ponatinib triggered apoptosis and inhibited vasculature development. We validated the proteomic data showing the inhibition of matrigel tube formation, an up-regulation of cleaved caspase-3 and a downregulation of phosphorylated AKT and phosphorylated eNOS. We delineated the signaling of ponatinib-induced vascular toxicity, demonstrating that ponatinib inhibits endothelial survival, reduces angiogenesis and induces endothelial senescence and apoptosis via the Notch-1 pathway. Ponatinib induced endothelial toxicity in vitro. Hyperactivation of Notch-1 in the vessels can lead to abnormal vascular development and vascular dysfunction. By hyperactivating Notch-1 in the vessels, ponatinib exerts an “on-target off tumor effect”, which leads to deleterious effects and may explain the drug’s vasculotoxicity. Selective blockade of Notch-1 prevented ponatinib-induced vascular toxicity. Full article
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11 pages, 239 KiB  
Article
Cranial Irradiation in Childhood Acute Lymphoblastic Leukemia Is Related to Subclinical Left Ventricular Dysfunction and Reduced Large Artery Compliance in Cancer Survivors
by Joanna Sulicka-Grodzicka, Bernadeta Chyrchel, Justyna Totoń-Żurańska, Ewelina Nowak, Paweł P. Wołkow, Andrzej Surdacki and Tomasz Grodzicki
J. Clin. Med. 2019, 8(11), 1952; https://doi.org/10.3390/jcm8111952 - 13 Nov 2019
Cited by 3 | Viewed by 2519
Abstract
Long-term survivors of acute lymphoblastic leukemia (ALL), the most common childhood malignancy, are at remarkably increased risk of heart failure (HF) in middle age, most likely due anthracycline cardiotoxicity. The role of cranial radiation therapy (CRT) in the development of left ventricular (LV) [...] Read more.
Long-term survivors of acute lymphoblastic leukemia (ALL), the most common childhood malignancy, are at remarkably increased risk of heart failure (HF) in middle age, most likely due anthracycline cardiotoxicity. The role of cranial radiation therapy (CRT) in the development of left ventricular (LV) dysfunction, a predecessor of overt HF, remains unclear. Our aim was to compare LV function and systemic arterial properties according to past CRT in young adult survivors of anthracycline-treated ALL. We studied young adult survivors of childhood ALL at a median of 16 years from diagnosis treated with anthracycline-based chemotherapy, with (n = 12) or without (n = 30) CRT. In addition to fractional shortening (FS) and ejection fraction (EF), LV function was quantified by tissue Doppler imaging of the mitral annulus. Aortic strain/distensibility and arterial compliance were derived from echocardiography and simultaneously recorded pulse pressure. Despite similar FS and EF, peak mitral annular systolic velocity (median (interquartile range): 9.0 (7.5–10.0) vs. 10.0 (8.8–11.5) cm/s, p = 0.05), and early diastolic velocity (13.8 (13.0–14.8) vs. 15.5 (14.0–17.3), p = 0.01) were decreased after chemotherapy combined with CRT compared to chemotherapy without CRT. Systemic arterial compliance was lower in post-CRT subjects (1.0 (0.8–1.2 vs. 1.4 (1.1–1.7) mL/mmHg, p = 0.002). Aortic strain and distensibility were similar regardless of prior CRT. In conclusion, lower arterial compliance and subclinical LV dysfunction may be possible late consequences of past CRT in adult survivors of childhood ALL. Whether arterial stiffening is associated with future HF development in CRT-exposed ALL survivors remains to be investigated. Full article

Review

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10 pages, 2163 KiB  
Review
The Role of Speckle Strain Echocardiography in the Diagnosis of Early Subclinical Cardiac Injury in Cancer Patients—Is There More Than Just Left Ventricle Global Longitudinal Strain?
by Michal Laufer-Perl, Dan Gilon, Livia Kapusta and Zaza Iakobishvili
J. Clin. Med. 2021, 10(1), 154; https://doi.org/10.3390/jcm10010154 - 5 Jan 2021
Cited by 14 | Viewed by 3906
Abstract
With the improvement in survival rate, cardiotoxicity has emerged as a significant adverse effect of cancer therapy. Early diagnosis of subclinical cardiac injury may allow the initiation of cardioprotective therapy and preventing the interruption of optimal cancer therapy and the development of irreversible [...] Read more.
With the improvement in survival rate, cardiotoxicity has emerged as a significant adverse effect of cancer therapy. Early diagnosis of subclinical cardiac injury may allow the initiation of cardioprotective therapy and preventing the interruption of optimal cancer therapy and the development of irreversible cardiac dysfunction. In this article, we review the role of two-dimensional speckle tracking echocardiography (2D-STE), beyond the common left ventricle global longitudinal strain in the diagnosis of early subclinical cardiac injury in patients treated with cancer therapies. Full article
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15 pages, 1296 KiB  
Review
Characteristics, Management, and Outcomes of Acute Coronary Syndrome Patients with Cancer
by Valentina Milazzo, Nicola Cosentino, Jeness Campodonico, Claudia Lucci, Daniela Cardinale, Carlo M. Cipolla and Giancarlo Marenzi
J. Clin. Med. 2020, 9(11), 3642; https://doi.org/10.3390/jcm9113642 - 12 Nov 2020
Cited by 20 | Viewed by 2898
Abstract
Patients with cancer are at increased risk of cardiovascular disease, with a reported prevalence of acute coronary syndrome (ACS) ranging from 3% to 17%. The increased risk of ACS in these patients seems to be due to the complex interaction of shared cardiovascular [...] Read more.
Patients with cancer are at increased risk of cardiovascular disease, with a reported prevalence of acute coronary syndrome (ACS) ranging from 3% to 17%. The increased risk of ACS in these patients seems to be due to the complex interaction of shared cardiovascular risk factors, cancer type and stage, and chemotherapeutic and radiotherapy regimens. The management of ACS in patients with cancer is a clinical challenge, particularly due to cancer’s unique pathophysiology, which makes it difficult to balance thrombotic and bleeding risks in this specific patient population. In addition, patients with cancer have largely been excluded from ACS trials. Hence, an evidence-based treatment for ACS in this group of patients is unknown and only a limited proportion of them is treated with antiplatelets or invasive revascularization, despite initial reports suggesting their beneficial prognostic effects in cancer patients. Finally, cancer patients experiencing ACS are also at higher risk of in-hospital and long-term mortality as compared to non-cancer patients. In this review, we will provide an overview on the available evidence of the relationship between ACS and cancer, in terms of clinical manifestations, possible underlying mechanisms, and therapeutic and prognostic implications. Full article
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22 pages, 1569 KiB  
Review
Hypertensive Cardiotoxicity in Cancer Treatment—Systematic Analysis of Adjunct, Conventional Chemotherapy, and Novel Therapies—Epidemiology, Incidence, and Pathophysiology
by Robin Chung, Sara Tyebally, Daniel Chen, Vikas Kapil, J. Malcolm Walker, Daniel Addison, Roohi Ismail-Khan, Avirup Guha and Arjun K Ghosh
J. Clin. Med. 2020, 9(10), 3346; https://doi.org/10.3390/jcm9103346 - 18 Oct 2020
Cited by 21 | Viewed by 5738
Abstract
Cardiotoxicity is the umbrella term for cardiovascular side effects of cancer therapies. The most widely recognized phenotype is left ventricular dysfunction, but cardiotoxicity can manifest as arrhythmogenic, vascular, myocarditic and hypertensive toxicities. Hypertension has long been regarded as one of the most prevalent [...] Read more.
Cardiotoxicity is the umbrella term for cardiovascular side effects of cancer therapies. The most widely recognized phenotype is left ventricular dysfunction, but cardiotoxicity can manifest as arrhythmogenic, vascular, myocarditic and hypertensive toxicities. Hypertension has long been regarded as one of the most prevalent and modifiable cardiovascular risk factors in the general population, but its relevance during the cancer treatment journey may be underestimated. Hypertensive cardiotoxicity occurs de novo in a substantial proportion of treated cancer patients. The pathology is incompletely characterized—natriuresis and renin angiotensin system interactions play a role particularly in conventional treatments, but in novel therapies endothelial dysfunction and the interaction between the cancer and cardiac kinome are implicated. There exists a treatment paradox in that a significant hypertensive response not only mandates anti-hypertensive treatment, but in fact, in certain cancer treatment scenarios, hypertension is a predictor of cancer treatment efficacy and response. In this comprehensive review of over 80,000 patients, we explored the epidemiology, incidence, and mechanistic pathophysiology of hypertensive cardiotoxicity in adjunct, conventional chemotherapy, and novel cancer treatments. Conventional chemotherapy, adjunct treatments, and novel targeted therapies collectively caused new onset hypertension in 33–68% of treated patients. The incidence of hypertensive cardiotoxicity across twenty common novel therapies for any grade hypertension ranged from 4% (imatinib) to 68% (lenvatinib), and high grade 3 or 4 hypertension in <1% (imatinib) to 42% (lenvatinib). The weighted average effect was all-grade hypertension in 24% and grade 3 or 4 hypertension in 8%. Full article
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18 pages, 1136 KiB  
Review
Management of Cardiac Toxicity Induced by Chemotherapy
by Dario Trapani, Paola Zagami, Eleonora Nicolò, Gabriella Pravettoni and Giuseppe Curigliano
J. Clin. Med. 2020, 9(9), 2885; https://doi.org/10.3390/jcm9092885 - 7 Sep 2020
Cited by 36 | Viewed by 9470
Abstract
Cardiotoxicity encompasses a spectrum of adverse cardiological effects experienced by cancer patients during and after receiving antineoplastic treatments. The intersection of cancer care with the management of the multiple comorbid non-communicable diseases carried by patients or related to cancer treatments motivates the need [...] Read more.
Cardiotoxicity encompasses a spectrum of adverse cardiological effects experienced by cancer patients during and after receiving antineoplastic treatments. The intersection of cancer care with the management of the multiple comorbid non-communicable diseases carried by patients or related to cancer treatments motivates the need for an integrated and multidisciplinary approach to therapeutic clinical decision-making. This present review aimed to provide a perspective and an update of the current pharmacotherapy approaches for the prevention and management of cardiotoxicity from antiblastic chemotherapy; as such, it addresses myocardial, vascular, and arrhythmic disorders associated to chemotherapy, by navigating the current knowledge and clinical indications in support of the medical interventions. Clinical scenarios of pharmacological interventions take place with patients receiving anthracycline and, by extrapolation, other agents with cardiotoxic potentials and non-chemotherapy agents, including various small molecules and immunotherapy agents. Analysis of these scenarios aims to provide practical evidence-based guidance for the management of drug-induced cardiac dysfunctions. The possible role of new biomarkers for the early recognition of cardiotoxicity is mentioned across the clinical studies, with reference to the pharmacological biomarker-driven interventions delivered. To best inform survivorship care, the management and context of cardio-oncology services are discussed within the broader network of providers and settings of care. Full article
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26 pages, 2355 KiB  
Review
Genetic Factors Involved in Cardiomyopathies and in Cancer
by María Sabater-Molina, Marina Navarro-Peñalver, Carmen Muñoz-Esparza, Ángel Esteban-Gil, Juan Jose Santos-Mateo and Juan R. Gimeno
J. Clin. Med. 2020, 9(6), 1702; https://doi.org/10.3390/jcm9061702 - 2 Jun 2020
Cited by 7 | Viewed by 4400
Abstract
Cancer therapy-induced cardiomyopathy (CCM) manifests as left ventricular (LV) dysfunction and heart failure (HF). It is associated withparticular pharmacological agents and it is typically dose dependent, but significant individual variability has been observed. History of prior cardiac disease, abuse of toxics, cardiac overload [...] Read more.
Cancer therapy-induced cardiomyopathy (CCM) manifests as left ventricular (LV) dysfunction and heart failure (HF). It is associated withparticular pharmacological agents and it is typically dose dependent, but significant individual variability has been observed. History of prior cardiac disease, abuse of toxics, cardiac overload conditions, age, and genetic predisposing factors modulate the degree of the cardiac reserve and the response to the injury. Genetic/familial cardiomyopathies (CMY) are increasingly recognized in general populations with an estimated prevalence of 1:250. Association between cardiac and oncologic diseases regarding genetics involves not only the toxicity process, but pathogenicity. Genetic variants in germinal cells that cause CMY (LMNA, RAS/MAPK) can increase susceptibility for certain types of cancer. The study of mutations found in cancer cells (somatic) has revealed the implication of genes commonly associated with the development of CMY. In particular, desmosomal mutations have been related to increased undifferentiation and invasiveness of cancer. In this article, the authors review the knowledge on the relevance of environmental and genetic background in CCM and give insights into the shared genetic role in the pathogenicity of the cancer process and development of CMY. Full article
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19 pages, 323 KiB  
Review
Cardiovascular Complications of Systemic Therapy in Non-Small-Cell Lung Cancer
by Magdalena Zaborowska-Szmit, Maciej Krzakowski, Dariusz M. Kowalski and Sebastian Szmit
J. Clin. Med. 2020, 9(5), 1268; https://doi.org/10.3390/jcm9051268 - 27 Apr 2020
Cited by 47 | Viewed by 5686
Abstract
Cardiovascular diseases may determine therapy outcomes of non-small-cell lung cancer (NSCLC). The evidence for how iatrogenic cardiovascular complications contribute to ceasing anticancer treatment, decreasing the quality of life or even premature death, is unclear. Older patients and smokers are at risk of atherosclerosis [...] Read more.
Cardiovascular diseases may determine therapy outcomes of non-small-cell lung cancer (NSCLC). The evidence for how iatrogenic cardiovascular complications contribute to ceasing anticancer treatment, decreasing the quality of life or even premature death, is unclear. Older patients and smokers are at risk of atherosclerosis and arterial thromboembolic events (TE), such as myocardial infarction or stroke. Venous TE can be observed in up to 15% of NSCLC patients, but the risk increases three to five times in ALK (anaplastic lymphoma kinase)-rearranged NSCLC. ALK inhibitors are associated with electrophysiological disorders. Cytotoxic agents and anti-VEGF inhibitors mainly cause vascular complications, including venous or arterial TE. Cardiac dysfunction and arrhythmias seem to be less frequent. Chemotherapy is often administered in two-drug regimens. Clinical events can be triggered by different mechanisms. Among epidermal growth factor inhibitors, erlotinib and gefitinib can lead to coronary artery events; however, afatinib and osimertinib can be associated with the development of heart failure. During anti-PD1/anti-PDL1 therapy, myocarditis is possible, which must be differentiated from acute coronary syndrome and heart failure. Awareness of all possible cardiovascular complications in NSCLC encourages vigilance in early diagnostics and treatment. Full article
14 pages, 272 KiB  
Review
Strategies to Prevent Cardiovascular Toxicity in Breast Cancer: Is It Ready for Primetime?
by Robin Kikuchi, Nishant P. Shah and Susan F. Dent
J. Clin. Med. 2020, 9(4), 896; https://doi.org/10.3390/jcm9040896 - 25 Mar 2020
Cited by 13 | Viewed by 4179
Abstract
Cardio-oncology is an emerging field tasked with identifying and treating cancer therapy related cardiac dysfunction (e.g., cytotoxic agents, immunotherapies, radiation, and hormone therapies) and optimizing the cardiovascular health of cancer patients exposed to these agents. Novel cancer therapies have led to significant improvements [...] Read more.
Cardio-oncology is an emerging field tasked with identifying and treating cancer therapy related cardiac dysfunction (e.g., cytotoxic agents, immunotherapies, radiation, and hormone therapies) and optimizing the cardiovascular health of cancer patients exposed to these agents. Novel cancer therapies have led to significant improvements in clinical outcomes for breast cancer patients. In this article, we review the current literature on assessing cardiovascular risk of breast cancer therapies and discuss strategies (including pharmacological and lifestyle interventions) to prevent cardiovascular toxicity. Full article
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