Abstract
Cardio-oncology has emerged as an exciting new field at the intersection of cardiology and oncology. While improved oncology treatment efficacy has increased survival rates in cancer patients, the long-term cardiovascular consequences of this life-saving treatment have become more clinically relevant. Both traditional and newer (targeted) cancer therapies can have cardiovascular and metabolic sequelae, resulting in heart failure, coronary artery disease, myocarditis, pericardial disease, hypertension, and vascular and metabolic perturbations (Moslehi JJ. Cardiovascular toxic effects of targeted cancer therapies. N Engl J Med 375: 1457-1467, 2016). Both acute and chronic cardiovascular toxicities have proven challenging for clinicians and patients, significantly contributing to morbidity and mortality. Although chronic cardiovascular disease affects a growing number of cancer survivors (~17 million in the United States in 2019), cardiovascular toxicities associated with cancer and cancer therapies are poorly understood mechanistically. To balance potential damage to the cardiovascular system with effective and efficient cancer treatment, novel strategies are sorely needed. This perspective focuses on an assembly of articles that discuss novel means of counteracting adverse cardiovascular events in response to anticancer therapy. In light of new clinical syndromes in cardiology due to cancer therapies, we hope to highlight promising research opportunities offered by cardio-oncology (Bellinger AM, Arteaga CL, Force T, Humphreys BD, Demetri GD, Druker BJ, Moslehi JJ. Cardio-oncology: how new targeted cancer therapies and precision medicine can inform cardiovascular discovery. Circulation 132: 2248-2258, 2015.).
PMID: 31172808 [PubMed - indexed for MEDLINE]
25 March 2020
12:37
Cardiotoxicity News
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A phase 2 study to assess the pharmacokinetics and pharmacodynamics of CPX-351 and its effects on cardiac repolarization in patients with acute leukemias.
//www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--production.springer.de-OnlineResources-Logos-springerlink.gif //www.ncbi.nlm.nih.gov/corehtml/query/egifs/https:--www.ncbi.nlm.nih.gov-corehtml-pmc-pmcgifs-pubmed-pmc.png Related Articles
A phase 2 study to assess the pharmacokinetics and pharmacodynamics of CPX-351 and its effects on cardiac repolarization in patients with acute leukemias.
Cancer Chemother Pharmacol. 2019 07;84(1):163-173
Authors: Lin TL, Newell LF, Stuart RK, Michaelis LC, Rubenstein E, Pentikis HS, Callahan T, Alvarez D, Liboiron BD, Mayer LD, Wang Q, Banerjee K, Louie AC
Abstract
PURPOSE: Daunorubicin can induce left ventricular dysfunction and QT interval prolongation. This study assessed the effects of CPX-351, a liposomal encapsulation of cytarabine and daunorubicin, on cardiac repolarization.
METHODS: Twenty-six adults with acute leukemia were treated with CPX-351 for 1-2 induction cycles and ≤ 4 consolidation cycles. The primary endpoint was mean change in QTcF from baseline.
RESULTS: Mean QTcF changes were < 10 ms30 h. Thirteen (50%) patients achieved remission. The most common adverse events were febrile neutropenia, fatigue, and nausea.
CONCLUSIONS: The cytarabine and daunorubicin in CPX-351 liposomes were metabolized and excreted similarly to conventional formulation; however, plasma pharmacokinetics were altered. CPX-351 did not prolong the QT interval, suggesting that CPX-351 may induce less cardiotoxicity than previously reported for conventional daunorubicin.
TRIAL REGISTRATION: Clinicaltrials.gov identifier: NCT02238925.
PMID: 31098682 [PubMed - indexed for MEDLINE]
27 March 2020
22:02
Cardiotoxicity News
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The Utility of Cardiac Reserve for the Early Detection of Cancer Treatment-Related Cardiac Dysfunction: A Comprehensive Overview.
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The Utility of Cardiac Reserve for the Early Detection of Cancer Treatment-Related Cardiac Dysfunction: A Comprehensive Overview.
Front Cardiovasc Med. 2020;7:32
Authors: Foulkes S, Claessen G, Howden EJ, Daly RM, Fraser SF, La Gerche A
Abstract
With progressive advancements in cancer detection and treatment, cancer-specific survival has improved dramatically over the past decades. Consequently, long-term health outcomes are increasingly defined by comorbidities such as cardiovascular disease. Importantly, a number of well-established and emerging cancer treatments have been associated with varying degrees of cardiovascular injury that may not emerge until years following the completion of cancer treatment. Of particular concern is the development of cancer treatment related cardiac dysfunction (CTRCD) which is associated with an increased risk of heart failure and high risk of morbidity and mortality. Early detection of CTRCD appears critical for preventing long-term cardiovascular morbidity in cancer survivors. However, current clinical standards for the identification of CTRCD rely on assessments of cardiac function in the resting state. This provides incomplete information about the heart's reserve capacity and may reduce the sensitivity for detecting sub-clinical myocardial injury. Advances in non-invasive imaging techniques have enabled cardiac function to be quantified during exercise thereby providing a novel means of identifying early cardiac dysfunction that has proved useful in several cardiovascular pathologies. The purpose of this narrative review is (1) to discuss the different non-invasive imaging techniques that can be used for quantifying different aspects of cardiac reserve; (2) discuss the findings from studies of cancer patients that have measured cardiac reserve as a marker of CTRCD; and (3) highlight the future directions important knowledge gaps that need to be addressed for cardiac reserve to be effectively integrated into routine monitoring for cancer patients exposed to cardiotoxic therapies.
PMID: 32211421 [PubMed]
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Correlation of HER2 codon 655 polymorphism with cardiotoxicity risk in Chinese HER2-positive breast cancer patients undergoing epirubicin/cyclophosphamide followed by docetaxel plus trastuzumab adjuvant chemotherapy.
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Correlation of HER2 codon 655 polymorphism with cardiotoxicity risk in Chinese HER2-positive breast cancer patients undergoing epirubicin/cyclophosphamide followed by docetaxel plus trastuzumab adjuvant chemotherapy.
Int J Clin Exp Pathol. 2020;13(2):286-294
Authors: Tan L, Su X, Li X, Li H, Hu B
Abstract
This study aimed to determine the correlation of human epidermal growth factor receptor 2 (HER2) codon 655 A>G polymorphism with cardiotoxicity risk in HER2-positive breast cancer patients undergoing epirubicin/cyclophosphamide followed by docetaxel plus trastuzumab (EC-D-T) adjuvant chemotherapy. Peripheral blood from 91 HER2-positive breast cancer patients was collected for HER2 codon 655 A>G genotyping before initiation of EC-D-T adjuvant chemotherapy (M0). Left ventricular ejection fraction (LVEF), cardiac troponin I (cTnI), and N terminal pro B type natriuretic peptide (NT-proBNP) levels were measured at M0, M3, M6, M9, M12 and M15. Cardiotoxicity was assessed at each time point after initiation of adjuvant chemotherapy. There were 77 cumulative cardiotoxicity events, and totally 26 patients had cardiotoxicity with incidence of 28.6% during the study. LVEF was decreased, cTnI was increased but NT-proBNP was similar in cardiotoxicity patients compared to non-cardiotoxicity patients at each time point. Additionally, the prevalences of HER2 codon 655 AA, AG, GG genotypes were 70.3%, 26.4% and 3.3% respectively. LVEF was lower at each time point after initiation of adjuvant chemotherapy and incidence of cardiotoxicity was increased in patients with HER2 codon 655 AG/GG genotypes compared to those with HER2 codon 655 AA genotype. Logistic regression analysis further revealed that HER2 codon 655 A>G, smoking and baseline cTnI were independent predictive factors for increased cardiotoxicity risk. In conclusion, HER2 codon 655 A>G was an independent predictive factor for increased cardiotoxicity risk in HER2-positive breast cancer patients undergoing EC-D-T adjuvant chemotherapy.
PMID: 32211111 [PubMed]
28 March 2020
14:21
Cardiotoxicity News
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Mitochondrial Determinants of Doxorubicin-Induced Cardiomyopathy.
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Mitochondrial Determinants of Doxorubicin-Induced Cardiomyopathy.
Circ Res. 2020 Mar 27;126(7):926-941
Authors: Wallace KB, Sardão VA, Oliveira PJ
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