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https://doi.org/10.15836/ccar2017.16

Kardiotoksičnost kao posljedica biološke terapije tumora

Ivo Darko Gabrić ; Klinički bolnički centar Sestre milosrdnice, Zagreb, Hrvatska

Puni tekst: hrvatski, pdf (243 KB) str. 16-22 preuzimanja: 105* citiraj
APA 6th Edition
Gabrić, I.D. (2017). Kardiotoksičnost kao posljedica biološke terapije tumora. Cardiologia Croatica, 12 (1-2), 16-22. https://doi.org/10.15836/ccar2017.16
MLA 8th Edition
Gabrić, Ivo Darko. "Kardiotoksičnost kao posljedica biološke terapije tumora." Cardiologia Croatica, vol. 12, br. 1-2, 2017, str. 16-22. https://doi.org/10.15836/ccar2017.16. Citirano 08.08.2020.
Chicago 17th Edition
Gabrić, Ivo Darko. "Kardiotoksičnost kao posljedica biološke terapije tumora." Cardiologia Croatica 12, br. 1-2 (2017): 16-22. https://doi.org/10.15836/ccar2017.16
Harvard
Gabrić, I.D. (2017). 'Kardiotoksičnost kao posljedica biološke terapije tumora', Cardiologia Croatica, 12(1-2), str. 16-22. https://doi.org/10.15836/ccar2017.16
Vancouver
Gabrić ID. Kardiotoksičnost kao posljedica biološke terapije tumora. Cardiologia Croatica [Internet]. 2017 [pristupljeno 08.08.2020.];12(1-2):16-22. https://doi.org/10.15836/ccar2017.16
IEEE
I.D. Gabrić, "Kardiotoksičnost kao posljedica biološke terapije tumora", Cardiologia Croatica, vol.12, br. 1-2, str. 16-22, 2017. [Online]. https://doi.org/10.15836/ccar2017.16
Puni tekst: engleski, pdf (243 KB) str. 16-22 preuzimanja: 237* citiraj
APA 6th Edition
Gabrić, I.D. (2017). Cardiotoxicity due to biological cancer therapy. Cardiologia Croatica, 12 (1-2), 16-22. https://doi.org/10.15836/ccar2017.16
MLA 8th Edition
Gabrić, Ivo Darko. "Cardiotoxicity due to biological cancer therapy." Cardiologia Croatica, vol. 12, br. 1-2, 2017, str. 16-22. https://doi.org/10.15836/ccar2017.16. Citirano 08.08.2020.
Chicago 17th Edition
Gabrić, Ivo Darko. "Cardiotoxicity due to biological cancer therapy." Cardiologia Croatica 12, br. 1-2 (2017): 16-22. https://doi.org/10.15836/ccar2017.16
Harvard
Gabrić, I.D. (2017). 'Cardiotoxicity due to biological cancer therapy', Cardiologia Croatica, 12(1-2), str. 16-22. https://doi.org/10.15836/ccar2017.16
Vancouver
Gabrić ID. Cardiotoxicity due to biological cancer therapy. Cardiologia Croatica [Internet]. 2017 [pristupljeno 08.08.2020.];12(1-2):16-22. https://doi.org/10.15836/ccar2017.16
IEEE
I.D. Gabrić, "Cardiotoxicity due to biological cancer therapy", Cardiologia Croatica, vol.12, br. 1-2, str. 16-22, 2017. [Online]. https://doi.org/10.15836/ccar2017.16

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Sažetak
Kardiotoksičnost je sve češća nuspojava onkološkog liječenja pa tako i novijih, bioloških ciljanih lijekova. Posebno razvijena monoklonska protutijela ili inhibitori tirozin-kinaze blokiraju bilo receptore HER-2 bilo VEGF bilo pak aktivnost Abl-kinaze. Međutim, time se ometaju i molekularni mehanzimi ključni za kardiovaskularno zdravlje. Anti-HER2 terapija najčešće uzrokuju reverzibilnu sistoličku disfunkciju lijevog ventrikula, a blokadom VEGF receptora razvija se arterijska hipertenzija i povećava sklonost tromboembolijskim incidentima. Ranim prepoznavanjem i liječenjem bolesnika u kojih se razvila kardiotoksičnost postiže se poboljšanje kliničkih ishoda i kvalitete života, a time je često moguće nastaviti specifično liječenja raka. Pri tome su ključni multidisciplinarni pristup kardiologa i onkologa te redovito kardiološko praćenje.

Ključne riječi
kardiotoksičnost; kardioonkologija; biološka terapija tumora; inhibitori tirozin-kinaze

Hrčak ID: 179870

URI
https://hrcak.srce.hr/179870

▼ Article Information



In the past 30 years, malignant disease mortality has been reduced, among other things, owing to advances in chemotherapeutic protocols. (1) However, prolonged survival frequently is achieved at the expense of damage to other organs including cardiovascular (CV) system. (2) Currently, CV diseases are the second leading cause of long-term morbidity and mortality among patients treated for carcinoma. (3) Both conventional chemotherapy and targeted biological therapy increase the risk of heart injury, left ventricular (LV) dysfunction and symptomatic heart failure (HF). (4) In addition, hypertensive reaction, vasospastic and/or thrombotic myocardial ischemia, rhythm and conductivity disorders may also occur. Some of these adverse effects are irreversible and cause progressive CV disease, whereas others cause only transient dysfunction without long-term sequels. (5) Predisposition to development of cardiotoxicity is multifactorial and is determined by the interaction of genetic and environmental factors. (6) Cardiotoxicity may manifest during or immediately after treatment (within days or weeks), or even long after completion of anti-cancer therapy. Some of the defined risk factors are for coronary artery disease or congestive HF positive family history, age, sex, arterial hypertension and dyslipidemia. An increased risk of cardiotoxicity has also been reported in patients with reduced systolic LV function and significant arrhythmias.

The ever-growing number of patients treated with chemotherapy and biological agents has resulted in the continuously increasing incidence of cardiotoxicity. (7) The extent of the problem is even greater taking into account that some of the patients have to take a combination of several cardiotoxic agents. (8) These unfavorable facts have pointed to the need of establishing cardio-oncologic teams and defining guidelines for follow up and treatment of these patients, such as those recently issued by the European Society of Cardiology in 2016. (9)

Tumor biological therapy with monoclonal antibodies or tyrosine kinase inhibitors (TKI) targets human epidermal growth factor 2 (HER2) receptors (e.g., trastuzumab, pertuzumab, etc.), vascular endothelial growth factor (VEGF) and VEGF receptors (e.g., bevacizumab, sunitinib, sorafenib, etc.), or Abl kinase activity (e.g., imatinib, nilotinib, dasatinib, etc.) (10) (Table 1). However, these therapies also impair molecular mechanisms that are crucial for CV health, resulting in cardiotoxicity. The aim of the article is to point to the potential CV side effects associated with particular biological drugs and antibodies used in the treatment of carcinoma in adult patients.

TABLE 1 Factors associated with risk of cardiotoxicity and incidence of left ventricular dysfunction following anti-HER2 compounds and VEGF inhibitors. Modified from Zamorano JL, Lancellotti P, Rodriguez Muńoz D, Aboyans V, Asteggiano R, Galderisi M, et al. Eur Heart J. 2016 Sep 21;37(36):2768-2801.
AgentIncidence of left ventricular dysfunction (%)Risk factors
Anti-HER2 compounds
AntibodiesPrevious or concomitant anthracycline treatment (short time between anthracycline and anti-HER2 treatment)
Age (>65 years)
High body mass index >30 kg/mg2
Previous left ventricular dysfunction
Arterial hypertension
Previous radiation therapy
Trastuzumab1.7-13
Pertuzumab0.7-1.2
Trastuzumab emtansine (T-DM1)1.7
Tyrosine kinase inhibitors
Lapatinib0.2-1.5
VEGF inhibitors
AntibodiesPre-existing heart failure, significant coronary artery disease or left side valvular heart disease (e.g. mitral regurgitation), chronic ischemic cardiomyopathy
Previous anthracycline
Bevacizumab1.6-4
Ramucirumab
Tyrosine kinase inhibitors
Sunitimib2.7-19Arterial hypertension
Pre-existing cardiac disease
Pazopanib7-11
Axitinib
Neratinib
Sorafenib4-8
Dasatinib2-4

HER2 = human epidermal growth factor receptor 2; VEGF = vascular endothelial growth factor.

Trastuzumab

Trastuzumab is a humanized monoclonal antibody that targets human epidermal HER2 receptor by inhibiting transfer of the signal induced by HER2 activation. (11, 12) In breast cancer patients with HER2 receptor overexpression, HER2 receptor blockade was found to improve survival and time of remission significantly, and has been used in the standard treatment protocol for metastatic or localized disease. (13, 14) The major side effect of trastuzumab therapy is the occurrence of cardiotoxicity independent of the drug cumulative dose, mostly manifesting as asymptomatic reduction of the left ventricular ejection fraction (LVEF), and less frequently as clinically symptomatic HF. (15) Unlike irreversible (type I) anthracycline induced damage, trastuzumab therapy results in reversible cardiac stunning in most cases, which resolves within 30 days (type II) in 65%-70% of patients. (16) However, in some patients it may progress to irreversible dilated cardiomyopathy. In large studies, the incidence of cardiotoxicity ranges from 8% to 13%, and similar data have also been reported from meta-analyses of randomized controlled studies, where the incidence of cardiotoxicity was around 10%. (17, 18) It appears that cardiotoxicity is mostly caused by direct cardiac HER2 protein blockade, however, other mechanisms cannot be excluded. (19) Risk factors for development of cardiotoxicity are pre-existent arterial hypertension, low LVEF at initiation of trastuzumab therapy, high body mass index (>25), coronary and valvular disease, and previous treatment with high anthracycline doses. (20, 21)

The incidence and type of cardiotoxicity of other anti-HER2 biological agents (pertuzumab and trastuzumab-emtansine) generally are similar to those associated with trastuzumab. (22) In recent protocols of neoadjuvant therapy for breast cancer and in the treatment of metastatic gastric cancer, trastuzumab is combined with other anti-HER2 drugs. According to data available so far, these combinations did not result in additional aggravation of CV side effects. (23) Yet, results of a large prospective randomized study (Aphinity) investigating a combination of pertuzumab and trastuzumab as adjuvant therapy are expecting to shed more light on the issue. (24) Another two studies of neoadjuvant therapy (Neosphere and Tryphaena) showed better results in women with breast cancer treated with chemotherapy and dual HER2 blockade (pertuzumab and trastuzumab) as compared with patients treated with chemotherapy and trastuzumab alone. In the Tryphaena study, the primary endpoint of CV safety with a low incidence of symptomatic and asymptomatic systolic LV dysfunction was achieved in all study groups. (25) Finally, it should be noted that the benefit of trastuzumab in terms of reducing the risk of the underlying malignant disease outweighs the increased risk of cardiotoxicity.

Bevacizumab

Bevacizumab is a humanized anti-VEGF antibody that is used in the treatment of patients with metastatic colon and breast cancer, non-small-cell lung carcinoma, renal cell and ovarian carcinoma, and glioblastoma multiforme. Bevacizumab cardiotoxicity generally manifests in the form of uncontrolled arterial hypertension. The most severe grade 3 and 4 arterial hypertension occurs in 9.2% of patients, with rare cases of hypertensive crisis including encephalopathy or intracranial hemorrhage. Hypertension may develop at any time during bevacizumab therapy, with some data suggesting an association of individual dose size and unfavorable outcomes. (26, 27) The mechanism of HF that occurs in 1.7%-3.0% of cases may be related to uncontrolled hypertension and inhibition of VEGF signaling. (28)

Fatal thromboembolic events such as myocardial infarction, ischemic stroke and pulmonary embolism may occur in 3.8% of patients on bevacizumab therapy. Thromboembolic events can occur at any time from therapy initiation. The mechanism of their occurrence remains obscure and does not appear to be related to either individual or cumulative drug dose. The risk is higher in elderly patients (age ≥65) and in those with a history of arterial thromboembolic event. (29) It is speculated that these events are induced by the antitumor therapy effect on the coagulation cascade with vascular intimal and endothelial cell continuity impairment, while anti-VEGF therapy reduces nitric oxide and prostacyclin levels, thus favoring development of thromboembolism. (30)

Tyrosine Kinase Inhibitors

Tyrosine kinase inhibitors can also be classified into HER2 pathway blockers such as lapatinib, and specific (axitinib) or nonspecific (sunitinib, sorafenib, vandetanib and pazopanib) VEGF pathway inhibitors.

Lapatinib is a TKI efficacious in the treatment of HER2p95 (aberrant form of HER2) positive breast cancer. It appears that lapatinib therapy is associated with a low prevalence of HF or other adverse CV effects. (31) In clinical studies, LVEF reduced by at least 20% was recorded in only 1.6% and symptomatic HF in 0.2% of patients. The prevalence of cardiotoxic complications was increased in patients having previously received anthracyclines or trastuzumab (32). In addition, reversible QT interval prolongation was recorded in some patients. In these patients, regular electrocardiographic (ECG) follow up along with dose adjustment or therapy discontinuation is recommended.

Sorafenib is a TKI used in the treatment of advanced renal cell and hepatocellular carcinoma, and advanced radioactive iodine-refractory thyroid carcinoma. Hypertension is the major side effect of sorafenib therapy, recorded in 17%-43% of cases. (33) Sorafenib therapy has been reported to be associated with development of acute coronary syndrome and of myocardial infarction in 2.9% of patients. Sorafenib toxicity can be explained by the inhibition of RAF1, which inhibits proapoptotic kinases. The occurrence of hypertension can be attributed to the VEGF receptor inhibition, which leads to reduced capillary permeability and increased volume load. (34)

Sunitinib is a TKI used in the treatment of renal cell carcinoma and gastrointestinal stromal tumor. Sunitinib acts on tumor cell proliferation and tumor angiogenesis. (35) Hypertension develops in a substantial proportion of sunitinib treated patients (47%), while 11% of patients experience CV events including acute myocardial infarction and HF. Asymptomatic LVEF reduction by at least 10% was recorded in nearly 28% of patients. (36) The mean time to HF development is 22-27 days; however, it appears to respond well to medical therapy. High-risk patients are those with a history of coronary disease, HF, LV dysfunction and previous anthracycline therapy. The true mechanism of cardiotoxicity remains unknown; however, it is most likely induced by inhibition of a series of growth factor receptors in cardiomyocytes. (37)

Ipilimumab, Nivolumab and Pembrolizumab

Antibodies for immune response modulation have proved efficacious in the treatment of various tumor types including melanoma (anti-CTLA-4 and PD-1), non-small-cell lung carcinoma and renal cell carcinoma. However, this therapy leads to a number of immune mediated side effects, so far including occasional cases of myocarditis and/or pericarditis. (38)

Follow up in Patients on Antitumor Biological Therapy

Thorough CV evaluation must be performed in all oncologic patients planned to be administered biological therapy with potentially cardiotoxic agents; yet CV complications will only develop in a minor proportion of patients. Therefore, it is of utmost importance to early identify and follow-up patients at high risk. All patients should undergo clinical examination and ECG before and during treatment. Detecting any ECG abnormalities such as tachycardia at rest, ST-T segment changes, conductivity impairment, QT-interval prolongation or arrhythmia may point to cardiotoxicity. Transthoracic echocardiography is the main diagnostic method for LV function assessment; it is recommended to perform it prior to therapy initiation, then at 3-month intervals, and upon completion of cardiotoxic therapy. Evaluation of LV function is crucial in anti-HER therapy since the majority of patients had received anthracyclines prior to targeted therapy introduction; it is of utmost importance to assess LV function after previous chemotherapy and before targeted therapy initiation. (39) LV function is assessed by two-dimensional (2D, Simson) method or by 3D echocardiography if available. (40) Other novel echocardiography techniques such as contrast echocardiography and stress echocardiography are indicated for assessment of borderline standard echocardiography findings. Tissue Doppler imaging and strain analysis are useful in early detection of LV dysfunction and should be used whenever possible. Assessment of the global longitudinal systolic strain is highly useful, as its reduction to less than 15% is an early sign of systolic dysfunction. (41) Therapy is suspended or temporarily discontinued in case of LVEF 15%-16% reduction from baseline or 10%-15% reduction from normal. Discontinuation of targeted therapy is recommended if LVEF fails to recover within 4 weeks. Monitoring cardiac biochemical markers (troponin and natriuretic peptides) during cardiotoxic therapy can help detect an early myocardial lesion. However, elevated levels of biochemical markers can only identify patients at high risk of cardiotoxicity because for the time being, there is no clear evidence that oncologic therapy should be suspended or discontinued in case of their pathologic finding. (42)

Treatment of anti-HER2 therapy induced cardiotoxicity does not differ from treatment of other HF patients; generally, angiotensin-converting enzyme inhibitors (ACEi) and beta-blockers are used, along with diuretics in case of symptomatic HF. (43) In patients administered VEGF signal pathway blockers, careful assessment of CV risk factors is required at therapy initiation, followed by regular blood pressure follow up and early introduction of antihypertensive therapy. In most patients, anti-VEGF therapy can be continued upon proper blood pressure regulation. (44)

Conclusion

Oncologic patients receiving targeted biological therapy associated with a high risk of cardiotoxicity require multidisciplinary approach and regular cardiologic follow up for timely recognition and appropriate treatment of CV side effects. Such an approach results in more favorable clinical outcomes and patient quality of life, along with optimal continuation of specific oncologic treatment if possible.

Literature

1 

Howlader N, Ries LA, Mariotto AB, Reichman ME, Ruhl J, Cronin KA. Improved estimates of cancer-specific survival rates from population-based data. J Natl Cancer Inst. 2010;102:1584–98. DOI: http://dx.doi.org/10.1093/jnci/djq366 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/20937991

2 

Dent S, Liu P, Brezden-Masley C, Lenihan D. Cancer and Cardiovascular Disease: The Complex Labyrinth. J Oncol. 2015;2015:516450. DOI: http://dx.doi.org/10.1155/2015/516450 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/26345724

3 

Bodai BI, Tuso P. Breast cancer survivorship: a comprehensive review of long-term medical issues and lifestyle recommendations. Perm J. 2015;19(2):48–79. DOI: http://dx.doi.org/10.7812/TPP/14-241 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/25902343

4 

Bowles EJ, Wellman R, Feigelson HS, Onitilo AA, Freedman AN, Delate T, et al. Pharmacovigilance Study Team. Risk of heart failure in breast cancer patients after anthracycline and trastuzumab treatment: a retrospective cohort study. J Natl Cancer Inst. 2012;104:1293–305. DOI: http://dx.doi.org/10.1093/jnci/djs317 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/22949432

5 

Aleman BM, Moser EC, Nuver J, Suter TM, Maraldo MV, Specht L, et al. Cardiovascular disease after cancer therapy. EJC Suppl. 2014;12:18–28. DOI: http://dx.doi.org/10.1016/j.ejcsup.2014.03.002 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/26217163

6 

Deng S, Wojnowski L. Genotyping the risk of anthracycline-induced cardiotoxicity. Cardiovasc Toxicol. 2007;7(2):129–34. DOI: http://dx.doi.org/10.1007/s12012-007-0024-2 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/17652817

7 

Hong RA, Iimura T, Sumida KN, Eager RM. Cardio-oncology/oncocardiology. Clin Cardiol. 2010 Dec;33(12):733–7. DOI: http://dx.doi.org/10.1002/clc.20823 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/21184556

8 

Raschi E, Vasina V, Ursino MG, Boriani G, Martoni A, De Ponti F. Anticancer drugs and cardiotoxicity: insights and perspectives in the era of targeted therapy. Pharmacol Ther. 2010 Feb;125(2):196–218. DOI: http://dx.doi.org/10.1016/j.pharmthera.2009.10.002 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/19874849

9 

Zamorano JL, Lancellotti P, Rodriguez Muńoz D, Aboyans V, Asteggiano R, Galderisi M, et al. Authors/Task Force Members. ESC Committee for Practice Guidelines (CPG). 2016 ESC Position Paper on cancer treatments and cardiovascular toxicity developed under the auspices of the ESC Committee for Practice Guidelines: The Task Force for cancer treatments and cardiovascular toxicity of the European Society of Cardiology (ESC). Eur Heart J. 2016 Sep 21;37(36):2768–801. DOI: http://dx.doi.org/10.1093/eurheartj/ehw211 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/27567406

10 

Force T, Kolaja KL. Cardiotoxicity of kinase inhibitors: the prediction and translation of preclinical models to clinical outcomes. Nat Rev Drug Discov. 2011 Feb;10(2):111–26. DOI: http://dx.doi.org/10.1038/nrd3252 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/21283106

11 

Zhang H, Wang Q, Montone KT, Peavey JE, Drebin JA, Greene MI, et al. Shared antigenic epitopes and pathobiological functions of anti-p185(her2/neu) monoclonal antibodies. Exp Mol Pathol. 1999 Sep;67(1):15–25. DOI: http://dx.doi.org/10.1006/exmp.1999.2266 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/10493889

12 

Sliwkowski MX, Lofgren JA, Lewis GD, Hotaling TE, Fendly BM, Fox JA. Nonclinical studies addressing the mechanism of action of trastuzumab (Herceptin). Semin Oncol. 1999 Aug;26(4 Suppl 12):60-70. PubMed: https://www.ncbi.nlm.nih.gov/pubmed/10482195

13 

Paik S, Bryant J, Tan-Chiu E, Yothers G, Park C, Wickerham DL, et al. HER2 and choice of adjuvant chemotherapy for invasive breast cancer: National Surgical Adjuvant Breast and Bowel Project protocol B-15. J Natl Cancer Inst. 2000 Dec 20;92(24):1991–8. DOI: http://dx.doi.org/10.1093/jnci/92.24.1991 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/11121461

14 

Thor AD, Berry DA, Budman DR, Muss HB, Kute T, Henderson IC, et al. erbB-2, p53, and efficacy of adjuvant therapy in lymph node-positive breast cancer. J Natl Cancer Inst. 1998;90(18):1346–60. DOI: http://dx.doi.org/10.1093/jnci/90.18.1346 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/9747866

15 

Perez EA, Rodeheffer R. Clinical cardiac tolerability of trastuzumab. J Clin Oncol. 2004 Jan 15;22(2):322–9. DOI: http://dx.doi.org/10.1200/JCO.2004.01.120 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/14722042

16 

Ewer MS, Vooletich MT, Durand JB, Woods ML, Davis JR, Valero V, et al. Reversibility of trastuzumab-related cardiotoxicity: new insights based on clinical course and response to medical treatment. J Clin Oncol. 2005 Nov 1;23(31):7820–6. DOI: http://dx.doi.org/10.1200/JCO.2005.13.300 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/16258084

17 

Viani GA, Afonso SL, Stefano EJ, De Fendi LI, Soares FV. Adjuvant trastuzumab in the treatment of her-2-positive early breast cancer: a meta-analysis of published randomized trials. BMC Cancer. 2007 Aug 8;7:153. DOI: http://dx.doi.org/10.1186/1471-2407-7-153 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/17686164

18 

Piccart-Gebhart MJ, Procter M, Leyland-Jones B, Goldhirsch A, Untch M, Smith I, et al. Herceptin Adjuvant (HERA) Trial Study Team. Trastuzumab after adjuvant chemotherapy in HER2-positive breast cancer. N Engl J Med. 2005 Oct 20;353(16):1659–72. DOI: http://dx.doi.org/10.1056/NEJMoa052306 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/16236737

19 

Keefe DL. Trastuzumab-associated cardiotoxicity. Cancer. 2002 Oct 1;95(7):1592–600. DOI: http://dx.doi.org/10.1002/cncr.10854 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/12237930

20 

Gabrić ID, Pintarić H, Vazdar LJ, Štefanović M, Jazvić M, Soldić Ž, et al. Influence of Angiotensin Conversion Enzyme Gene Polymorphism on Cardiotoxicity Caused by Immunotherapy with Trastuzumab. Circulation. 2012;126:A16961. Available at http://circ.ahajournals.org/content/126/Suppl_21/A16961

21 

Gabrić ID, Vazdar LJ, Pintarić H, Planinc D, Stefanovic M, Trbusic M, et al. Risk factors for the occurrence and irreversibility of cardiotoxicity caused by trastuzumab therapy. Eur J Heart Fail. 2015;17 Suppl. 1:26. Available at http://onlinelibrary.wiley.com/doi/10.1002/ejhf.277/epdf

22 

Piccart-Gebhart M, Holmes E, Baselga J, de Azambuja E, Dueck AC, Viale G, et al. Adjuvant Lapatinib and Trastuzumab for Early Human Epidermal Growth Factor Receptor 2-Positive Breast Cancer: Results From the Randomized Phase III Adjuvant Lapatinib and/or Trastuzumab Treatment Optimization Trial. J Clin Oncol. 2016 Apr 1;34(10):1034–42. DOI: http://dx.doi.org/10.1200/JCO.2015.62.1797 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/26598744

23 

Gianni L, Pienkowski T, Im YH, Roman L, Tseng LM, Liu MC, et al. Efficacy and safety of neoadjuvant pertuzumab and trastuzumab in women with locally advanced, inflammatory, or early HER2positive breast cancer (NeoSphere): a randomised multicentre, open-label, phase 2 trial. Lancet Oncol. 2012 Jan;13(1):25–32. DOI: http://dx.doi.org/10.1016/S1470-2045(11)70336-9 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/22153890

24 

Reynolds K, Sarangi S, Bardia A, Dizon DS. Precision medicine and personalized breast cancer: combination pertuzumab therapy. Pharmgenomics Pers Med. 2014 Mar 20;7:95–105. DOI: http://dx.doi.org/10.2147/PGPM.S37100 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/24715764

25 

Sevcikova K, Vertakova-Krakovska B, Spanik S. Neoadjuvant Treatment in Patients with HER2-Positive Breast Cancer. ISRN Oncol. 2013 May 23;2013:362467. DOI: http://dx.doi.org/10.1155/2013/362467 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/23762609

26 

Scartozzi M, Galizia E, Chiorrini S, Giampieri R, Berardi R, Pierantoni C, et al. Arterial hypertension correlates with clinical outcome in colorectal cancer patients treated with first-line bevacizumab. Ann Oncol. 2009 Feb;20(2):227–30. DOI: http://dx.doi.org/10.1093/annonc/mdn637 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/18842611

27 

Chen J, Lu Y, Zheng Y. Incidence and risk of hypertension with bevacizumab in non-small-cell lung cancer patients: a meta-analysis of randomized controlled trials. Drug Des Devel Ther. 2015 Aug 18;9:4751–60. DOI: http://dx.doi.org/10.2147/DDDT.S87258 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/26316712

28 

Vaklavas C, Lenihan D, Kurzrock R, Tsimberidou AM. Antivascular endothelial growth factor therapies and cardiovascular toxicity: what are the important clinical markers to target? Oncologist. 2010;15(2):130–41. DOI: http://dx.doi.org/10.1634/theoncologist.2009-0252 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/20139170

29 

Kamba T, McDonald DM. Mechanisms of adverse effects of anti-VEGF therapy for cancer. Br J Cancer. 2007 Jun 18;96(12):1788–95. DOI: http://dx.doi.org/10.1038/sj.bjc.6603813 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/17519900

30 

Dincer M, Altundag K. Angiotensin-converting enzyme inhibitors for bevacizumab-induced hypertension. Ann Pharmacother. 2006 Dec;40(12):2278–9. DOI: http://dx.doi.org/10.1345/aph.1H244 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/17105834

31 

Orphanos GS, Ioannidis GN, Ardavanis AG. Cardiotoxicity induced by tyrosine kinase inhibitors. Acta Oncol. 2009;48(7):964–70. DOI: http://dx.doi.org/10.1080/02841860903229124 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/19734999

32 

Perez EA, Koehler M, Byrne J, Preston AJ, Rappold E, Ewer MS. Cardiac safety of lapatinib: pooled analysis of 3689 patients enrolled in clinical trials. Mayo Clin Proc. 2008 Jun;83(6):679–86. DOI: http://dx.doi.org/10.1016/S0025-6196(11)60896-3 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/18533085

33 

Escudier B, Eisen T, Stadler WM, Szczylik C, Oudard S, Siebels M, et al. TARGET Study Group. Sorafenib in advanced clear-cell renal-cell carcinoma. N Engl J Med. 2007 Jan 11;356(2):125–34. DOI: http://dx.doi.org/10.1056/NEJMoa060655 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/17215530

34 

Shiojima I, Sato K, Izumiya Y, Schiekofer S, Ito M, Liao R, et al. Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure. J Clin Invest. 2005 Aug;115(8):2108–18. DOI: http://dx.doi.org/10.1172/JCI24682 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/16075055

35 

Faivre S, Demetri G, Sargent W, Raymond E. Molecular basis for sunitinib efficacy and future clinical development. Nat Rev Drug Discov. 2007 Sep;6(9):734–45. DOI: http://dx.doi.org/10.1038/nrd2380 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/17690708

36 

Chu TF, Rupnick MA, Kerkela R, Dallabrida SM, Zurakowski D, Nguyen L, et al. Cardiotoxicity associated with tyrosine kinase inhibitor sunitinib. Lancet. 2007 Dec 15;370(9604):2011–9. DOI: http://dx.doi.org/10.1016/S0140-6736(07)61865-0 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/18083403

37 

Force T, Krause DS, Van Etten RA. Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition. Nat Rev Cancer. 2007 May;7(5):332–44. DOI: http://dx.doi.org/10.1038/nrc2106 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/17457301

38 

Heinzerling L, Ott PA, Hodi FS, Husain AN, Tajmir-Riahi A, Tawbi H, et al. Cardiotoxicity associated with CTLA4 and PD1 blocking immunotherapy. J Immunother Cancer. 2016 Aug 16;4:50. DOI: http://dx.doi.org/10.1186/s40425-016-0152-y PubMed: http://www.ncbi.nlm.nih.gov/pubmed/27532025

39 

Plana JC, Galderisi M, Barac A, Ewer MS, Ky B, Scherrer-Crosbie M, et al. Expert consensus for multimodality imaging evaluation of adult patients during and after cancer therapy: a report from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging. 2014 Oct;15(10):1063–93. DOI: http://dx.doi.org/10.1093/ehjci/jeu192 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/25239940

40 

Lang RM, Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015 Jan;28(1):1–39.e14. DOI: http://dx.doi.org/10.1016/j.echo.2014.10.003 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/25559473

41 

Negishi K, Negishi T, Hare JL, Haluska BA, Plana JC, Marwick TH. Independent and incremental value of deformation indices for prediction of trastuzumab-induced cardiotoxicity. J Am Soc Echocardiogr. 2013 May;26(5):493–8. DOI: http://dx.doi.org/10.1016/j.echo.2013.02.008 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/23562088

42 

Cardinale D, Sandri MT, Colombo A, Colombo N, Boeri M, Lamantia G, et al. Prognostic value of troponin I in cardiac risk stratification of cancer patients undergoing high-dose chemotherapy. Circulation. 2004 Jun 8;109(22):2749–54. DOI: http://dx.doi.org/10.1161/01.CIR.0000130926.51766.CC PubMed: http://www.ncbi.nlm.nih.gov/pubmed/15148277

43 

Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG, et al. American College of Cardiology. American Heart Association Task Force on Practice Guidelines; American College of Chest Physicians; International Society for Heart and Lung Transplantation; Heart Rhythm Society. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society. Circulation. 2005 Sep 20;112(12):e154–235. DOI: http://dx.doi.org/10.1161/CIRCULATIONAHA.105.167586 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/16160202

44 

Kabbinavar FF, Schulz J, McCleod M, Patel T, Hamm JT, Hecht JR, et al. Addition of bevacizumab to bolus fluorouracil and leucovorin in first-line metastatic colorectal cancer: results of a randomized phase II trial. J Clin Oncol. 2005 Jun 1;23(16):3697–705. DOI: http://dx.doi.org/10.1200/JCO.2005.05.112 PubMed: http://www.ncbi.nlm.nih.gov/pubmed/15738537


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