Generic placeholder image

Current Hypertension Reviews

Editor-in-Chief

ISSN (Print): 1573-4021
ISSN (Online): 1875-6506

General Review Article

Arterial Hypertension and Multiple Myeloma: Physiopathology and Cardiovascular Risk and ‘Practical’ Indications in Patients Receiving Carfilzomib

Author(s): Alberto Milan*, Giulia Bruno, Ilaria Maffei, Andrea Iannaccone, Agnese Ravera, Domenica Schiavone and Franco Veglio

Volume 15, Issue 1, 2019

Page: [47 - 53] Pages: 7

DOI: 10.2174/1573402114666180611110547

Price: $65

Abstract

The introduction of carfilzomib in the treatment of relapsing and refractory multiple myeloma has allowed a significant increase in survival. The most frequent adverse effect of Carfilzomib treatment is arterial hypertension, even though the exact physiopathological mechanism are still unclear. MM patients, on the other hand, often present significant cardiovascular risk factors and comorbidities. Uncontrolled hypertension is frequently the cause of cardiovascular complications. It has been estimated that up to 50% of subjects in the general population are unaware of their hypertensive condition and only half of those who are aware of this risk factor present good control of blood pressure. Although the management of arterial hypertension is clearly important in reducing the risk of cardiovascular events, and is well described by the current guidelines, no clear indications are provided on how to approach and treat specifically MM patients undergoing treatment with proteasome inhibitors. The aim of our work is to summarize a practical approach to the stratification of cardiovascular risk of hypertensive in patients who are candidates for or actively treated with carfilzomib for refractory multiple myeloma (MMR). MM patients eligible for carfilzomib treatment should preliminary undergo a careful cardiovascular risk stratification. Perspective studies will help to better identify the specific risk factors that should be considered and treated in these patients.

Keywords: Arterial hypertension, cardiovascular toxicity, carfilzomib, multiple myeloma, cardiovascular risk.

Graphical Abstract

[1]
Raab MS, Podar K, Breitkreutz I, Richardson PG, Anderson KC. Multiple myeloma. Lancet 2009; 374(9686): 324-39.
[2]
Dimopoulos MA, Moreau P, Palumbo A, et al. Carfilzomib and dexamethasone versus bortezomib and dexamethasone for patients with relapsed or refractory multiple myeloma (ENDEAVOR): A randomised, phase 3, open-label, multicentre study. Lancet Oncol 2016; 17(1): 27-38.
[3]
Herrmann J, Yang EH, Iliescu CA, et al. Vascular toxicities of cancer therapies: The old and the new - an evolving avenue. Circulation 2016; 133(13): 1272-89.
[4]
Stewart AK, Rajkumar SV, Dimopoulos MA, et al. Carfilzomib, lenalidomide, and dexamethasone for relapsed multiple myeloma. N Engl J Med 2015; 372(2): 142-52.
[5]
Chari A, Mezzi K, Zhu S, Werther W, Felici D, Lyon AR. Incidence and risk of hypertension in patients newly treated for multiple myeloma: A retrospective cohort study. BMC Cancer 2016; 16(1): 912.
[6]
Kistler KD, Kalman J, Sahni G, et al. Incidence and risk of cardiac events in patients with previously treated multiple myeloma versus matched patients without multiple myeloma: An observational, retrospective, cohort study. Clin Lymphoma Myeloma Leuk 2017; 17(2): 89-96.e3.
[7]
Groll M, Huber R. Inhibitors of the eukaryotic 20S proteasome core particle: A structural approach. Biochim Biophys Acta 2004; 1695(1-3): 33-44.
[8]
Crawford LJ, Irvine AE. Targeting the ubiquitin proteasome system in haematological malignancies. Blood Rev 2013; 27(6): 297-304.
[9]
Stangl K, Stangl V. The ubiquitin-proteasome pathway and endothelial (dys)function. Cardiovasc Res 2010; 85(2): 281-90.
[10]
Wang Z, Yang J, Kirk C, et al. Clinical pharmacokinetics, metabolism, and drug-drug interaction of carfilzomib. Drug Metab Dispos 2013; 41(1): 230-7.
[11]
Demo SD, Kirk CJ, Aujay MA, et al. Antitumor activity of PR-171, a novel irreversible inhibitor of the proteasome. Cancer Res 2007; 67(13): 6383-91.
[12]
Govers R, de Bree P, Rabelink TJ. Involvement of the proteasome in activation of endothelial nitric oxide synthase. Life Sci 2003; 73(17): 2225-36.
[13]
Chen-Scarabelli C, Corsetti G, Pasini E, et al. Spasmogenic effects of the proteasome inhibitor carfilzomib on coronary resistance, vascular tone and reactivity. EBioMedicine 2017; 21: 206-12.
[14]
Chen Y, Ooi M, Lim SF, et al. Thrombotic microangiopathy during carfilzomib use: Case series in Singapore. Blood Cancer J 2016; 6(7): e450.
[15]
Bringhen S, De Wit E, Dimopoulos MA. New agents in multiple myeloma: An examination of safety profiles. Clin Lymphoma Myeloma Leuk 2017; 17(7): 391-407.e5.
[16]
Rosenthal A, Luthi J, Belohlavek M, et al. Carfilzomib and the cardiorenal system in myeloma: An endothelial effect? Blood Cancer J 2016; 6: e384.
[17]
Dimopoulos MA, Roussou M, Gavriatopoulou M, et al. Cardiac and renal complications of carfilzomib in patients with multiple myeloma. Blood Adv 2017; 1(7): 449-54.
[18]
Ranek MJ, Zheng H, Huang W, et al. Genetically induced moderate inhibition of 20S proteasomes in cardiomyocytes facilitates heart failure in mice during systolic overload. J Mol Cell Cardiol 2015; 85: 273-81.
[19]
Herrmann J, Saguner AM, Versari D, et al. Chronic proteasome inhibition contributes to coronary atherosclerosis. Circ Res 2007; 101(9): 865-74.
[20]
Spur EM, Althof N, Respondek D, et al. Inhibition of chymotryptic-like standard proteasome activity exacerbates doxorubicin-induced cytotoxicity in primary cardiomyocytes. Toxicology 2016; 353-354: 34-47.
[21]
Zamorano JL, Lancellotti P, Rodriguez Muñoz D, et al. 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; 37(36): 2768-801.
[22]
Mancia G, Fagard R, Narkiewicz K. et al. 2013 ESH/ESC Guidelines for the management of arterial hypertension: The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Eur Heart J 2013; 31(10): 1925-38.
[23]
Conroy RM, Pyörälä K, Fitzgerald AP, et al. Estimation of ten-year risk of fatal cardiovascular disease in Europe: The SCORE project. Eur Heart J 2003; 24(11): 987-1003.
[24]
Lopez-Fernandez T. Martín García A2, Santaballa Beltrán A, et al. Cardio-onco-hematology in clinical practice. Position paper and recommendations. Rev Esp Cardiol (Engl Ed), 2017; 70(6): 474-86 In:
[25]
Mozos I, Borzak G, Caraba A, Mihaescu R. Arterial stiffness in hematologic malignancies. OncoTargets Ther 2017; 10: 1381-8.
[26]
Marwick TH, Gillebert TC, Aurigemma G, et al. Recommendations on the use of echocardiography in adult hypertension: A report from the European Association of Cardiovascular Imaging (EACVI) and the American Society of Echocardiography (ASE)dagger. Eur Heart J Cardiovasc Imaging 2015; 16(6): 577-605.
[27]
Perrone-Filardi P, Coca A, Galderisi M, et al. Non-invasive cardiovascular imaging for evaluating subclinical target organ damage in hypertensive patients: A consensus paper from the European Association of Cardiovascular Imaging (EACVI), the European Society of Cardiology Council on Hypertension, and the European Society of Hypertension (ESH). Eur Heart J Cardiovasc Imaging 2017; 18(9): 945-60.
[28]
Reboldi G, Angeli F, de Simone G, Staessen JA, Verdecchia P. Cardio-Sis Investigators. Tight versus standard blood pressure control in patients with hypertension with and without cardiovascular disease. Hypertension 2014; 63(3): 475-82.
[29]
Lang RM, Badano LP, Mor-Avi V, 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; 28(1): 1-39 e14.
[30]
Thavendiranathan P, Grant AD, Negishi T, Plana JC, Popović ZB, Marwick TH. Reproducibility of echocardiographic techniques for sequential assessment of left ventricular ejection fraction and volumes: Application to patients undergoing cancer chemotherapy. J Am Coll Cardiol 2013; 61(1): 77-84.
[31]
Gong FF, Campbell DJ, Prior DL. Noninvasive cardiac imaging and the prediction of heart failure progression in preclinical stage A/B subjects. JACC 2017; 10(12): 1504-19.
[32]
Yang H, Marwick TH, Fukuda N, et al. Improvement in strain concordance between two major vendors after the strain standardization initiative. J Am Soc Echocardiogr 2015; 28(6): 642-8 e7.

Rights & Permissions Print Cite
© 2024 Bentham Science Publishers | Privacy Policy