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2013 | 3 | 3 | 149-162; 163-176
Article title

Leczenie celowane przewlekłej białaczki szpikowej a układ sercowo-naczyniowy

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EN
Targeted therapies for chronic myeloid leukemia and cardiovascular system
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PL EN
Abstracts
EN
Morbidity of chronic myeloid leukemia is recorded in elderly population, in patients with coexisting significant risk factors for atherosclerosis and heart diseases. Molecularly targeted therapy, imatinib, dasatinib and nilotinib, improve significantly the prognosis. However, the similar molecular targets in the form of different kinases are essential for cardiovascular system and blocking their pathways may have adverse effects. There is evidence about risk of systolic heart failure related to imatinib, pulmonary arterial hypertension induced by dasatinib and ischemic events associated with peripheral arterial disease and observed during nilotinib therapy. Some groups of patients with defined risk factors need appropriate cardiac monitoring.
PL
Zachorowania na przewlekłą białaczkę szpikową dotykają głównie osób starszych, u których występują istotne czynniki ryzyka miażdżycy, a często również organiczne choroby serca. Leki ukierunkowane molekularnie, takie jak imatynib, dazatynib i nilotynib, bardzo istotnie poprawiają rokowanie tej grupy chorych. Jednak podobne cele molekularne w postaci kinaz tyrozynowych są także istotne dla prawidłowej funkcji układu sercowo-naczyniowego i ich blokowanie może mieć niekorzystne skutki w tym układzie. Efektami klinicznymi są skurczowa niewydolność serca związana z terapią imatynibem, tętnicze nadciśnienie płucne związane z terapią dazatynibem oraz niedokrwienie kończyn związane z miażdżycą tętnic obwodowych obserwowane podczas terapii nilotynibem. Podkreśla się rolę odpowiedniego monitoringu kardiologicznego, zwłaszcza w podgrupach ze zdefiniowanymi czynnikami ryzyka powikłań.
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Journal
Year
Volume
3
Issue
3
Pages
149-162; 163-176
Physical description
Contributors
  • Klinika Krążenia Płucnego i Chorób Zakrzepowo-Zatorowych, Centrum Medyczne Kształcenia Podyplomowego, s.szmit@gmail.com
  • Katedra i Klinika Hematologii, Onkologii i Chorób Wewnętrznych, Warszawski Uniwersytet Medyczny
author
  • Klinika Krążenia Płucnego i Chorób Zakrzepowo-Zatorowych, Centrum Medyczne Kształcenia Podyplomowego
References
  • Swords R., Mahalingam D., Padmanabhan S. et al.: Nilotinib: optimal therapy for patients with chronic myeloid leukemia and resistance or intolerance to imatinib. Drug Des. Devel. Ther. 2009; 3: 89-101.
  • National Cancer Institute. US National Institutes of Health: Surveillance Epidemiology and End Results web site: Finding Cancer Statistics: Cancer Stat Fact Sheets: Chronic Myeloid Leukemia [online: http://seer.cancer.gov/statfacts/html/ cmyl.html] (dostęp: 20 sierpnia 2008 r.).
  • Rohrbacher M., Hasford J.: Epidemiology of chronic myeloid leukaemia (CML). Best Pract. Res. Clin. Haematol. 2009; 22(3): 295-302.
  • McDonald M., Hertz R.P., Unger A.N. et al.: Prevalence, awareness, and management of hypertension, dyslipidemia, and diabetes among United States adults aged 65 and older. J. Gerontol. A Biol. Sci. Med. Sci. 2009; 64(2): 256-63.
  • Pencina M.J., D’Agostino R.B. Sr, Larson M.G. et al.: Predicting the 30-year risk of cardiovascular disease: the Framingham Heart Study. Circulation 2009; 119(24): 3078-84.
  • Islam T.M., Fox C.S., Mann D. et al.: Age-related associations of hypertension and diabetes mellitus with chronic kidney disease. BMC Nephrol. 2009; 10: 17.
  • Coresh J., Selvin E., Stevens L.A. et al.: Prevalence of chronic kidney disease in the United States. JAMA 2007; 298(17): 2038-47.
  • Libby P.: Current concepts of the pathogenesis of the acute coronary syndromes. Circulation 2001; 104(3): 365-72.
  • Strait J.B., Lakatta E.G.: Aging-associated cardiovascular changes and their relationship to heart failure. Heart Fail. Clin. 2012; 8(1): 143-64.
  • Tuzcu E.M., Kapadia S.R., Tutar E. et al.: High prevalence of coronary atherosclerosis in asymptomatic teenagers and young adults: evidence from intravascular ultrasound. Circulation 2001; 103(22): 2705-10.
  • Cohen M.H., Williams G., Johnson J.R. et al.: Approval summary for imatinib mesylate capsules in the treatment of chronic myelogenous leukemia. Clin. Cancer Res. 2002; 8: 935-42.
  • Cheng H., Force T.: Why do kinase inhibitors cause cardiotoxicity and what can be done about it? Prog. Cardiovasc. Dis. 2010; 53(2): 114-20.
  • Cheng H., Force T.: Molecular mechanisms of cardiovascular toxicity of targeted cancer therapeutics. Circ. Res. 2010; 106: 21-34.
  • Hasinoff B.B., Patel D.: The lack of target specificity of small molecule anticancer kinase inhibitors is correlated with their ability to damage myocytes in vitro. Toxicol. Appl. Pharmacol. 2010; 249(2): 132-9.
  • Kerkela R., Grazette L., Yacobi R. et al.: Cardiotoxicity of the cancer therapeutic agent imatinib mesylate. Nat. Med. 2006; 12: 908-916.
  • Breccia M.: Is imatinib-related cardiotoxicity still an open issue? Leuk. Res. 2011; 35: 34-5.
  • Orphanos G.S., Ioannidis G.N., Ardavanis A.G.: Cardiotoxicity induced by tyrosine kinase inhibitors. Acta Oncol. 2009; 48(7): 964-70.
  • Steinberg S.F.: Distinctive activation mechanisms and functions for protein kinase C delta. Biochem. J. 2004; 384: 449-59.
  • Park Y.H., Park H.J., Kim B.S. et al.: BNP as a marker of the heart failure in the treatment of imatinib mesylate. Cancer Lett. 2006; 243: 16-22.
  • Tiribelli M., Colatutto A., Marin L. et al.: Brain natriuretic peptide level as marker of cardiac function in imatinib-treated chronic myeloid leukemia patients: No evidence of cardiotoxicity of imatinib therapy. Am. J. Hematol. 2008; 83: 517-8.
  • Fernandez A., Sanguino A., Peng Z. et al.: An anticancer C-Kit kinase inhibitor is reengineered to make it more active and less cardiotoxic. J. Clin. Invest. 2007; 117: 4044-54.
  • Aoki H., Kang P.M., Hampe J. et al.: Direct activation of mitochondrial apoptosis machinery by c-Jun N-terminal kinase in adult cardiac myocytes. J. Biol. Chem. 2002; 277: 10244-50.
  • Francis J., Ahluwalia M.S., Wetzler M. et al.: Reversible cardiotoxicity with tyrosine kinase inhibitors. Clin. Adv. Hematol. Oncol. 2010; 8(2): 128-32.
  • Kantarjian H., Pasquini R., Hamerschlak N. et al.: Dasatinib or high-dose imatinib for chronic-phase chronic myeloid leukemia after failure of first-line imatinib: A randomized phase 2 trial. Blood 2007; 109: 5143-50.
  • Cortes J., Kim D.W., Raffoux E. et al.: Efficacy and safety of dasatinib in imatinib-resistant or -intolerant patients with chronic myeloid leukemia in blast phase. Leukemia 2008; 22(12): 2176-83.
  • Talpaz M., Shah N., Kantarjian H. et al.: Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias. N. Engl. J. Med. 2006; 354: 2531-41.
  • Masiello D., Gorospe G. 3rd, Yang A.S.: The occurrence and management of fluid retention associated with TKI therapy in CML, with a focus on dasatinib. J. Hematol. Oncol. 2009; 2: 46.
  • Brixey A.G., Light R.W.: Pleural effusions due to dasatinib. Curr. Opin. Pulm. Med. 2010; 16(4): 351-6.
  • Quintás-Cardama A., Kantarjian H., O’Brien S. et al.: Pleural effusion in patients with chronic myelogenous leukemia treated with dasatinib after imatinib failure. J. Clin. Oncol. 2007; 25(25): 3908-14.
  • Goldblatt M., Huggins J.T., Doelken P. et al.: Dasatinib-induced pleural effusions: a lymphatic network disorder? Am. J. Med. Sci. 2009; 338(5):
  • Kim D., Goh H.G., Kim S.H. et al.: Long-term pattern of pleural effusion from chronic myeloid leukemia patients in second-line dasatinib therapy. Int. J. Hematol. 2011; 94(4): 361-71.
  • Breccia M., Alimena G.: Pleural/pericardic effusions during dasatinib treatment: incidence, management and risk factors associated to their development. Expert Opin. Drug Saf. 2010; 9(5): 713-21.
  • Krauth M.T., Herndlhofer S., Schmook M.T. et al.: Extensive pleural and pericardial effusion in chronic myeloid leukemia during treatment with dasatinib at 100 mg or 50 mg daily. Haematologica 2011; 96(1): 163-6.
  • Tinsley S.M.: Safety profiles of second-line tyrosine kinase inhibitors in patients with chronic myeloid leukaemia. J. Clin. Nurs. 2010; 19(9-10): 1207-18.
  • Wolf A., Couttet P., Dong M. et al.: Preclinical evaluation of potential nilotinib cardiotoxicity. Leuk. Res. 2011; 35(5): 631-7.
  • Kantarjian H., Hochhaus A., Saglio G. et al.: Nilotinib versus imatinib for the treatment of patients with newly diagnosed chronic phase, Philadelphia chromosome-positive, chronic myeloid leukemia: 24-month minimum follow-up of the phase 3 randomised ENESTnd trial. Lancet Oncol. 2011; 12: 841-51.
  • Haverkamp W., Breithardt G., Camm A.J. et al.: The potential for QT prolongation and proarrhythmia by non-antiarrhythmic drugs: clinical and regulatory implications. Report on a policy conference of the European Society of Cardiology. Eur. Heart J. 2000; 21(15): 1216- 31.
  • Strevel E.L., Ing D.J., Siu L.L.: Molecularly targeted oncology therapeutics and prolongation of the QT interval. J. Clin. Oncol. 2007; 25(22): 3362-71.
  • Breccia M., Efficace F., Alimena G.: Progressive arterial occlusive disease (PAOD) and pulmonary hypertension (PAH) as new adverts events of second generation TKIs in CML treatment: who’s afraid of the big bad wolf? Leuk. Res. 2012; 36: 813-814.
  • Breccia M., Alimena G.: Occurrence and current management of side effects in chronic myeloid leukemia patients treated frontline with tyrosine kinase inhibitors. Leuk. Res. 2013; 37(6): 713-20.
  • Humbert M., Simonneau G., Dinh-Xuan A.T.: Whistleblowers. Eur. Respir. J. 2011; 38(3): 510-1.
  • EMEA: Sprycel-Scientific discussion. European Public Assessment Report (EPAR 2011).
  • Kantarjian H., Shah N.P., Cortes J.E. et al.: Dasatinib or imatinib in newly diagnosed chronic-phase chronic myeloid leukemia: 2-year follow-up from a randomized phase 3 trial (DASISION). Blood 2012; 119: 1123-9.
  • Montani D., Bergot E., Günther S. et al.: Pulmonary arterial hypertension in patients treated by dasatinib. Circulation 2012; 125: 2128-2137.
  • Rasheed W., Flaim B., Seymour J.F.: Reversible severe pulmonary hypertension secondary to dasatinib in a patient with chronic myeloid leukemia. Leuk. Res. 2009; 33: 861-4.
  • Mattei D., Feola M., Orzan F. et al.: Reversible dasatinib-induced pulmonary arterial hypertension and right ventricle failure in a previously allografted CML patient. Bone Marrow Transplant. 2009; 43: 967-8.
  • Dumitrescu D., Seck C., ten Freyhaus H. et al.: Fully reversible pulmonary arterial hypertension associated with dasatinib treatment for chronic myeloid leukemia. Eur. Respir. J. 2011; 38: 218-20.
  • Hennigs J.K., Keller G., Baumann H.J. et al.: Multi tyrosine kinase inhibitor dasatinib as novel cause of severe pre-capillary pulmonary hypertension? BMC Pulm. Med. 2011; 23: 11-30.
  • Orlandi E.M., Rocca B., Pazzano A.S. et al.: Reversible pulmonary arterial hypertension likely related to long-term, low dose dasatinib treatment for chronic myeloid leukemia. Leuk. Res. 2012; 36: e4-6.
  • Patkowska E., Lech-Marańda E., Darocha S. et al.: Odwracalne tętnicze nadciśnienie płucne jako powikłanie leczenia dazatynibem, ze skuteczną i bezpieczną kontynuacją terapii przewlekłej białaczki szpikowej nilotynibem. Hematologia 2013; 4(1): 76-83.
  • Olschewski H., Nagaraj C., Tang B. et al.: Novel role of src family tyrosine kinase (srctk) in response of potassium channels in human pulmonary artery smooth muscle cells to hypoxia. Am. J. Respir. Crit. Care Med. 2011; 183: A5484.
  • Oda Y., Renaux B., Bjorge J. et al.: Csrc is a major cytosolic tyrosine kinase in vascular tissue. Can. J. Physiol. Pharmacol. 1999; 77: 606-617.
  • Girerd B., Montani D., Eyries M. et al.: Absence of influence of gender and BMPR2 mutation type on clinical phenotypes of pulmonary arterial hypertension. Respir. Res. 2010; 11: 73.
  • Austin E.D., Cogan J.D., West J.D. et al.: Alterations in oestrogen metabolism: implications for higher penetrance of familial pulmonary arterial hypertension in females. Eur. Respir. J. 2009; 34: 1093-1099.
  • Schermuly R.T., Dony E., Ghofrani H.A. et al.: Reversal of experimental pulmonary hypertension by PDGF inhibition. J. Clin. Invest. 2005; 115: 2811-2821.
  • Perros F., Montani D., Dorfmüller P. et al.: Platelet-derived growth factor expression and function in idiopathic pulmonary arterial hypertension. Am. J. Respir. Crit. Care Med. 2008; 178: 81-88.
  • Izikki M., Guignabert C., Fadel E. et al.: Endothelial-derived fgf2 contributes to the progression of pulmonary hypertension in humans and rodents. J. Clin. Invest. 2009; 119: 512-523.
  • Tu L., Dewachter L., Gore B. et al.: Autocrine FGF2 signaling contributes to altered endothelial phenotype in pulmonary hypertension. Am. J. Respir. Cell Mol. Biol. 2011; 45: 311-22.
  • Montani D., Perros F., Gambaryan N. et al.: C-kit-positive cells accumulate in remodeled vessels of idiopathic pulmonary arterial hypertension. Am. J. Respir. Crit. Care Med. 2011; 184: 116-123.
  • Dahal B.K., Cornitescu T., Tretyn A. et al.: Role of epidermal growth factor inhibition in experimental pulmonary hypertension. Am. J. Respir. Crit. Care Med. 2010; 181: 158-167.
  • Merklinger S.L., Jones P.L., Martinez E.C. et al.: Epidermal growth factor receptor blockade mediates smooth muscle cell apoptosis and improves survival in rats with pulmonary hypertension. Circulation 2005; 112: 423-431.
  • Adir Y., Humbert M.: Pulmonary hypertension in patients with chronic myeloproliferative disorders. Eur. Respir. J. 2010; 35(6): 1396-406.
  • Guilpain P., Montani D., Damaj G. et al.: Pulmonary hypertension associated with myeloproliferative disorders: a retrospective study of ten cases. Respiration 2008; 76(3): 295-302.
  • García-Manero G., Schuster S.J., Patrick H. et al.: Pulmonary hypertension in patients with myelofibrosis secondary to myeloproliferative diseases. Am. J. Hematol. 1999; 60: 130-135.
  • Dingli D., Utz J.P., Krowka M.J. et al.: Unexplained pulmonary hypertension in chronic myeloproliferative disorders. Chest 2001; 120: 801-808.
  • Altintas A., Karahan Z., Pasa S. et al.: Pulmonary hypertension in patients with essentials thrombocythemia and reactive hrombocytosis. Leuk. Lymphoma 2007; 48: 1981-1987.
  • Garypidou V., Vakalopoulou S., Dimitriadis D. et al.: Incidence of pulmonary hypertension in patients with chronic myeloproliferative disorders. Haematologica 2004; 89: 245-246.
  • Gupta R., Perumandla S., Patsiornik Y. et al.: Incidence of pulmonary hypertension in patients with chronic myeloproliferative disorders. J. Natl. Med. Assoc. 2006; 98: 1779-1782.
  • Souza R., Sitbon O., Parent F. et al.: Long term imatinib treatment in pulmonary arterial hypertension. Thorax 2006; 61(8): 736.
  • Ghofrani H.A., Morrell N.W., Hoeper M.M. et al.: Imatinib in pulmonary arterial hypertension patients with inadequate response to established therapy. Am. J. Respir. Crit. Care Med. 2010; 182(9): 1171-7.
  • Galie N., Hoeper M.M., Humbert M. et al.: Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur. Respir. J. 2009; 34: 1219-1263.
  • Ghio S., Gavazzi A., Campana C. et al.: Independent and additive prognostic value of right ventricular systolic function and pulmonary artery pressure in patients with chronic heart failure. J. Am. Coll. Cardiol. 2001; 37: 183-188.
  • Vahanian A., Baumgartner H., Bax J. et al.; Task Force on the Management of Valvular Hearth Disease of the European Society of Cardiology; ESC Committee for Practice Guidelines: Guidelines on the management of valvular heart disease: The Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology. Eur. Heart J. 2007; 28: 230-268.
  • Simonneau G., Robbins I., Beghetti M. et al.: Updated clinical classification of pulmonary hypertension. J. Am. Coll. Cardiol. 2009; 54: S43-S54.
  • Gabbay E., Yeow W., Playford D.: Pulmonary arterial hypertension (PAH) is an uncommon cause of pulmonary hypertension (PH) in an unselected population: the Armadale echocardiography study. Am. J. Resp. Crit. Care Med. 2007; 175: A713.
  • Abraham W.T., Raynolds M.V., Gottschall B. et al.: Importance of angiotensin-converting enzyme in pulmonary hypertension. Cardiology 1995; 10(Suppl. 1): 9-15.
  • Peacock A.J., Murphy N.F., McMurray J.J.V. et al.: An epidemiological study of pulmonary arterial hypertension. Eur. Respir. J. 2007; 30: 104-109.
  • Humbert M., Sitbon O., Chaouat A. et al.: Pulmonary arterial hypertension in France: results from a national registry. Am. J. Respir. Crit. Care Med. 2006; 173: 1023-1030.
  • Kim T.D., le Coutre P., Schwarz M. et al.: Clinical cardiac safety profile of nilotinib. Haematologica 2012; 97(6): 883-9.
  • Ferri N., Carragher N.O., Raines E.W.: Role of discoidin domain receptors 1 and 2 in human smooth muscle cell-mediated collagen remodeling: potential implications in atherosclerosis and lymphangioleiomyomatosis. Am. J. Pathol. 2004; 164: 1575-1585.
  • Aichberger K.J., Herndlhofer S., Schernthaner G.H. et al.: Progressive peripheral arterial occlusive disease and other vascular events during nilotinib therapy in CML. Am. J. Hematol. 2011; 86(7): 533-9.
  • Valent P.: Severe adverse events associated with the use of second-line BCR/ABL tyrosine kinase inhibitors: preferential occurrence in patients with comorbidities. Haematologica 2011; 96(10): 1395-7.
  • Tefferi A., Letendre L.: Nilotinib treatment-associated peripheral artery disease and sudden death: yet another reason to stick to imatinib as front-line therapy of chronic myelogenous leukemia. Am. J. Hematol. 2011; 86(7): 610-611.
  • Quintas-Cardama A., Kantarjian H., Cortes J.: Nilotinib-associated vascular events. Clin. Lymphoma Myeloma Leuk. 2012; 12(5): 337-40.
  • Kantarjian H.M., Kim D.W., Issaragrisil S. et al.: ENESTnd 4-year update: continued superiority of nilotinib vs imatinib in patients with newly diagnosed Philadelphia chromosome-positive (Ph+) chronic myeloid leukemia in chronic phase (CML-CP). Poster Presentation at American Society of Hematology – 54th Annual Meeting; December 8-11, 2012; Altanta, GA. Poster 1676.
  • le Coutre P., Rea D., Abruzzese E. et al.: Severe peripheral arterial disease during nilotinib therapy. J. Natl. Cancer Inst. 2011; 103: 1347-8.
  • Levato L., Cantaffa R., Kropp M. et al.: Progressive peripheral arterial occlusive disease and other vascular events during nilotinib therapy in chronic myeloid leukemia. W: Proceedings from the American Society of Hematology – 54th Annual Meeting; December 8-11, 2012; Atlanta, GA. Abstract 1679.
  • Labussiere-Wallet H., Guillermin Y., Etienne M. et al.: Analysis of clinical arterial and metabolic parameters in chronic phase CML patients on nilotinib in a single center cohort. W: Proceedings from the American Society of Hematology – 54th Annual Meeting; December 8-11, 2012; Atlanta, GA. Abstract 3756.
  • Kim T.D., Rea D., Schwarz M. et al.: Peripheral artery occlusive disease in chronic phase chronic myeloid leukemia patients treated with nilotinib or imatinib. Leukemia 2013; 27(6): 1316-21.
  • Giles F.J., Mauro M.J., Hong F. et al.: Rates of peripheral arterial occlusive disease in patients with chronic myeloid leukemia in the chronic phase treated with imatinib, nilotinib, or non-tyrosine kinase therapy: a retrospective cohort analysis. Leukemia 2013; 27(6): 1310-5.
  • Saglio G., Kim D.W., Issaragrisil S. et al.: Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia. N. Engl. J. Med. 2010; 362: 2251-2259.
  • Cortes J.E., Baccarani M., Guilhot F. et al.: Phase III, randomized, open-label study of daily imatinib mesylate 400 mg versus 800 mg in patients with newly diagnosed, previously untreated chronic myeloid leukemia in chronic phase using molecular end points: tyrosine kinase inhibitor optimization and selectivity study. J. Clin. Oncol. 2010; 28: 424-430.
  • O’Brien S.G., Guilhot F., Larson R.A. et al.: Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia. N. Engl. J. Med. 2003; 348: 994-1004.
  • Nakamura K., Akagi S., Ogawa A. et al.: Pro-apoptotic effects of imatinib on PDGF-stimulated pulmonary artery smooth muscle cells from patients with idiopathic pulmonary arterial hypertension. Int. J. Cardiol. 2011; 159: 100-106.
  • Li L., Blumenthal D.K., Masaki T. et al.: Differential effects of imatinib on PDGF-induced proliferation and PDGF receptor signaling in human arterial and venous smooth muscle cells. J. Cell. Biochem. 2006; 99: 1553-1563.
  • Agostino N.M., Chinchilli V.M., Lynch C.J. et al.: Effect of the tyrosine kinase inhibitors (sunitinib, sorafenib, dasatinib, and imatinib) on blood glucose levels in diabetic and nondiabetic patients in general clinical practice. J. Oncol. Pharm. Pract. 2011; 17: 197-202.
  • Lassila M., Allen T.J., Cao Z. et al.: Imatinib attenuates diabetes-associated atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 2004; 24: 935-942.
  • Larson R.A., Hochhaus A., Hughes T.P. et al.: Nilotinib vs imatinib in patients with newly diagnosed Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase: ENESTnd 3-year follow-up. Leukemia 2012; 26: 2197-2203.
  • Murabito J.M., Evans J.C., Larson M.G. et al.: The ankle-brachial index in the elderly and risk of stroke, coronary disease, and death: The Framingham Study. Arch. Intern. Med. 2003; 163: 939-942.
  • Leng G.C., Fowkes F.G., Lee A.J. et al.: Use of ankle-brachial pressure index to predict cardiovascular events and death: A cohort study. BMJ 1996; 313: 1440-1444.
  • McDermott M.M., Liu K., Greenland P. et al.: Functional decline in peripheral arterial disease: Associations with the ankle-brachial index and leg symptoms. JAMA 2004; 292: 453-461.
  • Curb J.D., Masaki K., Rodriguez B.L. et al.: Peripheral artery disease and cardiovascular risk factors in the elderly: the Honolulu Heart Program. Arterioscler. Thromb. Vasc. Biol. 1996; 16: 1495-1500.
  • Zheng Z.J., Sharrett A.R., Chambless L.E. et al.: Associations of ankle-brachial index with clinical coronary heart disease, stroke and preclinical carotid and popliteal atherosclerosis: the Atherosclerosis Risk in Communities (ARIC) Study. Atherosclerosis 1997; 131: 115-125.
  • Newman A.B., Shemanski L., Manolio T.A. et al.: Ankle-arm index as a predictor of cardiovascular disease and mortality in the Cardiovascular Health Study: the Cardiovascular Health Study Group. Arterioscler. Thromb. Vasc. Biol. 1999; 19: 538-545.
  • Murabito J.M., Evans J.C., Nieto K. et al.: Prevalence and clinical correlates of peripheral arterial disease in the Framingham Offspring Study. Am. Heart J. 2002; 143: 961-965.
  • Newman A.B., Siscovick D.S., Manolio T.A. et al.: Ankle-arm index as a marker of atherosclerosis in the Cardiovascular Health Study. Cardiovascular Heart Study (CHS) Collaborative Research Group. Circulation 1993; 88: 837-845.
  • Meijer W.T., Grobbee D.E., Hunink M.G. et al.: Determinants of peripheral arterial disease in the elderly: The Rotterdam Study. Arch. Intern. Med. 2000; 160: 2934-2938.
  • Selvin E., Erlinger T.P.: Prevalence and risk factors for peripheral arterial disease in the United States: results from the National Health and Nutrition Examination Survey 1999-2000. Circulation 2004; 110: 738-43.
  • Ridker P.M., Stampfer M.J., Rifai N.: Novel risk factors for systemic atherosclerosis: a comparison of C-reactive protein, fibrinogen, homocysteine, lipoprotein(a), and standard cholesterol screening as predictors of peripheral arterial disease. JAMA 2001; 285: 2481-2485.
  • McDermott M.M., Green D., Greenland P. et al.: Relation of levels of hemostatic factors and inflammatory markers to the ankle-brachial index. Am. J. Cardiol. 2003; 92: 194-199.
  • Ostchega Y., Paulose-Ram R., Dillon C.F. et al.: Prevalence of peripheral arterial disease and risk factors in persons aged 60 and older: data from the National Health and Nutrition Examination Survey 1999-2004. J. Am. Geriatr. Soc. 2007; 55(4): 583-9.
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