Detalhes bibliográficos
Título da fonte: Biblioteca Digital de Teses e Dissertações da UFTM
id UFTM_86b274cc531f7f05705931602eea8386
oai_identifier_str oai:bdtd.uftm.edu.br:tede/792
network_acronym_str UFTM
network_name_str Biblioteca Digital de Teses e Dissertações da UFTM
repository_id_str
reponame_str Biblioteca Digital de Teses e Dissertações da UFTM
instacron_str UFTM
institution Universidade Federal do Triangulo Mineiro (UFTM)
instname_str Universidade Federal do Triangulo Mineiro (UFTM)
spelling Avaliação morfológica e histopatológica de indivíduos autopsiados com cardiopatia hipertensivaAutópsia.Cardiopatia hipertensiva.Mastócitos.Autopsy.Hypertensive heart disease.Mast cells.MorfologiaObjetivo: Analisar as alterações histopatológicas na cardiopatia hipertensiva e descrever e comparar os achados para esclarecer os fatores determinantes. Métodos: 42 fragmentos do miocárdio do ventrículo esquerdo e do ramo circunflexo da artéria coronária esquerda foram obtidos de indivíduos autopsiados no Hospital das Clínicas da Universidade Federal do Triângulo Mineiro (UFTM) no período de 1984 a 2018. Os grupos foram divididos em indivíduos com cardiopatia hipertensiva (CH) e indivíduos sem cardiopatia (SC). A espessura da parede livre do ventrículo esquerdo foi medida com um paquímetro digital e tomografia computadorizada. A quantificação das fibras de colágeno foi realizada por morfometria computadorizada e a densidade de mastócitos foi avaliada por métodos imunohistoquímicos. Resultados: O peso cardíaco do grupo CH foi significativamente maior do que no grupo SC (p=0.0002). A espessura da parede do ventrículo esquerdo do grupo CH foi significativamente maior do que do grupo SC (p=0.04). A densidade de fibras colágenas no ventrículo esquerdo do grupo CH foi significativamente maior do que do grupo SC (p<0.0001). A densidade de mastócitos no ventrículo esquerdo imunomarcados por anti-quimase/anti-triptase foi significativamente maior do que do grupo SC (p<0.0001). A densidade de mastócitos no ramo circunflexo da artéria coronária esquerda imunomarcados por anti-quimase/anti-triptase foi significativamente maior do que do grupo SC (p=0.01). Conclusões: Os mastócitos parecem estar envolvidos no desenvolvimento de cardiopatia hipertensiva, contribuindo para a remodelação das fibras de colágeno nessa doença.Objective: To analyze morphological changes in hypertensive cardiopathy and to describe and compare findings in order to help clarify determinant factors. Methods: 42 fragments of the left ventricular myocardium and circumflex branch of the left coronary artery were obtained from individuals autopsied at the Clinical Hospital of the Federal University of Triângulo Mineiro (UFTM) in the period ranging from 1984 to 2018. Groups were split into individuals with hypertensive heart disease (HD) and individuals without heart disease (ND). The thickness of the free wall of the left ventricle was measured with a digital caliper and Computed Tomography. Quantification of collagen fibers was conducted by computerized morphometry and mast cell density was assessed by immunohistochemical methods. Results: There was a significant increase of heart weight in the HD group compared to the ND group, (p=0.0002). There was a significant increase of thickness of the middle third of the free wall in the HD group compared to the ND group, (p=0.04). There was a significant increase of collagen fibers in the left ventricle in the HD group compared to the ND group, (p<0.0001). Concerning mast cell density, there was a significant increase in the left ventricle of individuals with HD immuno-labeled by the set antichymase/anti-tryptase (p<0.0001). Theres was a significant increase of mast cell density in the circumflex branch of the left coronary artery of individuals with HD immuno-labeled by the set anti-chymase/anti-tryptase (p=0.01). Conclusions: Mast cells appear to be involved in the development of hypertensive heart disease, contributing to the remodeling of collagen fibers in this disease.Conselho Nacional de Desenvolvimento Científico e TecnológicoCoordenação de Aperfeiçoamento de Pessoal de Nível SuperiorFundação de Amparo à Pesquisa do Estado de Minas GeraisFundação de Ensino e Pesquisa de UberabaUniversidade Federal do Triângulo MineiroUniversidade Federal do Triângulo MineiroInstituto de Ciências da Saúde - ICS::Programa de Pós-Graduação em Ciências da SaúdeBrasilUFTMPrograma de Pós-Graduação em Ciências da SaúdeFERRAZ, Mara Lúcia da Fonseca64044270600http://lattes.cnpq.br/9852478909273401ANTUNES, Vicente de Paula Antunes19278063649http://lattes.cnpq.br/6788700810093027JULIANO, Guilherme Ribeiro2019-07-25T14:38:53Z2019-06-10info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/doctoralThesisapplication/pdfapplication/pdfJULIANO, Guilherme Ribeiro. Avaliação morfológica e histopatológica de indivíduos autopsiados com cardiopatia hipertensiva. 2019. 76f. Tese (Doutorado em Ciências da Saúde) - Programa de Pós-Graduação em Ciências da Saúde, Universidade Federal do Triângulo Mineiro, Uberaba, 2019.http://bdtd.uftm.edu.br/handle/tede/792porANGUITA, M. et al. Hipertensíon arterial, cardiopatía hipertensiva e insuficiência cardíaca. Papel de los diuréticos de asa. Med Clin (Barc), v. 131, n. 17, p. 660-664, 2008. ARNETT, D. K. et al. Pharmacogenetic approaches tohypertension therapy: design and rationale for the genetics of hypertensionassociated treatment (GenHAT) study. Pharmacogenomics J, v. 2, p. 309-317, 2002. BADAM, R. K. et al. Virtopsy: Touch-free autopsy. J Forensic Dent Sci, v. 9, n. 1, p. 42, 2017. BARRETO, M. L. et al. O nascimento, a vida, o adoecimento, a morte e a atenção à saúde da população brasileira durante 20 anos de Sistema Único de Saúde: uma síntese. In: BRASIL. Ministério da Saúde (Org.) Saúde Brasil 2008: 20 anos de Sistema Único de Saúde (SUS). Brasília: Ministério da Saúde, 2009. p. 407-4016. BERK, B. C.; FUJIWARA, K.; LEHOUX, S. ECM remodeling in hypertensive heart disease. J Clin Invest, v. 117, p.568–575, 2007. BHOGAL, R. K.; BONA, C. A. Regulatory effect of extracellular signal-regulated kinases (ERK) on type 1 collagen synthesis in human dermal fibroblasts stimulated by IL-4 and IL-13. Int Rev Immunol, v. 27, p. 472-496, 2008. BOMBIG, M. T. N.; POVÓA, R. Cardiopatia hipertensiva: aspectos epidemiológicos, prevalência e fator de risco cardiovascular. Rev Bras Hipertens, v. 15, n. 2, p. 75-80, 2008. BOT, I.; VAN BERKEL, T. J. C.; BIESSEN, E. A. L. Mast cells: pivotal players in cardiovascular diseases. Current Cardiology Reviews, v. 4, p. 170-178, 2008. Cardiol do Rio Grande do Sul, v. 12, n. 3, p. 5-15, 2003. CALDERÓN-GARCIDUENAS, L. et al. Canines as sentinel species for assessing chronic exposures to air pollutants: Part 2. Cardiac pathology. Toxicol Sci, v. 61, p. 356-367, 2001. CARDOSO, E. et al. Alterações eletrocardiográficas e sua relação com os fatores de risco para doença isquêmica do coração em população da área metropolitana de São Paulo. Rev Assoc Med Bras (1992), v. 48, p. 231-6, 2002. CARVALHO, R. F.; NILSSON, G.; HARVIMA, I. T. Increased mast cell expression of PAR-2 in skin inflammatory diseases and release of IL-8 upon PAR-2 activation. Exp Dermatol, v. 19, p. 117-122, 2010. CAUGHEY, G. H. Mast cell tryptases and chymases in inflammation and host defense. Immunol Rev, n. 217, p. 141-154, 2007. CHAHAL, N.S. et al. Ethnicity-related differences in left ventricular function, structure and geometry: a population study of UK Indian Asian and European White subjects. Heart, v. 96, n. 6, p. 466-71, 2010. CHANG, E. Y. et al. Functional effects of overexpression of protein kinase C -alpha, -beta, -delta, -epsilon, and -eta in the mast cell line RBL-2H3. J Immunol, v. 159, p. 2624-2632, 1997. CHENG, Y. et al. Large Accumulation of Collagen and Increased Activation of Mast Cells in Hearts of Mice with Hyperlipidemia. Arq Bras Cardiol, v. 109, p. 404-409, 2017. COMPTON, S. J. et al. Human mast cell tryptase stimulates the release of an IL-8- dependent neutrophil chemotactic activity from human umbilical vein endothelial cells (HUVEC). Clin Exp Immunol, v. 121, p. 31-36, 2000. DELIARGYRIS, E. M. et al. Mast cell tryptase: a new biomarker in patients with stable coronary artery disease. Atherosclerosis, v. 178, n. 2, p. 381-386, 2005. DICKSON, M. E.; SIGMUND, C. D. Genetic Basis of Hypertension: Revisiting Angiotensinogen. Hypertension, v.48, n. 1, p. 14-20, 2006. DÍEZ, J.; FROHLICH, E. D. A Translational Approach to Hypertensive Heart Disease. Hypertension, v. 55, p. 1-8, 2010. DOGGRELL, S. A.; WANSTALL, J. C. Vascular chymase: pathophysiological role andtherapeutic potential of inhibition. Casdiovasc Res, v. 61, p. 653-662, 2004. DOMINICZAK, A. F.; KUO, D. Hypertension: update 2017. Hypertension, v. 69, p. 3- 4, 2017. DRAZNER, M. H. et al. Left ventricular hypertrophy is more prevalent in blacks than whites in the general population: the Dallas Heart Study. Hypertension, v. 46, p. 124- 129, 2005. DRAZNER, M. H. The Progression of Hypertensive Heart Disease. Circulation, v. 123, p. 327-334, 2011. FERRAZ, M. L. et al. Correlation of lifetime progress of atherosclerosis and morphologic markers of severity in humans: new tools for a more sensitive evaluation. Clinics (Sao Paulo), v. 67, p. 1071-5, 2012. FERREIRA FILHO, P.R.P. Padrões de Hipertrofia e Geometria do Ventrículo Esquerdo pela Ecocardiografia Transtorácica. Rev bras ecocardiogr imagem cardiovasc, v. 25, n. 2, p. 103-115, 2012. FOREMAN, K.J. et al. Forecasting life expectancy, years of life lost, and all-cause and cause-specific mortality for 250 causes of death: reference and alternative scenarios for 2016-40 for 195 countries and territories. Lancet, v. 392, n. 10159, p. 2052–90, 2018. FRAZER, K. A. et al. Human genetic variation and its contribution to complex traits. Nature Reviews Genetics, v. 10, p. 241-251, 2009. GAUDIERI, V. et al. Coronary vascular function in patients with resistant hypertension and normal myocardial perfusion: a propensity score analysis. Eur Heart J Cardiovasc Imaging, 2019. GILFILLAN, A. M.; TKACZYK, C. Integrated signalling pathways for mast-cell activation. Nat Rev, v. 6, p. 218-230, 2006. GOMES, E. R. et al. Anggiotensin-(1-7) prevents cardiomyocyte pathological remodeling through a nitric oxide/guanosine 3´, 5´-cyclic monophosphate-dependent pathway. Hypertension, v. 55, p. 153-160, 2010. GONZÁLES, A. et al. Biochemical markers of myocardial remodeling in hypertensive heart disease. Cardiovasc Res, v. 81, p. 509-518, 2009. GRADMAN, A. H.; ALFAYOUMI, F. From left ventricular hypertrophy to congestive heart failure: management of hypertensive heart disease. Prog Cardiovasc Dis, v. 48, p. 326-41, 2006. GRUBER, B. L. et al. Synovial procollagenase activation by human mast cell tryptase dependence upon matrix metalloproteinase 3 activation. J Clin Invest, v. 84, p. 1657– 1662, 1989. HARA, M. et al. Evidence for a role of mast cells in the evolution to congestive heart failure. J Exp Med, v. 195, p. 375-381, 2002. HEIKKILA, H. M. et al. Activated mast cells induce endothelial cell apoptosis by a combined action of chymase and tumor necrosis factor-alpha. Arterioscler Thromb Vasc Biol, v. 28, p. 309–314, 2008. HILL, J. A.; OLSON, E. N. Cardiac plasticity. N Engl J Med, v. 358, p. 1370-1380, 2008. JIMÉNEZ-NAVARRO, M. F. et al. Collagen synthesis and heart failure. Rev Esp Cardiol (Engl Ed), v. 58, p. 975-8; 2005. JORGE, A. C. et al. Avaliação Histológica da Fibrose Cardíaca de Indivíduos Urêmicos Hipertensos: Estudo Caso e Controle. J Bras Nefrol, v. 26, n. 4, p. 190- 195, 2004. JUNQUEIRA, L. C. U.; BIGNOLAS, G.; BRENTANI, R. R. A simple and sensitive 6 method for the quantitative estimation of collagen. Anal Biochem, v. 94, n. 7 p. 96-99, 1979. KAARTINEN, M.; PENTTILA, A.; KOVANEN, P.T. Accumulation of activated mast cells in the shoulder region of human coronary atheroma, the predilection site of atheromatous rupture. Circulation, v. 90, p. 1669-78, 1994. KANNEL, W. B.; GORDON, T.; OFFUT, D. Left ventricular hypertrophy by electrocardiogram. Prevalence, incidence, and mortality in the Framingham study. Ann Intern Med, V. 71, N. 1, P. 89-105, 1969. KANNEL, W. Left ventricular hypertrophy as a risk factor: The Framingham experience. J Hypertens, v. 9, p. 2-9, 1991. KANELLAKIS, P. et al. A pro-fibrotic role for interleukin-4 in cardiac pressure overload. Cardiovasc Res, v. 95, n. 1, p. 77-85, 2012. KAPUKU, G. K. et al. Early markers of cardiovascular disease. Vasc Pharmacol, v. 45, p. 277-280, 2006. KAWEL, N. et al. Normal left ventricular myocardial thickness for middle aged and older subjects with SSFP cardiac MR: The Multi-Ethnic Study of Atherosclerosis Circ Cardiovasc Imaging, v. 5, p. 500-508, 2012. KINET, J. The essential role of mast cells in orchestring inflammation. Immunol Rev, v.217, p. 5-7, 2007. KIZER, J. R.; ARNETT, D. K.; BELLA, J. N. Differences in left ventricular structure between black and white hypertensive adults: the Hypertension Genetic Epidemiology Network study. Hypertension, v. 43, p. 1182, 2004. KONSTANTINOV, I.E. et al. Anichkov and his theory of atherosclerosis. Tex Heart Inst J, v. 33n. 4, p. 417-23, 2006. KOVANEN, P. T. Mast cells: multipotent local effector cells in atherothrombosis. Immunol Rev, n. 217, p. 105-122, 2007. KOVANEN, P.T.; KAARTINEN, M.; PAAVONEN, T. Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction. Circulation, v. 92, p. 1087-8, 1995. KUMAR, N. T. et al. Postmortem heart weight: relation to body size and effects of cardiovascular disease and cancer. Cardiovasc Pathol, v. 23, p. 5-11, 2014. LEES, M.; TAYLOR, D. J.; WOOLLEY, D. E. Mast cell proteinases activate precursor forms of collagenase and stromelysin, but not of gelatinases A and B. Eur J Biochem, v. 223, p. 171–177, 1994. LESKINEN, M. J. et al. Mast cell chymase induces smooth muscle cell apoptosis by a mechanism involving fibronectin degradation and disruption of focal adhesions. Arterioscler Thromb Vasc Biol, v. 23, p. 238-243, 2003. LEVICK, S. P. et al. Cardiac mast cells mediate left ventricular fibrosis in the hypertensive rat heart. Hypertension, v. 53, p. 1041–1047, 2009. LEVICK, S. P. et al. Cardiac mast cells: the centrepiece in adverse myocardial remodelling. Cardiovasc Res, v. 89, p. 12–19, 2011. LÓPEZ, B. et al. Biochemical Assessment of Myocardial Fibrosis in Hypertensive Heart Disease. Hypertension, v. 38, p. 1222-1226, 2001. LOVIC, D.; ERDINE, S.; ÇATAKOĞLU, A. B. How to estimate left ventricular hypertrophy in hypertensive patients. Anadolu Kardiyol, v. 14, p. 389-95, 2014. LUITEL, H. et al. Pressure overload leads to an increased accumulation and activity of mast cells in the right ventricle. Physiol Rep, v. 5, n. 6, p. e13146, 2017. LYNGBAKKEN, M. N. et al. Novel biomarkers of cardiovascular disease: Applications in clinical practice. Crit Rev Clin Lab Sci, v. 20, p. 1-28, 2018. MANCIA, G. et al. Prevalence of left ventricular hypertrophy in hypertensive patients without and with blood pressure control: data from the PAMELA population. Hypertension, v. 39, p. 744-9, 2002. MATSUMOTO, T. et al. Chymase inhibition prevents cardiac fibrosis and improves diastolic dysfunction in the progression of heart failure. Circulation, v. 107, p. 2555–8, 2003. MEHTA, N. J.; KHAN, I. A. Cardiology's 10 greatest discoveries of the 20th century. Tex Heart Inst J, v. 29, n. 2, p. 167-71, 2002. MELVILLE, S.; BYRD, J.B. Personalized Medicine and the Treatment of Hypertension. Curr Hypertens Rep, v. 21, n. 2, p. 13, 2019. METCALFE, D. D.; BARAM, D.; MEKORI, Y. A. Mast cells. Physiol Rev, v. 77, p. 1033-1079, 1997. METCALFE, D. D. Mast cells and mastocitosis. Blood J, v. 112, p. 946-956, 2008. MUJUMDAR, V. S.; TYAGI, S.C. Temporal regulation of extracellular matrix components in transition from compensatory hypertrophy to decompensatory heart failure. J Hypertens, v. 17, p. 261-70, 1999. MORGAN, L. G. et al. A novel technique for isolating functional mast cells from the heart. Inflamm Res, v. 57, p. 1-6, 2008 MURRAY, D. B. et al. Endothelin-1 mediates cardiac mast cell degranulation, matrix metalloproteinase activation, and myocardial remodeling in rats. Am J Physiol Heart Circ Physiol, v. 287, p. 2295-2299, 2004. NADRUZ, W. Myocardial remodeling in hypertension. J Hum Hypertens, v. 29, n. 1, p. 1-6, 2015. NEELAND, I. J. et al. Relation of regional fat distribution to left ventricular structure and function. Circ Cardiovasc Imaging, v. 6, p. 800-7, 2013. OKAYAMA, Y.; KAWAKAMI, T. Development, migration, and survival of mast cells. Immunol Res, v. 34, p. 97-115, 2006. OLIVETTI, G. et al. Long-term pressure-induced cardiac hypertrophy: capillary and mast cell proliferation. Am J Physiol Heart Circ Physiol, v. 257, p. 1766–1772, 1989. OMRAN, A. R. The epidemiologic Transition: a theory of epidemiology of population change. Milbank Mem Fund Q, v. 49, p. 509-538, 1971. PALANIYANDI, S. S. et al. Chymase inhibition reduces the progression to heart failure after autoimmune myocarditis in rats. Exp Biol Med; v. 232, p. 1213–1221, 2007. PALANYIANDI, S. S.; INAGAKI, K.; MOCHLY-ROSEN, D. Mast cells and epsilonPKC: a role in cardiac remodeling in hypertension-induced heart failure. J Mol Cell Cardiol, v. 45, p. 779-786, 2008. PANIZO, A. et al. Are mast cells involved in hypertensive heart disease? J Hypertens, v. 13, p. 1201–1208, 1995. PANT, S. et al. Inflammation and atherosclerosis--revisited. J Cardiovasc Pharmacol Ther, v. 19, n. 2, p. 170-178, 2014. PASTORELLO, E. A. et al. Serum Tryptase: A New Biomarker in Patients with Acute Coronary Syndrome? Int Arch Allergy Immunol, v. 164, p. 97-105, 2014. PATELLA, V. et al. Stem cell factor in mast cells and increased mast cell density in idiopathic and ischemic cardiomyopathy. Circulation, v. 17, p. 971-978, 1998. PEREIRA, F. E. L. Hipertrofia cardíaca: Aspectos Morfológicos e Clínicos. In: Contratilidade Miocárdica. Aspectos Básicos e Clínicos, 1.ed. São Paulo,1993. cap. II, p.29-40. PETRETTO, E. R. et al. Integrated genomic approaches implicate osteoglycin(Ogn) in the regulation of left ventricular mass. Nat Genet, v. 40, n. 5, p. 546-552, 2008. POST, W. S. et al. Heritability of leftventricular mass: The Framingham Heart Study. Hypertension, v. 30, 1025-1028, 1997. REID, A. C. et al. Targeting Cardiac Mast Cells: Pharmacological Modulation of the Local Renin-Angiotensin System. Curr Pharm, v. 17, n. 34, 3744-3752, 2011. REILLY, C. F. et al. Rapid conversion of angiotensin I to angiotensin II by neutrophil and mast cell proteinases. J Biol Chem, v. 257, n. 15, p. 8619-8622, 1982. RIBEIRO, A. L. et al. Cardiovascular Health in Brazil: Trends and Perspectives. Circulation, v. 133, n. 4, p. 422-33, 2016. RIVERA, S.L.; MARTIN, J.; LANDRY J. Acute and Chronic Hypertension: What Clinicians Need to Know for Diagnosis and Management. Crit Care Nurs Clin North Am, v. 31, n. 1, p. 97-108, 2019. RIZZI, E. et al. Matrix Metalloproteinase Inhibition Improves Cardiac Dysfunction and Remodeling in 2-Kidney, 1-Clip Hypertension. J Card Fail, v. 16, n. 7, p. 599-607, 2010. RIZZI, E. et al. Tempol inhibits TGF-β and MMPs upregulation and prevents cardiac hypertensive changes. Int J Cardiol, v. 165, p. 165-173, 2011. RIZZI, E. et al. Temporal changes in cardiac matrix metalloproteinase activity oxidative stress, and TGF-β in renovascular hypertension-induced cardiac hypertrophy. Exp Mol Pathol, v. 94, p. 1-9, 2013. ROBERTS, I. S. et al. Post-mortem imaging as an alternative to autopsy in the diagnosis of adult deaths: a validation study. Lancet, v. 14, p. 136-42, 2012. RODRIGUES, S.L.; PIMENTEL, E. B.; MILL, J. G. Peso dos ventrículos cardíacos determinado em necropsia de indivíduos saudáveis mortos por causas externas. Arq Bras Cardiol, v. 89, p. 279-84, 2007. RODRIGUES, F. R. et al. O decréscimo vertiginoso das autópsias em um hospital universitário do Brasil nos últimos 20 anos. J Bras Patol Med Lab, v. 47, n. 4, p. 445- 450, 2011. ROSSI, M. A. Pathologic fibrosis and connective tissue matrix in left ventricular hypertrophy due to chronic arterial hypertension in humans. J Hypertens, v. 16, p. 1031-1041, 1998. ROTHENBERG K. The Autopsy through History. In Ayn Embar-seddon, Allan D. Pass (eds). Forensic Science. Salem Press, p. 100–100, 2008. SALTON, C. M. L. et al. Gender differences and normal left ventricular anatomy in an adult population free of hypertension: a cardiovascular magnetic ressonance study of the Framingham Heart Study Offspring Cohort. J Am Coll Cardiol, v. 39, p. 1055-60, 2002. SANT’ANNA, M. P. et al. Hipertrofia cardíaca esquerda e direita em necropsias de hipertensos. Rev Assoc Med Bras (1992), v. 58, p. 41-47, 2012. SCHMIDT, M.I. et al. Chronic non-communicable diseases in Brazil: burden and current challenges. Lancet; v. 377, p. 1949–1961, 2011. SCHOEN, F. J.; MITCHELL, R. N. O Coração. In: KUMAR, V.; ABBAS, A. K; FAUSTO, N. Robbins & Cotran. Patologia: bases patológicas das doenças. 8ª ed. Rio de Janeiro: Elsevier; 2010. p. 538. SCHWARTZKOPFF, B. et al. Structural and functional alterations of the intramyocardial coronary arterioles in patients with arterial hypertension. Circulation, v. 88, p. 993-1003, 1993. SHAHBAZ, A. U. et al. Fibrosis in hypertensive heart disease: molecular pathways and cardioprotective strategies. J Hypertens, v. 28, n. 1, p. 25–32, 2010. SHIOTA, N. et al. A role for cardiac mast cells in the pathogenesis of hypertensive heart disease. Journal of Hypertension, v. 21, p.1935-1944, 2003. SILVA, R. P.; AMODEO, C.; RAMIRES, J. A. F. O ventrículo direito e a hipertensão arterial: aspectos ecocardiográficos. Arq Bras Cardiol, v. 79, p. 313-8, 2002. SPINALE, F. G. Myocardial matrix remodeling and the matrix metalloproteinases: influence on cardiac form and function. Physiol Rev, v. 87, n.4, p. 1285-342, 2007. STARY, H.C. Natural history and histological classification of atherosclerotic lesions: an update. Arterioscler Thromb Vasc Biol, v. 20, p. 1177-8, 2000. SUZUKI, K. et al. Activation of precursors for matrix metalloproteinases 1 (interstitial collagenase) and 3 (stromelysin) by rat mast-cell proteinases I and II. Biochem J; v. 305, p. 301–306, 1995. TANAKA, M. et al. Quantitative analysis of myocardial fibrosis in normals, hypertensive hearts, and hypertrophic cardiomyopathy. Br Heart J, v. 55, p. 575-581, 1986. TCHOUGOUNOVA, E. et al. A key role for mast cell chymase in the activation of promatrix metalloprotease-9 and pro-matrix metalloprotease-2. J Biol Chem, v. 280, p. 9291–9296, 2005. TEEKAKIRIKUL, P. et al. Cardiac fibrosis in mice with hypertrophic cardiomyopathy is mediated by non-myocyte proliferation and requires TGF-beta. J Clin Invest, v. 120, p. 3520-3529, 2010. THEOHARIDES, T. C. et al. Differential release of mast cell mediators and the pathogenesis of inflammation. Immunol. Rev, v. 217, p. 65-78, 2007. TSURUDA, T. et al. Adrenomedullin in mast cells of abdominal aortic aneurysm. Cardiovasc Res, v. 70, p. 158-164, 2006. VAKILI, B. A.; OKIN, P. M.; DEVEREUX, R. B. Prognostic implications of left ventricular hypertrophy. Am Heart J, v. 141 n. 3, p. 334-341, 2001. VASAN, R. S. et al. Association of leukocyte telomere length with echocardiographic left ventricular mass: the Framingham heart study. Circulation, v. 120, p. 1195-1202, 2009. WILLIAMS, M. A. Quantitative methods in biology. In: Pratical methods in electron microscopy. Editted by Glaubert A. M. Elsevier North-Holland Biomedical Press. Amsterdam, The Nederlands, p. 233, 1977. WILSON, P. W. F. et al. Prediction of Coronary Heart Disease Using Risk Factor Categories. Circulation, v. 97, n. 18, p. 1837-1847, 1998. World Health Organization. Cardiovascular diseases (CVDs). 2017. Disponível em: http://www.who.int/en/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds). Acesso em: 23 nov 2018. World Health Organization. Noncommunicable Diseases Progress Monitor. 2017. Disponível em: http://www.who.int/nmh/publications/ncd-progress-monitor-2017/en/. Acesso em: 24 nov 2018.http://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessreponame:Biblioteca Digital de Teses e Dissertações da UFTMinstname:Universidade Federal do Triangulo Mineiro (UFTM)instacron:UFTM2019-07-26T04:00:16Zoai:bdtd.uftm.edu.br:tede/792Biblioteca Digital de Teses e Dissertaçõeshttp://bdtd.uftm.edu.br/PUBhttp://bdtd.uftm.edu.br/oai/requestbdtd@uftm.edu.br||bdtd@uftm.edu.bropendoar:2024-04-24T09:59:15.842145Biblioteca Digital de Teses e Dissertações da UFTM - Universidade Federal do Triangulo Mineiro (UFTM)false
_version_ 1809186159465594880