Heart 1999;82:279-285 ( September )

Different microcirculatory and interstitial matrix patterns in idiopathic dilated cardiomyopathy and Chagas' disease: a three dimensional confocal microscopy study

M de Lourdes Higuchi^a, S Fukasawa^a, T De Brito^b, L C Parzianello^c, G Bellotti^d, J A F Ramires^d

^a Service of Pathology, Heart Institute of São Paulo University Medical School, Av Dr Eneas C Aguiar, 44São Paulo, CEP 05403/000, Brazil, ^b Institute of Tropical Medicine of São Paulo University Medical School, São Paulo, Brazil, ^c Computer Division, Heart Institute of São Paulo University Medical School, São Paulo, Brazil, ^d Clinical Division, Heart Institute of São Paulo University Medical School, São Paulo, Brazil

Correspondence to: Dr de Lourdes Higuchi.

Accepted for publication 14 January 1999

OBJECTIVETo analyse the morphological aspects of the extracellular matrix and microcirculation to clarify whether chronic Chagas' cardiopathy (CCC) is an accurate model to study the pathogenesis of idiopathic dilated cardiomyopathy (IDCM).
DESIGNThick histological myocardial sections were prepared to analyse collagen, and microcirculation was examined during confocal laser and light microscopy.
SETTINGThe specimens were prepared at the pathology service of the Heart Institute of São Paulo, Brazil.
PATIENTSNine control hearts, eight IDCM hearts, and 10 CCC hearts were studied after necropsy.
MAIN OUTCOME MEASURESThe number of collagen struts per 100× field, the area of fibrosis (%), and the diameters of arterioles and capillaries were measured in each heart to establish outcome.
RESULTSA smaller number (mean (SD)) of collagen struts was seen in the hearts in the IDCM group (9.1 (4.1)) than in the control (22.4 (3.2)) (p < 0.05) or CCC (15.7 (7.4)) (p > 0.05) groups. Fibrosis was greater in the CCC hearts (13.8 (10.5)%) than in the IDCM hearts (5.9 (6.6)%) (p > 0.05). Major increases in arteriole (65.4 (9.9) µm) and capillary (9.9 (1.7) µm) diameters were seen in the CCC hearts but not in the IDCM hearts (arteriole diameter 40.3 (7.9) µm; capillary diameter 7.9 (1.3) µm).
CONCLUSIONSHearts demonstrating CCC and IDCM present different extracellular and microvessel alterations. This suggests that distinct pathogenic mechanisms are responsible for each condition and that CCC is not an effective model to study IDCM.


Keywords: microcirculation; Chagas' disease; dilated cardiomyopathy; extracellular matrix

---

© 1999 by Heart
CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

• Waghabi, M. C., de Souza, E. M., de Oliveira, G. M., Keramidas, M., Feige, J.-J., Araujo-Jorge, T. C., Bailly, S. (2009). Pharmacological Inhibition of Transforming Growth Factor {beta} Signaling Decreases Infection and Prevents Heart Damage in Acute Chagas' Disease. Antimicrob. Agents Chemother. 53: 4694-4701 [Abstract] [Full Text]  
• Schmitz, V., Svensjo, E., Serra, R. R., Teixeira, M. M., Scharfstein, J. (2009). Proteolytic generation of kinins in tissues infected by Trypanosoma cruzi depends on CXC chemokine secretion by macrophages activated via Toll-like 2 receptors. J. Leukoc. Biol. 85: 1005-1014 [Abstract] [Full Text]  
• Hiss, F. C., Lascala, T. F., Maciel, B. C., Marin-Neto, J. A., Simoes, M. V. (2009). Changes in myocardial perfusion correlate with deterioration of left ventricular systolic function in chronic Chagas' cardiomyopathy.. J Am Coll Cardiol Img 2: 164-172 [Abstract] [Full Text]  
• Rochitte, C. E., Oliveira, P. F., Andrade, J. M., Ianni, B. M., Parga, J. R., Avila, L. F., Kalil-Filho, R., Mady, C., Meneghetti, J. C., Lima, J. A.C., Ramires, J. A.F. (2005). Myocardial Delayed Enhancement by Magnetic Resonance Imaging in Patients With Chagas' Disease: A Marker of Disease Severity. J Am Coll Cardiol 46: 1553-1558 [Abstract] [Full Text]  
• Waghabi, M. C., Keramidas, M., Bailly, S., Degrave, W., Mendonca-Lima, L., Soeiro, M. d. N. C., Meirelles, M. d. N. L., Paciornik, S., Araujo-Jorge, T. C., Feige, J.-J. (2005). Uptake of Host Cell Transforming Growth Factor-{beta} by Trypanosoma cruzi Amastigotes in Cardiomyocytes: Potential Role in Parasite Cycle Completion. Am. J. Pathol. 167: 993-1003 [Abstract] [Full Text]  
• Marino, A. P. M.P., da Silva, A., dos Santos, P., Pinto, L. M. d. O., Gazzinelli, R. T., Teixeira, M. M., Lannes-Vieira, J. (2004). Regulated on Activation, Normal T Cell Expressed and Secreted (RANTES) Antagonist (Met-RANTES) Controls the Early Phase of Trypanosoma cruzi-Elicited Myocarditis. Circulation 110: 1443-1449 [Abstract] [Full Text]  
• Michailowsky, V., Celes, M. R. N., Marino, A. P., Silva, A. A., Vieira, L. Q., Rossi, M. A., Gazzinelli, R. T., Lannes-Vieira, J., Silva, J. S. (2004). Intercellular Adhesion Molecule 1 Deficiency Leads to Impaired Recruitment of T Lymphocytes and Enhanced Host Susceptibility to Infection with Trypanosoma cruzi. J. Immunol. 173: 463-470 [Abstract] [Full Text]  
• SCHIJMAN, A. G., VIGLIANO, C. A., VIOTTI, R. J, BURGOS, J. M., BRANDARIZ, S., LOCOCO, B. E., LEZE, M. I., ARMENTI, H. A., LEVIN, M. J. (2004). TRYPANOSOMA CRUZI DNA IN CARDIAC LESIONS OF ARGENTINEAN PATIENTS WITH END-STAGE CHRONIC CHAGAS HEART DISEASE. Am J Trop Med Hyg 70: 210-220 [Abstract] [Full Text]  
• Higuchi, M. d. L., Benvenuti, L. A., Martins Reis, M., Metzger, M. (2003). Pathophysiology of the heart in Chagas' disease: current status and new developments. Cardiovasc Res 60: 96-107 [Abstract] [Full Text]  
• HAYWARD, M P (1999). Dynamic cardiomyoplasty: time to wrap it up?. Heart 82: 263-264 [Full Text]