9 research outputs found

    N-terminal prohormone brain natriuretic peptide (NT-proBNP) as a noninvasive marker for restrictive syndromes

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    Constrictive pericarditis (CP) and restrictive cardiomyopathy share many similarities in both their clinical and hemodynamic characteristics and N-terminal prohormone brain natriuretic peptide (NT-proBNP) is a sensitive marker of cardiac diastolic dysfunction. The objectives of the present study were to determine whether serum NT-proBNP was high in patients with endomyocardial fibrosis (EMF) and CP, and to investigate how this relates to diastolic dysfunction. Thirty-three patients were divided into two groups: CP (16 patients) and EMF (17 patients). The control group consisted of 30 healthy individuals. Patients were evaluated by bidimensional echocardiography, with restriction syndrome evaluated by pulsed Doppler of the mitral flow and serum NT-proBNP measured by immunoassay and detected by electrochemiluminescence. Spearman correlation coefficient was used to analyze the association between log NT-proBNP and echocardiographic parameters. Log NT-proBNP was significantly higher (P < 0.05) in CP patients (log mean: 2.67 pg/mL; 95%CI: 2.43-2.92 log pg/mL) and in EMF patients (log mean: 2.91 pg/mL; 95%CI: 2.70-3.12 log pg/mL) compared with the control group (log mean: 1.45; 95%CI: 1.32-1.60 log pg/mL). There were no statistical differences between EMF and CP patients (P = 0.689) in terms of NT-proBNP. The NT-proBNP log tended to correlate with peak velocity of the E wave (r = 0.439; P = 0.060, but not with A wave (r = -0.399; P = 0.112). Serum NT-proBNP concentration can be used as a marker to detect the presence of diastolic dysfunction in patients with restrictive syndrome; however, serum NT-proBNP levels cannot be used to differentiate restrictive cardiomyopathy from CP

    Leptin levels in different forms of Chagas' disease

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    Leptin is produced primarily by adipocytes. Although originally associated with the central regulation of satiety and energy metabolism, increasing evidence indicates that leptin may be an important mediator in cardiovascular pathophysiology. The aim of the present study was to investigate plasma leptin levels in patient with Chagas' heart disease and their relation to different forms of the disease. We studied 52 chagasic patients and 30 controls matched for age and body mass index. All subjects underwent anthropometric, leptin and N-terminal pro-brain natriuretic peptide (NT-proBNP) measurements and were evaluated by echocardiography, 12-lead electrocardiogram (ECG), and chest X-ray. All patients had fasting blood samples taken between 8:00 and 9:00 am. Chagasic patients were divided into 3 groups: group I (indeterminate form, IF group) consisted of 24 subjects with 2 positive serologic reactions for Chagas' disease and no cardiac involvement as evaluated by chest X-rays, ECG and two-dimensional echocardiography; group II (showing ECG abnormalities and normal left ventricular systolic function, ECG group) consisted of 14 patients; group III consisted of 14 patients with congestive heart failure (CHF group) and left ventricular dysfunction. Serum leptin levels were significantly lower (P < 0.001) in the CHF group (1.4 ± 0.8 ng/mL) when compared to the IF group (5.3 ± 5.3 ng/mL), ECG group (9.7 ± 10.7 ng/mL), and control group (8.1 ± 7.8 ng/mL). NT-proBNP levels were significantly higher (P < 0.001) in the CHF group (831.8 ± 800.1 pg/mL) when compared to the IF group (53.2 ± 33.3 pg/mL), ECG group (83.3 ± 57.4 pg/mL), and control group (32 ± 22.7 pg/mL). Patients with Chagas' disease and an advanced stage of CHF have high levels of NT-ProBNP andlow plasma levels of leptin. One or more leptin-suppressing mechanisms may operate in chagasic patients

    Association of angiotensin-converting enzyme activity and polymorphism with echocardiographic measures in familial and nonfamilial hypertrophic cardiomyopathy

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    Angiotensin-converting enzyme (ACE) activity and polymorphism contribute significantly to the prognosis of patients with cardiomyopathy. The aim of this study was to determine the activity and type of ACE polymorphism in patients with familial and nonfamilial hypertrophic cardiomyopathy (HCM) and to correlate these with echocardiographic measurements (echo-Doppler). We studied 136 patients (76 males) with HCM (69 familial and 67 nonfamilial cases). Mean age was 41 ± 17 years. DNA was extracted from blood samples for the polymerase chain reaction and the determination of plasma ACE levels. Left ventricular mass, interventricular septum, and wall thickness were measured. Mean left ventricular mass index, interventricular septum and wall thickness in familial and nonfamilial forms were 154 ± 63 and 174 ± 57 g/m² (P = 0.008), 19 ± 5 and 21 ± 5 mm (P = 0.02), and 10 ± 2 and 12 ± 3 mm (P = 0.0001), respectively. ACE genotype frequencies were DD = 35%, ID = 52%, and II = 13%. A positive association was observed between serum ACE activity and left ventricular mass index (P = 0.04). Logistic regression showed that ACE activity was twice as high in patients with familial HCM and left ventricular mass index &#8805;190 g/m² compared with the nonfamilial form (P = 0.02). No other correlation was observed between ACE polymorphisms and the degree of myocardial hypertrophy. In conclusion, ACE activity, but not ACE polymorphisms, was associated with the degree of myocardial hypertrophy in the patients with HCM

    Venous Endothelial Dysfunction In Chagas' Disease Patients Without Heart Failure [disfunção Endotelial Venosa Em Pacientes Com Doença De Chagas Sem Insuficiência Cardíaca]

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    OBJECTIVE: To analyze the venous endothelial function in Chagas' disease patients without heart failure. METHODS: The Chagas' disease Group (G1) was composed by 14 women and 2 men aged 46 ± 2,7 and the Control Group (G0) by 7 women and 1 man matched by age, weight and height. Dorsal Hand Vein Compliance Technique was used to evaluate the venous endothelial function. Crescent doses of phenylephrine were infused to get a 70% preconstriction of the vein; after that, acetylcholine and sodium nitroprusside were respectively administrated to analyze the endothelium-dependent and -independent venodilation. RESULTS: No significant systemic hemodynamic changes were observed in both groups during the experiment. The necessary phenylephrine dose to reach 70% preconstriction of the vein was significantly higher in the G1 (1116 ± 668,2 ng/ml) compared to G0 (103 ± 28 ng/ml) p = 0,05. The endothelium-dependent venous dilation was significantly lower in G1 (65,5 ± 8%) compared to G0 (137 ± 20 %) p = 0,009. No difference was observed in the endothelium-independent venous dilatation between groups. CONCLUSION: Patients with Chagas' disease without heart failure presented venous endothelial dysfunction.866466471Schmunis, G.A., American Trypanosomiasis as a public health problem (1994) Chagas' Disease and the Nervous System, pp. 3-29. , Pan American Health Organization (ed.). Washington, DC: Pan American OrganizationMarin-Neto, J.A., Simões, M.V., Sarabanda, A.V., Chagas'heart disease (1999) Arq Bras Cardiol, 72, pp. 247-280Mady, C., Barreto, A.C., Stolf, N., Lopes, E.A., Dauar, D., Wajngarten, M., Biopsia miocárdica na forma indeterminada da doença de Chagas (1981) Arq Bras Cardiol, 36, pp. 387-390Consolim-Colombo, F.M., Lopes, H.F., Rosetto, E.A., Endothelial function is preserved in Chagas' heart disease patients without heart failure (2004) Endothelium, 11 (5-6), pp. 241-246Guzman, Juan, C., Leon, Hernando, Casa, S., Juan, P., Disfunción autonómica y vascular en la fase asintomática de la enfermedad de Chagas (2004) Rev Colomb Cardiol, 11 (2), pp. 105-113Leiby, D.A., Rentas, F.J., Nelson, K.E., Evidence of Trypanosoma cruzi infection (Chagas' disease) among patients undergoing cardiac surgery (2000) Circulation, 102 (24), pp. 2978-2982Moncayo, A., Chagas disease: Current epidemiological trends after the interruption of vectorial and transfusional transmission in the Southern Cone countries (2003) Mem Inst Oswaldo Cruz, 5, pp. 577-591Ramos, S.G., Rossi, M.A., Microcirculation and Chagas' disease: Hypothesis and recent results (1999) Inst Med Trop São Paulo, 41 (2), pp. 123-129Soares Barreto-Filho, J.A., Consolim-Colombo, F.M., Ferreira Lopes, H., Martins Sobrinho, C.R., Guerra-Riccio, G.M., Krieger, E.M., Dysregulation of peripheral and central chemorefl ex responses in Chagas' heart disease patients without heart failure (2000) Circulation, 104 (15), pp. 1792-1798Rossi, M.A., Ramos, S.G., Coronary microvascular abnormalities in Chagas' disease (1996) Am Heart J, 132 (1), pp. 207-210Ianni, B.M., Arteaga, E., Frim, C.C., Pereira, C., Barreto, A.C., Mady, C., Chagas' heart disease: Evolutive evaluation of electrocardiographic and echocardiographic parameters in patients with the indeterminate form (2001) Arq Bras Cardiol, 77, pp. 59-62Consolim-Colombo, F.M., Filho, J.A., Lopes, H.F., Sobrinho, C.R., Otto, M.E., Riccio, G.M., Mady, C., Krieger, E.M., Decreased cardiopulmonary barorefl ex sensitivity in Chagas' heart disease (2000) Hypertension, 36 (6), pp. 1035-1039Anderson, T.J., Assessment and treatment of endothelial dysfunction in humans (1999) J Am Coll Cardiol, 34, pp. 631-638Drexler, H., Hornig, B., Endothelial dysfunction in human disease Endothelial dysfunction: A novel therapeutic target (1999) Mol Cell Cardiol, 31, pp. 51-60Schächinger, V., Britten, M.B., Zeiher, A.M., Prognostic impact of coronary vasodilator dysfunction on adverse long-term outcome of coronary heart disease (2000) Circulation, 101 (16), pp. 1899-1906Rossi, M.A., Aortic endothelial cell changes in the acute septicemic phase of experimental Trypanosoma cruzi infection in rats: Scanning and transmission electron microscopic study (1997) Am J Trop Med Hyg, 57 (3), pp. 321-327Camargos, E.R., Machado, C.R., Teixeira Jr., A.L., Rocha, L.L., Ferreira, A.J., Almeida, A.P., Barton, M., Teixeira, M.M., Role of endothelin during experimental Trypanosoma cruzi infection in rats (2002) Clin Sci, 103 (48 SUPPL.), pp. 64S-67S. , LondMorris, S.A., Tanowitz, H., Makman, M., Hatcher, V.B., Bilezikian, J.P., Trypanosoma cruzi: Alteration of cAMP metabolism following infection of human endothelial cell (1992) Exp Parasit, 74 (1), pp. 69-76Sunnemark, D., Frostegard, J., Orn, A., Harris, R.A., Cellular and cytokine characterization of vascular infl ammation in CBA/J mice chronically infected with Trypanosoma cruzi (1998) Scand J Immunol, 48 (5), pp. 480-484Tanowitz, H.B., Wittner, M., Morris, S.A., The putative mechanistic basis for the modulatory role of endothelin-1 in the altered vascular tone induced by Trypanosoma cruzi (1999) Endothelium, 6 (3), pp. 217-220Cardoni, R.L., Garcia, M.M., De Rissio, A.M., Proinfl ammatory and antiinflammatory cytokines in pregnant women chronically infected with Trypanosoma cruzi (2004) Acta Trop, 90 (1), pp. 65-72Ferreira, R.C., Ianni, B.M., Abel, L.C., Buck, P., Mady, C., Kalil, J., Cunha-Neto, E., Increased plasma levels of tumor necrosis factor-alpha in symptomatic "indeterminate" and Chagas disease cardiomyopathy patients (2003) Mem Inst Oswaldo Cruz, 98 (3), pp. 407-411Malvezi, A.D., Cecchini, R., De Souza, F., Tadokoro, C.E., Rizzo, L.V., Pinge-Filho, P., Involvement of nitric oxide (NO) and TNF-alpha in the oxidative stress associated with anemia in experimental Trypanosoma cruzi infection (2004) FEMS Immunol Med Microbiol, 41 (1), pp. 69-77Silva, J.S., Machado, F.S., Martins, G.A., The role of nitric oxide in the pathogenesis of Chagas disease (2003) Front Biosci, pp. s314-25Teichholz, L.E., Kreulen, T., Herman, M.V., Gorlin, R., Problems in echocardiographic volume determinations: Echocardiographic- angiographic correlation in the present or absence of a synergy (1976) Am J Cardiol, 37 (1), pp. 7-11Junqueira Jr., L.F., Discriminação entre as manifestações eletrocardiográficas normais, anormais e "borderline" na doença de Chagas (1992) Rev Soc Bras Med Trop, 25 (3 SUPPL.), p. 83Chalon, S., Bedarida, G.V., Moreno Jr., H., Tejura, B., Urae, A., Hoffman, B.B., Blaschke, T.F., Angiotensin-converting enzyme inhibition improves venous endothelial dysfunction in chronic smokers (1999) Clin Pharmacol Ther, 65, pp. 295-303Moreno Jr., H., Chalon, S., Urae, A., Tangphao, O., Abiose, A.K., Hoffman, B.B., Blaschke, T.F., Endothelial dysfunction in human hand veins is rapidly reversible after smoking cessation (1998) Am J Physiol, 275, pp. H1040-5Sousa, M.G., Yugar-Toledo, J.C., Rubira, M., Ascorbic acid improves impaired venous and arterial endothelium-dependent dilation in smokers (2005) Acta Pharmacol Sin, 26 (4), pp. 447-452Tangphao, O., Chalon, S., Moreno Jr., H., Hoffman, B.B., Blaschke, T.F., Pharmacokinetics of L-arginine during chronic administration to patients with hypercholesterolaemia (1999) Clin Sci, 96, pp. 199-207. , LondFurchgott, R.F., Zawadzki, J.V., The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine (1980) Nature, 288, pp. 373-376Li, H., Forstermann, U., Nitric oxide in the pathogenesis of vascular disease (2000) J Pathol, 190, pp. 244-254Costa, P.C., Fortes, F.S., Machado, A.B., Sera from chronic chagasic patients depress cardiac electrogenesis and conduction (2000) Braz J Med Biol Res, 33 (4), pp. 439-446Masuda, M.O., Levin, M., De Oliveira, S.F., Functionally active cardiac antibodies in chronic Chagas' disease are specifically blocked by Trypanosoma cruzi antigens (1998) FASEB J, 12 (14), pp. 1551-1558Ogawa, S., Yoshikawa, T., Autoantibodies: Emerging upstream targets of arrhythmias and sudden death in patients with idiopathic dilated cardiomyopathy (2001) J Mol Cell Cardiol, 33 (10), pp. 1761-1763Pedrosa, R.C., (1998) Contribuição Ao Estudo Da Etiopatogenia Do Distúrbio de Condução e Da Eletrogênese Na Cardiopatia Chagásica Crônica: Efeitos de Anticorpos IgG de Pacientes Chagásicos Crônicos Na Eletrogênese e No Sistema de Condução Do Coração Isolado de Mamíferos, , Rio de Janeiro, Tese (Doutorado) - Universidade Federal do Rio de JaneiroSchulte, K.L., Laber, E., Meyer-Sabellek, W.A., Distler, A., Gotzen, R., Specific alpha-adrenoceptor-mediated vasoconstriction in human veins and interaction with the calcium entry blockers nifedipine and diltiazem (1985) J Hypertens (Suppl), pp. S239-41Simões, M.V., Pintya, A.O., Bromberg-Marin, G., Sarabanda, A.V., Antloga, C.M., Pazin-Filho, A., Maciel, B.C., Marin-Neto, J.A., Relation of regional sympathetic denervation and myocardial perfusion disturbance to wall motion impairment in Chagas' cardiomyopathy (2000) Am J Cardiol, 86 (9), pp. 975-981Davila, D.F., Bellabarba, G., Hernandez, L., Calmon, G., Torres, A., Donis, J.H., Barboza, J.S., Gonzalez, J.G., Plasma norepinephrine, myocardial damage and left ventricular systolic function in Chagas' heart disease (1995) Int J Cardiol, 24-52 (2), pp. 145-15
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