Artículos de revistas
Infliximab Reduces Cardiac Output In Rheumatoid Arthritis Patients Without Heart Failure [infliximabe Reduz Débito Cardíaco Em Pacientes Com Artrite Reumatoide Sem Insuficiência Cardíaca]
Revista Da Associacao Medica Brasileira. , v. 58, n. 6, p. 698 - 702, 2012.
Moreno Jr. H.
Objective: Human anti-tumor necrosis factor (TNF-α) monoclonal antibody (infliximab) is used to treat autoimmune diseases such as rheumatoid arthritis (RA). Although the risk of worsening heart failure has been described in patients under chronic treatment, the acute cardiovascular effects of this drug are unknown in RA patients without heart failure. Methods: 14 RA patients with normal echocardiography and no history of heart failure were evaluated during the 2-hour infliximab (3-5 mg/kg) infusion period, using a noninvasive hemodynamic beat-to-beat system (Portapres). Stroke volume (SV); systolic, diastolic and mean blood pressures (SBP, DBP and MBP, respectively); cardiac output (CO); heart rate (HR); and total peripheral vascular resistance (PVR) were recorded. All patients also received saline infusion instead of infliximab as a control. Significant differences in hemodynamic parameters were determined using Tuckey's test. All values were expressed as mean ± standard deviation (SD). Results: Fourteen RA patients (6M/8F) with mean age of 47.2 ± 8.8 years were evaluated. A significant decrease was found in cardiac output and stroke volume (7.04 ± 2.3 to 6.12 ± 2.1 l/min and 91 ± 29.0 to 83 ± 28.8 mL/beat, respectively) after infliximab infusion. Although not statistically significant, a progressive increase was detected in SBP, DBP and total PVR during infusion. Saline infusion did not cause significant hemodynamic changes in the same group of RA patients. No adverse effects were observed during the infusion period. Conclusion: Acute infliximab administration decreased cardiac output due to low stroke volume in RA patients without heart disease. The results also demonstrated that, in spite of its negative inotropic effect, infliximab enhanced BP, probably by increasing PVR. © 2012 Elsevier Editora Ltda. All rights reserved.586698702Smolen, J.S., Aletaha, D., Koeller, M., Weisman, M.H., Emery, P., New therapies for treatment of rheumatoid arthritis (2007) Lancet., 370, pp. 1861-1874Doan, T., Massarotti, E., Rheumatoid arthritis: An overview of new and emerging therapies (2005) J Clin Pharmacol., 45, pp. 751-762Mann, D.L., Inflammatory mediators and the failing heart: Past, present, and the foreseeable future (2002) Circ Res., 91, pp. 988-998Lysander, W.J., van Lieshout, J.J., Non-invasive pulsatile arterial pressure and stroke volume changes from the human finger (2005) Exp Physiol., 90, pp. 437-446Wallberg-Jonsson, S., Johansson, H., Ohman, M.L., Rantapaa-Dahlqvist, S., Extent of inflammation predicts cardiovascular disease and overall mortality in seropositive rheumatoid arthritis. A retrospective cohort study from disease onset (1999) J Rheumatol., 26, pp. 2562-2571Wolfe, F., Flowers, N., Burke, T.A., Arguelles, L.M., Pettitt, D., Increase in lifetime adverse drug reactions, service utilization, and disease severity among patients who will start COX-2 specific inhibitors: Quantitative assessment of channeling bias and confounding by indication in 6689 patients with rheumatoid arthritis and osteoarthritis (2002) J Rheumatol., 29, pp. 1015-1022Bértolo, M.B., Brenol, C.V., Schainberg, C.G., Neubarth, F., Lima, F.A.C., Laurindo, I.M., Atualização do consenso brasileiro no diagnóstico e tratamento da artrite reumatóide (2007) Rev Bras Reumatol., 47, pp. 151-159Aletaha, D., Neogi, T., Silman, A.J., Funovits, J., Felson, D.T., Bingham III, C.O., 2010 rheumatoid arthritis classification criteria: An American College of Rheumatology/European League Against Rheumatism collaborative initiative (2010) Arthritis Rheum., 62, pp. 2569-2581Lang, E.A., Recommendations for chamber quantification: A report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group (2005) J Am Soc Echocardiogr., 18, pp. 1440-1463El Assaad, M.A., Topouchian, J.A., Darne, B.M., Asmar, R.G., Validation of the Omron HEM-907 device for blood pressure measurement (2002) Blood Press Monit., 7, pp. 237-241Chobanian, A.V., Bakris, G.L., Black, H.R., Cushman, W.C., Green, L.A., Izzo Jr., J.L., The Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 report (2003) JAMA., 289, pp. 2560-2572Langewouters, G.J., Settels, J.J., Roelandt, R., Wesseling, K.H., Why use Finapres or Portapres rather than intra-arterial or intermittent non-invasive techniques of blood pressure measuremant? (1998) J Med Eng Technol., 22, pp. 37-43Jansen, J.R.C., Schreuder, J.J., Mulier, J.P., Smith, N.T., Settels, J.J., Wesseling, K.H., A comparison of cardiac output derived from the arterial pressure wave against thermodilution in cardiac surgery patients (2001) Br J Anaesth., 87, pp. 212-222Leonetti, P., Audat, F., Girard, A., Laude, D., Lefrère, F., Elghozi, J., Stroke volume monitored by modeling flow from finger arterial pressure waves mirrors blood volume withdrawn by phlebotomy (2004) Clin Auton Res., 14, pp. 176-181Ramey, D.R., Raynauld, J.P., Fries, J.F., The health assessment questionnaire 1992: Status and review (1992) Arthritis Care Res., 5, pp. 119-129Wolfe, F., A reappraisal of HAQ disability in rheumatoid arthritis (2000) Arthritis Rheum., 43, pp. 2751-2761Kumar, A., Anel, R., Bunnell, E., Habet, K., Neumann, A., Wolff, D., Effect of large volume infusion on left ventricular volumes, performance and contractility parameters in normal volunteers (2004) Intensive Care Med., 30, pp. 1361-1369Ku, I.A., Imboden, J.B., Hsue, P.Y., Ganz, P., Rheumatoid arthritis: Model of systemic inflammation driving atherosclerosis (2009) Circ J., 73, pp. 977-985van de Putte, L.B., Atkins, C., Malaise, M., Sany, J., Russell, A.S., van Riel, P.L., Efficacy and safety of adalimumab as monotherapy in patients with rheumatoid arthritis for whom previous disease modifying antirheumatic drug treatment has failed (2004) Ann Rheum Dis., 63, pp. 508-516Weinblatt, M.E., Keystone, E.C., Furst, D.E., Moreland, L.W., Weisman, M.H., Birbara, C.A., Adalimumab, a fully human anti-tumor necrosis factor alpha monoclonal antibody, for the treatment of rheumatoid arthritis in patients taking concomitant methotrexate: The ARMADA trial (2003) Arthritis Rheum., 48, pp. 35-45Mann, D.L., McMurray, J.J., Packer, M., Swedberg, K., Borer, J.S., Colucci, W.S., Targeted anticytokine therapy in patients with chronic heart failure: Results of the Randomized Etanercept Worldwide Evaluation (RENEWAL) (2004) Circulation., 109, pp. 1594-1602Chung, E.S., Packer, M., Lo, K.H., Fasanmade, A.A., Willerson, J.T., Randomized, double-blind, placebo-controlled, pilot trial of infliximab, a chimeric monoclonal antibody to tumor necrosis factor-alpha, in patients with moderate-to-severe heart failure: Results of the anti-TNF Therapy Against Congestive Heart Failure (ATTACH) trial (2003) Circulation., 107, pp. 3133-3140Kubota, T., Bounoutas, G.S., Miyagishima, M., Kadokami, T., Sanders, V.J., Bruton, C., Soluble tumor necrosis factor receptor abrogates myocardial inflammation but not hypertrophy in cytokine-induced cardiomyopathy (2000) Circulation., 101, pp. 2518-2525Kadokami, T., Frye, C., Lemster, B., Wagner, C.L., Feldman, A.M., McTiernan, C.F., Anti-tumor necrosis factor-alpha antibody limits heart failure in a transgenic model (2001) Circulation., 104, pp. 1094-1097Zink, A., Strangfeld, A., Schneider, M., Herzer, P., Hierse, F., Stoyanova-Scholz, M., Effectiveness of tumor necrosis factor inhibitors in rheumatoid arthritis in an observational cohort study: Comparison of patients according to their eligibility for major randomized clinical trials (2006) Arthritis Rheum., 54, pp. 3399-3407Khaper, N., Bryan, S., Dhingra, S., Singal, R., Bajaj, A., Pathak, C.M., Targeting the vicious inflammation-oxidative stress cycle for the management of heart failure (2010) Antioxid Redox Signal., 13, pp. 1033-1049Giordano, F.J., Oxygen, oxidative stress, hypoxia, and heart failure (2005) J Clin Invest., 115, pp. 500-508Matsuzawa, A., Ichijo, H., Redox control of cell fate by MAP kinase: Physiological roles of ASK1-MAP kinase pathway in stress signaling (2008) Biochim Biophys Acta., 1780, pp. 1325-1336Scallon, B.J., Moore, M.A., Trinh, H., Knight, D.M., Ghrayeb, J., Chimeric anti-TNFalpha monoclonal antibody cA2 binds recombinant transmembrane TNFalpha and activates immune effector functions (1995) Cytokine., 7, pp. 251-259