Produção Nacional
Revisado por pares
Respiratory function and functional capacity in Chagas cardiomyopathy
2013; Elsevier BV; Volume: 168; Issue: 5 Linguagem: Inglês
10.1016/j.ijcard.2013.07.206
ISSN1874-1754
AutoresErika Alves Baião, Manoel Otávio da Costa Rocha, Márcia Maria Oliveira Lima, Francilu Rodrigues Beloti, Danielle Aparecida Gomes Pereira, Verônica Franco Parreira, Antônio Luiz Pinho Ribeiro, Raquel Rodrigues Britto,
Tópico(s)Cardiovascular Function and Risk Factors
ResumoApproximately 30% of patients with Chagas cardiomyopathy (ChC) develop severe chronic cardiomyopathy, having heart failure (HF) as a common complication [[1]Ribeiro A.L. Nunes M.P. Teixeira M.M. Rocha M.O. Diagnosis and management of Chagas disease and cardiomyopathy.Nat Rev Cardiol. Oct 2012; 9: 576-589Crossref PubMed Scopus (172) Google Scholar]. HF patients usually present dyspnea and fatigue as symptoms limiting the physical and daily life activities [1Ribeiro A.L. Nunes M.P. Teixeira M.M. Rocha M.O. Diagnosis and management of Chagas disease and cardiomyopathy.Nat Rev Cardiol. Oct 2012; 9: 576-589Crossref PubMed Scopus (172) Google Scholar, 2Piepoli M.F. Conraads V. Corrà U. et al.Exercise training in heart failure: from theory to practice. A consensus document of the Heart Failure Association and the European Association for Cardiovascular Prevention and Rehabilitation.Eur J Heart Fail. Apr 2011; 13: 347-357Crossref PubMed Scopus (400) Google Scholar]. The reduced functional capacity on ChC is associated with neurohumoral and inflammatory markers [[3]Sousa L. Botoni F.A. Britto R.R. et al.Six-minute walk test in Chagas cardiomyopathy.Int J Cardiol. Mar 28 2008; 125: 139-141Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar] which could improve the respiratory muscle weakness observed in HF patients. In this study we compared the respiratory function, muscle strength and endurance of patients with ChC and patients with HF for other etiologies as well as the relation with the functional capacity. We evaluated 45 subjects, 15 in each group of patients (ChC group and HF for other etiologies — HF group) and 15 healthy subjects (control group). The inclusion criteria were: age < 65, no smoking, without musculoskeletal or other conditions that could compromise exercise tests, no participation on regular physical activity program from the last six months, without diabetes mellitus or other metabolic diseases and no use of pacemakers. For the ChC group, Chagas disease was diagnosed based on the presence of at least two positive serological tests (ELISA, indirect hemagglutination or indirect immunofluorescence). Exclusion criteria included the presence of ventilatory alterations on spirometry, clinical instability or inability to execute any procedures. The Ethic and Research Committee approved the study and volunteers signed the informed consent. Forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), FEV1/FVC and 25–75% of expiratory forced flow (FEF25–75%) expressed in liter (l) and in percentage (%) of the predicted value [[4]Neder J.A. Andreone S. Leratio M.C. et al.Reference values for lung function test. II. Maximal respiratory pressures and voluntary ventilation.Braz J Biol Res. 1999; 32: 719-727PubMed Google Scholar] were evaluated by standardized pulmonary function tests considering 80% as normal. Respiratory muscle strength was assessed by the maximal inspiratory muscle pressure (MIP) and maximal expiratory muscle pressure (MEP), at residual volume and total lung capacity, respectively, using a manovacuometer (MTR, GERAR® SP/Brazil) with a conventional mouthpiece and nose clip [[4]Neder J.A. Andreone S. Leratio M.C. et al.Reference values for lung function test. II. Maximal respiratory pressures and voluntary ventilation.Braz J Biol Res. 1999; 32: 719-727PubMed Google Scholar]. The Threshold® IMT, a device calibrated in centimeters of water, was used to assess the inspiratory muscle endurance. Briefly it consisted of breathing during 2 min at 50% of MIP, and subsequently, 10% of MIP added every 2 min until the subjects stopped because of fatigue or dyspnea. The greatest pressure sustained for at least 1 min (maximal peak pressure — Pm-peak) was considered [[5]ATS/ERS statement on respiratory muscle testing.Am J Respir Crit Care Med. 2002; 166: 518-624Crossref PubMed Scopus (1503) Google Scholar]. The maximal functional capacity, expressed as estimated oxygen consumption achieved (peak V02), was evaluated by a symptom-limited exercise test using Bruce protocol. Normal continuous variables were expressed as mean and standard deviation (mean ± SD) and nonnormal (Shapiro–Wilk) data as median and interquartile range. Comparisons were made by ANOVA one-way plus Tukey test or Kruskal–Wallis plus Wilcoxon and correlations by Spearman coefficient considering the significance level of 0.05. Table 1 shows the main group characteristics. The HF group was characterized by 40% of dilated cardiomyopathy and 60% of ischemic cardiomyopathy. The main results (Table 2) were: 1) patients with Chagas cardiomyopathy presented a reduced respiratory muscle strength and endurance as well as reduced functional capacity; 2) the respiratory function, the respiratory muscle strength and endurance and the functional capacity of these patients were similar to the ones with non-Chagas cardiomyopathy, except for forced vital capacity (HF < ChC, p = 0.043) and 3) the ChC group presented reduced chronotropic response to the same level of exercise compared with the HF group. In cardiomyopathy patients' peak V02 significantly (p < 0.0001) correlated with the respiratory variables, MIP, MEP and Pm-peak (r = 0.52, 0.53 and 0.55, respectively) but not with the left ventricular function (r = −0.25, p = 0.22).Table 1Demographic, anthropometric and ecocardiography data.VariablesControl(n = 15)HF(n = 15)Ch(n = 15)p valueGender (F:M)7:87:87:8–Age (year)47.27 ± 9.1248.60 ± 8.9550.27 ± 5.680.59Weight (kg)64.47 ± 12.1472.87 ± 16.3264.91 ± 12.910.19Height (m)1.64 ± 0.081.65 ± 0.091.61 ± 0.100.31BMI (kg/m2)23.70 ± 3.5926.93 ± 5.6024.93 ± 4.030.15NYHA (II:III)–12:313:2–LVEF (%)a–40.00 (30.22–57.38)36.00 (34.45–2.88)0.72LVD (mm)a–69.00 (62.56–75.84)62.00 (59.95–65.11)0.07Data expressed as media and standard deviation or median (interquartile range). ANOVA and Mann–Whitney Testa.ChC: Chagas cardiomyopathy, HF: heart failure, F: female, M: male, BMI: body mass index, NYHA: New York Heart Association, LVEF: left ventricular ejection fraction, LVD: left ventricular end-diastolic diameter. Open table in a new tab Table 2Spirometric, respiratory muscle function and symptom-limited exercise test variables.VariablesControl(n = 15)HF(n = 15)ChC(n = 15)p valueFVC (L)3.68 ± 0.653.22 ± 0.983.39 ± 0.750.30% previsto96.2 ± 7.9483.4 ± 13.4595.7 ± 17.430.02p = 0.013aIn relation to control group.p = 0.017bIn relation to HF group.FEV1 (L)2.93 ± 0.532.55 ± 0.832.51 ± 0.570.17% previsto93.6 ± 9.2280.5 ± 15.1887.0 ± 14.930.04p = 0.010aIn relation to control group.FEV1/FVC81.26 ± 5.7181.33 ± 8.1677.69 ± 9.340.36% previsto99.6 ± 6.8899.0 ± 10.0195.9 ± 11.250.54FEF25–75% (L/s)2.60 (2.28–3.38)2.35 (2.10-3.52)1.81 (1.60–2.63)0.12c% previsto82.00 (74.56–104.51)83.00 (63.27–123.11)68.00 (56.83–87.44)0.28cMIP (cmH2O)80 (73.65–98.35)50.00 (53.20–73.46)50.00 (46.70–75.97)0.01cp = 0.009aIn relation to control group.p = 0.02aIn relation to control group.% previsto84.1 ± 21.0062.3 ± 13.1360.4 ± 23.320.003p = 0.011aIn relation to control group.p = 0.005aIn relation to control group.MEP (cmH2O)102.6 ± 43.9190.0 ± 45.3573.3 ± 42.280.20% previsto97.7 ± 43.8180.1 ± 28.4368.1 ± 31.55aIn relation to control group.0.08Pm-peak (cmH2O)72.00 (59.36–83.04)38.00 (31.35–48.65)35.00 (34.64–57.90)0.001cp < 0.001aIn relation to control group.p < 0.001aIn relation to control group.V02 (mL/kg/min)38.53 ± 7.8130.80 ± 9.5828.46 ± 6.580.004p = 0.032aIn relation to control group.p = 0.004aIn relation to control group.MET10.64 ± 2.698.80 ± 2.738.13 ± 1.880.023NS (p = 0.11)p = 0.022aIn relation to control group.HRpeak (bpm)164.5 ± 19.88147.1 ± 19.50116.1 ± 14.72<0.0001p = 0.032aIn relation to control group.p < 0.0001aIn relation to control group.Data are presented as media and standard deviation or median (interquartile range). NS: no significant. Bold: significant between groups. ANOVA or Kruskall-Wallis Testc plus post-hoc Tukey or Wilcoxon.ChC: Chagas cardiomyopathy, HF: heart failure, FVC: forced vital capacity, FEV1: forced expiratory volume in 1 s, FEF25–75%: 25–75% of expiratory forced flow, MIP: maximal inspiratory pressure, MEP: maximal expiratory pressure, Pm-peak: maximal peak pressure, V02: peak oxygen consumption, MET: metabolic index, HRpeak: peak heart rate.a In relation to control group.b In relation to HF group. Open table in a new tab Data expressed as media and standard deviation or median (interquartile range). ANOVA and Mann–Whitney Testa. ChC: Chagas cardiomyopathy, HF: heart failure, F: female, M: male, BMI: body mass index, NYHA: New York Heart Association, LVEF: left ventricular ejection fraction, LVD: left ventricular end-diastolic diameter. Data are presented as media and standard deviation or median (interquartile range). NS: no significant. Bold: significant between groups. ANOVA or Kruskall-Wallis Testc plus post-hoc Tukey or Wilcoxon. ChC: Chagas cardiomyopathy, HF: heart failure, FVC: forced vital capacity, FEV1: forced expiratory volume in 1 s, FEF25–75%: 25–75% of expiratory forced flow, MIP: maximal inspiratory pressure, MEP: maximal expiratory pressure, Pm-peak: maximal peak pressure, V02: peak oxygen consumption, MET: metabolic index, HRpeak: peak heart rate. This study reinforces hypothesis presented in a previous study conducted by our group [[2]Piepoli M.F. Conraads V. Corrà U. et al.Exercise training in heart failure: from theory to practice. A consensus document of the Heart Failure Association and the European Association for Cardiovascular Prevention and Rehabilitation.Eur J Heart Fail. Apr 2011; 13: 347-357Crossref PubMed Scopus (400) Google Scholar] that increased level of circulating proinflammatory chemokines could provoke respiratory and limb weakness and cause reduced physical activity and dyspnea in these patients. Oca et al. [[6]Oca M. Torres S.H. Loyo J.G. et al.Exercise performance and skeletal muscles in patients with advanced Chagas disease.Chest. 2004; 125: 1306-1314Crossref PubMed Scopus (18) Google Scholar] demonstrate more glycolytic and less oxidative capacity of the peripheral muscle in patients with advanced Chagas disease. These alterations could be related to the auto-immune process present during the chronic phase of Chagas disease, whereas the autoimmunity is considered a pathological mechanism for heart and muscle injuries. Although reduced values of pulmonary function variables were found, they are between the clinically normal ranges. The reduced MIP observed in the patient groups is similar to that in other studies with HF patients for different etiologies [[7]Chua T.P. Anker S.D. Harrington D. et al.Inspiratory muscle strength is a determinant of maximum oxygen consumption in chronic heart failure.Br Heart J. 1995; 74: 381-385Crossref PubMed Scopus (71) Google Scholar]. Considered as an important parameter to represent the respiratory effort necessary to daily activities [[8]Lima M.M. Rocha M.O. Nunes M.C. et al.A randomized trial of the effects of exercise training in Chagas cardiomyopathy.Eur J Heart Fail. Aug 2010; 12: 866-873Crossref PubMed Scopus (38) Google Scholar], the lowest respiratory muscle endurance (Pm-peak) in HF and ChC patients was also reported by previous study [[9]Dall'Ago P. Chiappa G.R. Guths H. Stein R. Ribeiro J.P. Inspiratory muscle training in patients with heart failure and inspiratory muscle weakness: a randomized trial.J Am Coll Cardiol. Feb 21 2006; 47: 757-763Abstract Full Text Full Text PDF PubMed Scopus (240) Google Scholar]. The %MEP lower than 70% of the predicted value on ChC patients is considered as a reference to prescribe the respiratory muscle training and could indicate the impairment of the peripheral muscle. A reduced peak VO2 and also a characteristic reduced chronotropic response were observed on ChC patients [[1]Ribeiro A.L. Nunes M.P. Teixeira M.M. Rocha M.O. Diagnosis and management of Chagas disease and cardiomyopathy.Nat Rev Cardiol. Oct 2012; 9: 576-589Crossref PubMed Scopus (172) Google Scholar]. The respiratory variables of cardiomyopathy patients correlate with VO2 as has been identified in HF [[7]Chua T.P. Anker S.D. Harrington D. et al.Inspiratory muscle strength is a determinant of maximum oxygen consumption in chronic heart failure.Br Heart J. 1995; 74: 381-385Crossref PubMed Scopus (71) Google Scholar]. On the other hand, the absence of correlation between functional capacity (peak VO2) and LFVE indicates that these phenomena are different, though related and have different determinants as described by Lima et al. [[10]Lima M.M. Nunes M.C. Rocha M.O. et al.Left ventricular diastolic function and exercise capacity in patients with Chagas cardiomyopathy.Echocardiography. May 2010; 27: 519-524Crossref PubMed Scopus (19) Google Scholar]. A study with ChC patients reported improvement on functional capacity and quality of life after aerobic training [[7]Chua T.P. Anker S.D. Harrington D. et al.Inspiratory muscle strength is a determinant of maximum oxygen consumption in chronic heart failure.Br Heart J. 1995; 74: 381-385Crossref PubMed Scopus (71) Google Scholar]. However, knowledge about the effect of respiratory muscle training in this population is still scarce. Other studies have to be conducted including patients with NYHA III and IV considering that there is a relationship between functional capacity and severity of ChC [[2]Piepoli M.F. Conraads V. Corrà U. et al.Exercise training in heart failure: from theory to practice. A consensus document of the Heart Failure Association and the European Association for Cardiovascular Prevention and Rehabilitation.Eur J Heart Fail. Apr 2011; 13: 347-357Crossref PubMed Scopus (400) Google Scholar]. In conclusion, patients with Chagas cardiomyopathy also present a reduced strength and resistance of respiratory muscles correlated to functional capacity. These results reinforce the useful strategy to considerer the evaluation and training of the respiratory muscles in the clinical management of these patients.
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