CAMILA PAIXAO JORDAO
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina
6 resultados
Resultados de Busca
Agora exibindo 1 - 6 de 6
- Exercise Training Preserves Myocardial Strain and Improves Exercise Tolerance in Doxorubicin-Induced Cardiotoxicity(2021) GOMES-SANTOS, Igor L.; JORDAO, Camila P.; PASSOS, Clevia S.; BRUM, Patricia C.; OLIVEIRA, Edilamar M.; CHAMMAS, Roger; CAMARGO, Anamaria A.; NEGRAO, Carlos E.Doxorubicin causes cardiotoxicity and exercise intolerance. Pre-conditioning exercise training seems to prevent doxorubicin-induced cardiac damage. However, the effectiveness of the cardioprotective effects of exercise training concomitantly with doxorubicin treatment remains largely unknown. To determine whether low-to-moderate intensity aerobic exercise training during doxorubicin treatment would prevent cardiotoxicity and exercise intolerance, we performed exercise training concomitantly with chronic doxorubicin treatment in mice. Ventricular structure and function were accessed by echocardiography, exercise tolerance by maximal exercise test, and cardiac biology by histological and molecular techniques. Doxorubicin-induced cardiotoxicity, evidenced by impaired ventricular function, cardiac atrophy, and fibrosis. Exercise training did not preserve left ventricular ejection fraction or reduced fibrosis. However, exercise training preserved myocardial circumferential strain alleviated cardiac atrophy and restored cardiomyocyte cross-sectional area. On the other hand, exercise training exacerbated doxorubicin-induced body wasting without affecting survival. Finally, exercise training blunted doxorubicin-induced exercise intolerance. Exercise training performed during doxorubicin-based chemotherapy can be a valuable approach to attenuate cardiotoxicity.
conferenceObject Sympathetic Neural Overdrive, Endothelial Dysfunction and Aortic Stiffness in Coronavirus Disease 2019 Survivors: A Short-Term Study of Cardiovascular Sequelae(2021) FARIA, Diego; TESTA, Laura; MOLL-BERNARDES, Renata; MONIZ, Camila; RODRIGUES, Erika; COSTA-NETO, Abel; SOUSA, Andrea; RODRIGUES, Amanda; OLIVEIRA, Patricia; ALVES, Maria Janieire; SANTOS, Gabriel; SALEMI, Vera; PIMENTA, Ruan; PAIXAO, Camila; SANTOS, Beatriz; RONDON, Maria U.; CRAIGHEAD, Daniel; ROSSMAN, Matthew; CONSOLIM-COLOMBO, Fernanda M.; IRIGOYEN, Maria C.; MARTINEZ-LEMUS, Luis A.- Sacubitril/valsartan versus enalapril on exercise capacity in patients with heart failure with reduced ejection fraction: A randomized, double-blind, active-controlled study(2021) SANTOS, Marcelo Rodrigues dos; ALVES, Maria-Janieire de Nazare Nunes; JORDAO, Camila Paixao; PINTO, Caio Eduardo Novaes; CORREA, Kelly Thayane Souza; SOUZA, Francis Ribeiro de; FONSECA, Guilherme Wesley Peixoto da; TOMAZ FILHO, Joaquim; COSTA, Marcel; PEREIRA, Rosa Maria Rodrigues; NEGRAO, Carlos Eduardo; BARRETTO, Antonio Carlos PereiraBackground Sacubitril/valsar tan reduces mortality in patients with heart failure with reduced ejection fraction (HFrEF) when compared with enalapril. However, it is unknown the effect of both treatments on exercise capacity. We compared sacubitril/valsartan versus enalapril in patients with HFrEF based on peak oxygen consumption (VO2) and 6-minute walk test (6-MWT). Methods We included 52 participants with HFrEF with a left ventricular ejection fraction <40% to receive either sacu-bitril/ valsartan (target dose of 400 mg daily) or enalapril (target dose of 40 mg daily). Peak VO2 was measured by using cardiopulmonary exercise testing. Six-minute walk test was also performed. Results At 12 weeks, the sacubitril/valsartan (mean dose 382.6 +/- 57.6 mg daily) group had increased peak VO2 of 13.1% (19.35 +/- 0.99 to 21.89 +/- 1.04 mL/kg/min) and enalapril (mean dose 34.4 +/- 9.2 mg daily) 5.6% (18.58 +/- 1.19 to 19.62 +/- 1.25 mL/kg/min). However, no difference was found between groups (P = .332 interaction). At 24 weeks, peak VO2 increased 13.5% (19.35 +/- 0.99 to 21.96 +/- 0.98 mL/kg/min) and 12.0% (18.58 +/- 1.19 to 20.82 +/- 1.18 mL/kg/min) in sacubitril/valsartan (mean dose 400 +/- 0 mg daily) and enalapril (mean dose 32.7 +/- 11.0 mg daily), respectively. However, no differences were found between groups (P = .332 interaction). At 12 weeks, 6-MWT increased in both groups (sacubitril/valsartan: 459 +/- 18 to 488 +/- 17 meters [6.3%] and enalapril: 443 +/- 22 to 477 +/- 21 meters [7.7%]). At 24 weeks, sacubitril/valsartan increased 18.3% from baseline (543 +/- 26 meters) and enalapril decreased slightly to 6.8% (473 +/- 31 meters), but no differences existed between groups (P = .257 interaction). Conclusions Compared to enalapril, sacubitril/valsartan did not substantially improve peak VO2 or 6-MWT after 12 or 24 weeks in participants with HFrEF.
- Visceral Obesity and High Systolic Blood Pressure as the Substrate of Endothelial Dysfunction in Obese Adolescents(2021) HUSSID, Maria Fernanda; CEPEDA, Felipe Xerez; JORDAO, Camila P.; LOPES-VICENTE, Rafaela R. P.; VIRMONDES, Leslie; KATAYAMA, Keyla Y.; OLIVEIRA, Ezequiel F. de; OLIVEIRA, Luis V. F.; CONSOLIM-COLOMBO, Fernanda Marciano; TROMBETTA, Ivani CredidioBackground: Obesity affects adolescence and may lead to metabolic syndrome (MetS) and endothelial dysfunction, an early marker of cardiovascular risk. Albeit obesity is strongly associated with obstructive sleep apnea (OSA), it is not clear the role of OSA in endothelial function in adolescents with obesity. Objective: To investigate whether obesity during adolescence leads to MetS and/or OSA; and causes endothelial dysfunction. In addition, we studied the possible association of MetS risk factors and apnea hypopnea index (AHI) with endothelial dysfunction. Methods: We studied 20 sedentary obese adolescents (OA; 14.2 +/- 1.6 years, 100.9 +/- 20.3kg), and 10 normal-weight adolescents (NWA, 15.2 +/- 1.2 years, 54.4 +/- 5.3kg) paired for sex. We assessed MetS risk factors (International Diabetes Federation criteria), vascular function (Flow-Mediated Dilation, FMD), functional capacity (VO(2)peak) and the presence of OSA (AHI>1event/h, by polysomnography). We considered statistically significant a P<0.05. Results: OA presented higher waist (WC), body fat, triglycerides, systolic (SBP) and diastolic blood pressure (DBP), LDL-c and lower HDL-c and VO(2)peak than NWA. MetS was presented in the 35% of OA, whereas OSA was present in 86.6% of OA and 50% of EA. There was no difference between groups in the AHI. The OA had lower FMD than NWA (6.17 +/- 2.72 vs. 9.37 +/- 2.20%, p=0.005). There was an association between FMD and WC (R=-0.506, p=0.008) and FMD and SBP (R=-0.493, p=0.006). Conclusion: In adolescents, obesity was associates with MetS and caused endothelial dysfunction. Increased WC and SBP could be involved in this alteration. OSA was observed in most adolescents, regardless of obesity.
- Adjuvant Treatment with 5-Fluorouracil and Oxaliplatin Does Not Influence Cardiac Function, Neurovascular Control, and Physical Capacity in Patients with Colon Cancer (vol 25, pg e1956, 2020)(2021) GROEHS, Raphaela V.; NEGRAO, Marcelo V.; HAJJAR, Ludhmila A.; JORDAO, Camila P.; CARVALHO, Bruna P.; TOSCHI-DIAS, Edgar; ANDRADE, Ana C.; HODAS, Fabiana P.; ALVES, Maria J. N. N.; SARMENTO, Adriana O.; TESTA, Laura; HOFF, Paulo M. G.; NEGRAO, Carlos E.; KALIL FILHO, Roberto
- Breast Cancer Promotes Cardiac Dysfunction Through Deregulation of Cardiomyocyte Ca2+-Handling Protein Expression That is Not Reversed by Exercise Training(2021) COSTA, Tassia S. R. da; URIAS, Ursula; V, Marcelo Negrao; JORDAO, Camila P.; PASSOS, Clevia S.; GOMES-SANTOS, Igor L.; SALEMI, Vera Maria C.; CAMARGO, Anamaria A.; BRUM, Patricia C.; OLIVEIRA, Edilamar M.; HAJJAR, Ludhmila A.; CHAMMAS, Roger; FILHO, Roberto K.; NEGRAO, Carlos E.Background Patients treated for breast cancer have a high incidence of cardiovascular complications. In this study, we evaluated the impact of breast cancer on cardiac function and cardiomyocyte Ca2+-handling protein expression. We also investigated whether exercise training (ET) would prevent these potential alterations. Methods and Results Transgenic mice with spontaneous breast cancer (mouse mammary tumor virus-polyomavirus middle T antigen [MMTV-PyMT+], n=15) and littermate mice with no cancer (MMTV-PyMT-, n=14) were studied. For the ET analysis, MMTV-PyMT+ were divided into sedentary (n=10) and exercise-trained (n=12) groups. Cardiac function was evaluated by echocardiography with speckle-tracking imaging. Exercise tolerance test was conducted on a treadmill. Both studies were performed when the tumor became palpable and when it reached 1 cm(3). After euthanasia, Ca2+-handling protein expression (Western blot) was evaluated. Exercise capacity was reduced in MMTV-PyMT+ compared with MMTV-PyMT- (P-interaction=0.031). Longitudinal strain (P-group <0.001) and strain rate (P-group=0.030) were impaired. Cardiomyocyte phospholamban was increased (P=0.011), whereas phospho-phospholamban and sodium/calcium exchanger were decreased (P=0.038 and P=0.017, respectively) in MMTV-PyMT+. No significant difference in sarcoplasmic or endoplasmic reticulum calcium 2 ATPase (SERCA2a) was found. SERCA2a/phospholamban ratio was reduced (P=0.007). ET was not associated with increased exercise capacity. ET decreased left ventricular end-systolic diameter (P-group=0.038) and end-diastolic volume (P-group=0.026). Other morphological and functional cardiac parameters were not improved by ET in MMTV-PyMT+. ET did not improve cardiomyocyte Ca2+-handling protein expression. Conclusions Breast cancer is associated with decreased exercise capacity and subclinical left ventricular dysfunction in MMTV-PyMT+, which is at least partly associated with dysregulation of cardiomyocyte Ca2+ handling. ET did not prevent or reverse these changes.