We investigated a potential link between genetic polymorphisms in genes XRCC1 (Arg399Gln), OGG1 (Ser326Cys), XRCC3 (Thr241Met), and XRCC4 (Ile401Thr) with the level of DNA damage and repair, accessed by comet and micronucleus test, in 51 COPD patients and 51 controls.

While the majority of individuals with coronavirus disease 2019 (COVID-19) recover completely, a significant percentage experience persistent symptom, which has been characterized as Long COVID and may be associated with cardiac and autonomic dysfunction. We evaluated heart rate variability (HRV) at rest and during deep-breathing (M-RSA) in patients with Long COVID. Case–control design involved 21 patients with Long COVID and 20 controls; the HRV was evaluated (POLAR system) at rest in the supine position and during M-RSA and expressed in time domain and non-linear analysis. In the supine position we found a reduction HRV measures in Long COVID’ patients compared to controls for: Mean_iRR (p < 0.001), STD_iRR (p < 0.001); STD_HR (p < 0.001); SD1 (p < 0.001); SD2 (p < 0.001); alpha2 (p < 0.001). In the M-RSA we found reduction Mean_iRR (p < 0.001), STD_iRR (p < 0.001), STD_HR (p < 0.001), rMSSD (p < 0.001), RR_tri-index (p < 0.001) in Long COVID’ patients except for highest Mean_HR p < 0.001. In conclusion, Long COVID reduced HRV at rest and during deep breathing. These findings may imply impairment of cardiac autonomic control when symptoms of COVID-19 persist following initial recovery.

Introduction: Chronic obstructive pulmonary disease (COPD) is recognized as a multisystemic inflammatory disease associated with extrapulmonary comorbidities, including respiratory muscle weakness and cardiovascular and cardiac autonomic regulation disorders. We investigated whether alterations in respiratory muscle strength (RMS) would affect cardiac autonomic modulation in COPD patients. Methods: This study was a cross-sectional study done in ten COPD patients affected by moderate to very severe disease. The heart rate variability (HRV) signal was recorded using a Polar cardiofrequencimeter at rest in the sitting position (10 minutes) and during a respiratory sinus arrhythmia maneuver (RSA-M; 4 minutes). Linear analysis in the time and frequency domains and nonlinear analysis were performed on the recorded signals. RMS was assessed using a digital manometer, which provided the maximum inspiratory pressure (Pimax) and the maximum expiratory pressure (Pemax). Results: During the RSA-M, patients presented an HRV power increase in the low-frequency band (LFnu) (46.9±23.7 vs 75.8±27.2; P=0.01) and a decrease in the high-frequency band (HFnu) (52.8±23.5 vs 24.0±27.0; P=0.01) when compared to the resting condition. Significant associations were found between RMS and HRV spectral indices: Pimax and LFnu (r=-0.74; P=0.01); Pimax and HFnu (r=0.74; P=0.01); Pemax and LFnu (r=-0.66; P=0.01); Pemax and HFnu (r=0.66; P=0.03); between Pemax and sample entropy (r=0.83; P<0.01) and between Pemax and approximate entropy (r=0.74; P=0.01). Using a linear regression model, we found that Pimax explained 44% of LFnu behavior during the RSA-M. Conclusion: COPD patients with impaired RMS presented altered cardiac autonomic control, characterized by marked sympathetic modulation and a reduced parasympathetic response; reduced HRV complexity was observed during the RSA-M.

RESUMO Objetivo Estabelecer ponto de corte entre as variáveis clínicas e funcionais para avaliar a prevalência de sarcopenia e dinapenia em pacientes com Doença Pulmonar Obstrutiva Crônica (DPOC), além de analisar o impacto da Disfunção Muscular Esquelética (DME) nestas variáveis. Métodos Realizado estudo transversal com pacientes diagnosticados com DPOC para determinar sarcopenia ou dinapenia por meio do índice de baixa massa muscular e Força de Preensão Palmar (FPP). Avaliadas a função pulmonar, força muscular respiratória e capacidade funcional (CF). A precisão das variáveis na determinação dos pontos de corte previstos para as doenças em questão foi obtida a partir da curva Receiver Operating Characteristic (ROC) e de uma análise bidirecional da variância. Resultados Ao final da análise, obtiveram-se 20 pacientes com DPOC estratificados por sarcopenia (n = 11) e dinapenia (n = 07). O grupo com sarcopenia apresentou menor massa magra e menor pressão inspiratória máxima (PImáx), diminuição da Força de Preensão Palmar (FPP) e redução da CF (p<0,050). O grupo com dinapenia apresentou redução da PImáx, menor FPP e menor distância percorrida no teste Incremental Shuttle Walk (ISWT) (p<0,050). Foram encontrados pontos de corte no Volume Expiratório Forçado (VEF1) durante o primeiro segundo na PImáx, na Pressão Expiratória Máxima (PEmáx) e no ISWT, o que possibilitou identificar sarcopenia ou dinapenia nestes pacientes. A partir destes resultados, foi possível encontrar coexistência das condições (efeito DME) na DPOC: redução da distância no ISWT (p = 0,002) e % ISWT (p = 0,017). Conclusões Em pacientes com DPOC moderada a muito grave, a sarcopenia pode ser prevista pelo VEF1 (% previsto) <52, PImáx <73 cm H2O, PEmáx <126 cm H2O e distância percorrida de <295 metros no ISWT. Já a dinapenia pode ser prevista pelo VEF1 <40%, PImáx <71 cm H2O, PEmáx <110 cm H2O e distância de <230 metros percorrida no ISWT.

Tuberculosis (TB), Lung Cancer (LC) and Chronic Obstructive Pulmonary Diseases (COPD) affect millions of individuals worldwide. Monitoring of DNA damage in pathological situations has been investigated because it can add a new dimension to clinical expression and may represent a potential target for therapeutic intervention. The aim of this study was to evaluate DNA damage and the frequency of cellular abnormalities in TB, LC and COPD patients by comparing them to healthy subjects. The detection of DNA damage by a buccal micronucleus cytome assay was investigated in patients with COPD (n = 28), LC (n = 18) and TB (n = 22) and compared to control individuals (n = 17). The COPD group had a higher frequency of apoptotic cells compared to TB and LC group. The TB group showed a higher frequency of DNA damage, defect in cytokinesis, apoptotic and necrotic cells. Patients with LC had low frequency of chromosomal aberrations than TB and COPD patients. COPD patients showed cellular abnormalities that corresponded to cell death by apoptosis and necrosis, while patients with TB presented defects in cytokinesis and dysfunctions in DNA repair that resulted in the formation of micronucleus (MN) besides apoptotic and necrotic cells. Patients with COPD, TB and LC had a low frequency of permanent DNA damage.