ABSTRACT
OBJECTIVES: The aim of our study was to evaluate the total atrial conduction time and its relationship to subclinical atherosclerosis, inflammation and echocardiographic parameters in patients with type 2 diabetes mellitus. METHODS: A total of 132 patients with type 2 diabetes mellitus (mean age 54.5±9.6 years; 57.6% male) and 80 age- and gender-matched controls were evaluated. The total atrial conduction time was measured by tissue-Doppler imaging and the carotid intima-media thickness was measured by B-mode ultrasonography. RESULTS: The total atrial conduction time was significantly longer in the patients with type 2 diabetes mellitus than in the control group (131.7±23.6 vs. 113.1±21.3, p<0.001). The patients with type 2 diabetes mellitus had significantly increased carotid intima-media thicknesses, neutrophil to lymphocyte ratios and high-sensitivity C-reactive protein levels than those of the controls. The total atrial conduction time was positively correlated with the high-sensitivity C-reactive protein level, neutrophil to lymphocyte ratio, carotid intima-media thickness and left atrial volume index and negatively correlated with the early diastolic velocity (Em), Em/late diastolic velocity (Am) ratio and global peak left atrial longitudinal strain. A multiple logistic regression analysis demonstrated that the neutrophil to lymphocyte ratio, carotid intima-media thickness and global peak left atrial longitudinal strain were independent predictors of the total atrial conduction time. CONCLUSIONS: We suggest that subclinical atherosclerosis and inflammation may represent a mechanism related to prolonged total atrial conduction time and that prolonged total atrial conduction time and impaired left atrial myocardial deformation may be represent early subclinical cardiac involvement in patients with type 2 diabetes mellitus. .
Subject(s)
Genotyping Techniques/methods , Hepacivirus/genetics , Molecular Diagnostic Techniques/methods , Reverse Transcriptase Polymerase Chain Reaction , Genotype , Hepacivirus/classificationABSTRACT
FUNDAMENTO: O levosimendan é conhecido pelo seu efeito bilateral de fortalecimento contração das miofibrilas sem aumentar a demanda de oxigênio no miocárdio. A anemia é uma deterioração que causa aumento da dosagem de fármacos em pacientes com insuficiência cardíaca. OBJETIVO: No presente estudo comparamos a eficácia do tratamento com levosimendan em pacientes com insuficiência cardíaca descompensada com ou sem anemia. MÉTODOS: Foram incluídos no estudo 23 pacientes anêmicos com insuficiência cardíaca classe 3 ou 4, segundo a New York Heart Association (NYHA) e fração de ejeção abaixo de 35%. Outros 23 pacientes com o mesmo diagnóstico cardíaco, mas sem anemia, serviu como grupo controle. Ao tratamento da insuficiência cardíaca tradicional desses pacientes foi acrescido um tratamento de 24 horas de levosimendan. Amostras foram tomadas para dosar os níveis séricos do fator de necrose tumoral alfa sérico (TNF-alfa), peptídeo natriurético cerebral aminoterminal (NT-proPNB) e metaloproteinase da matriz 1 (MMP-1), antes e após a administração. RESULTADOS: Não houve diferença significativa entre os níveis séricos de TNF-alfa e MMP-1, antes e depois do tratamento (p > 0,05). Embora o nível de NT-proBNP tenha diminuído em ambos os grupos após o tratamento, não foi estatisticamente significativo (p = 0,531 e p = 0,913 para os grupos de anemia e de controle, respectivamente). Uma restauração significativa da capacidade funcional foi observada em ambos os grupos avaliados, de acordo com a NYHA (p < 0,001 e p = 0,001 para os grupos de anemia e controle, respectivamente). CONCLUSÃO: O tratamento com levosimendan apresenta efeitos semelhantes em pacientes com insuficiência cardíaca, com anemia e sem anemia. No entanto, o efeito precoce desse tratamento sobre os níveis de TNF-alfa, NT-proPNB e MMP-1 não é evidente. Ele oferece uma melhora significativa na capacidade funcional, sem a influência da anemia.
BACKGROUND: Levosimendan is known with its two-sided effects of strengthening myofibril contraction without increasing myocardial oxygen demand. Anemia is a deteriorating situation that causes increase of drug dosing in patients with heart failure. OBJECTIVES: In this study, we compared the effectiveness of levosimendan treatment in decompensated heart failure patients with or without anemia. METHODS: Twenty-three anemic patients having class 3 or 4 heart failure according to New York Heart Association (NYHA) and an ejection fraction of below 35% were included to the study. Another 23 patients with the same cardiac diagnosis but without anemia served as control group. Twenty-four hours levosimendan treatment was added to the traditional heart failure treatment of these patients. Samples were taken to measure serum tumor necrotizing factor alpha (TNF-alpha), aminoterminal pro-brain natriuretic peptide (NT-proBNP) and matrix metalloproteinase-1 (MMP-1) levels before and after the administration. RESULTS: There was no significant difference between serum TNF-alpha and MMP-1 levels before and after the treatment (p>0.05). Although NT-proBNP level decreased in both groups after the treatment this was not statistically significant (p=0.531 and p=0.913 for anemia and control groups respectively). Significant restoration of functional capacity was seen in both groups assessed according to NYHA (p<0.001 and p=0.001 for anemia and control groups respectively). CONCLUSION: Levosimendan treatment shows similar effects in heart failure patients with anemia to that of patients without anemia. However, the early effect of this treatment on TNF-alpha, NT-proBNP and MMP-1 levels is not evident. It provides significant improvement in functional capacity without influence from anemia.