Abstract
Low spot urinary creatinine concentration (SUCR) is a marker of muscle wasting and clinical outcome. The risk factors for low SUCR in heart failure (HF) remain poorly understood. We explored the risk factors for low SUCR related to poor outcomes. In 721 HF patients (age: 52.3 ± 11 years, female: 14%, NYHA: 2.7 ± 0.7) SUCR and Dexa body composition scans were performed. BMI prior HF-onset, weight loss, and appendicular muscle mass were obtained. Each patient was classified as malnutrition or normal by GLIM criteria and three other biochemical indices (CONUT, PNI, and GRNI). Sarcopenia index (SI) as creatinine to cystatin C ratio was also calculated. Within 1 year, 80 (11.1%) patients died. In ROC curve we identified a SUCR value of 0.628 g/L as optimally discriminating surviving from dead. In low SUCR group more advanced HF, higher weight loss and catabolic components of weight trajectory (CCWT), more frequent under-nutrition by GLIM, and lower SI were observed. In multivariate analysis the independent predictors of low SUCR were SI, CCWT, and GNRI score. In conclusion: the risk of low SUCR was associated with a worse outcome. Low SUCR was associated with greater catabolism and sarcopenia but not with biochemical indices of malnutrition.
Highlights
Heart failure (HF) has become an epidemic with the number of affected exceeding64 million worldwide [1]
Phosphocreatine is a central compound of energy metabolism, serving to regenerate adenosine triphosphate from the product of its hydrolysis–adenosine diphosphate [6]
Patients with HF and reduced left ventricle ejection fraction (LVEF) ≤ 40%, diagnosed according to criteria published by the European Society of Cardiology, aged > 18 years and with HF duration of more than 6 months, recruited in outpatient settings from January 2004 to March 2013, on the best tolerated medical therapy, for whom HF could be confirmed with 1 month precision and with available records concerning body weight before the first diagnosis of HF and minimal weight during HF
Summary
Heart failure (HF) has become an epidemic with the number of affected exceeding. 64 million worldwide [1]. Despite modern therapy and some improvements in prognosis, still the morbidity and mortality associated with HF remains unacceptably high [2,3]. There is an increasing awareness among medical professionals that HF is a complex multiorgan syndrome with a significant contribution of noncardiac diseases in the overall risk [4]. The reciprocal interaction between various organs is the key issue. Well-known cross-talk between the heart and skeletal muscles stands behind the development of myopathy, which is one of the most important factors affecting symptoms and prognosis [5]. Phosphocreatine is a central compound of energy metabolism, serving to regenerate adenosine triphosphate from the product of its hydrolysis–adenosine diphosphate [6]
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