心不全の栄養管理の新知見

もう１つ、5th Cachexia Conferenceの資料の中から、心不全の栄養管理の新知見の抄録を紹介します。

http://www.lms-events.com/19/5th_Cachexia_Conference_2009_Abstracts.pdf

慢性心不全における悪液質が、心不全の栄養ではもっとも大きな問題です。5-15％の慢性心不全患者に悪液質を認めます。悪液質でなくても筋肉量の低下・筋萎縮は、慢性心不全患者の68％に認めます。

慢性心不全における鉄欠乏に対して、静脈から鉄剤を投与すると心機能が有意に改善したというランダム化比較試験があります。

貧血の存在は心不全を確実に悪化させますので、鉄だけでなくビタミンB12、葉酸の欠乏も問題となります。また、ビタミンB1が不足している場合にも心不全が悪化し、ビタミンB1の投与とともに心機能が改善することがあります。これらのビタミン、微量元素は、慢性心不全の栄養管理では特に重要です。

慢性心不全における悪液質に対して、異化を抑える治療か同化を促す治療を併用しなければ、栄養サポートだけで有意な改善を得ることは難しいとあります。運動療法のアウトカムも、栄養サポートを併用することでより改善するかもしれません。

New insights on nutrition in heart failure
Stefan Anker
Center for Applied Cachexia Research and Therapy, Department of Cardiology, Charité Medical School, Campus Virchow-Klinikum, Berlin, Germany

The biggest nutritional problem of heart failure is the development of muscle wasting and cachexia in chronic heart failure (CHF). Depending on disease severity and co-morbidities, cachexia occurs in 5 to 15% of patients with CHF (review Ref: von Haehling et al. Pharmacol Ther 2009). Muscle wasting (with or without weight loss) is found in up to 68% of patients. Cardiac cachexia is a major cause of poor symptom status, increased hospitalization rate and higher mortality in CHF patients (see: Anker et al. Lancet 1997 & Lancet 2003).

It is well known that the heart of patients with CHF can be considered as an “engine out of fuel”. Micro- and macro-nutritional support may be a new way forward to improve outcome in CHF patients. Results of recent studies will be discussed in the presentation.

Peripheral tissue wasting is thought to be due to catabolic / anabolic imbalance. Nutritional deficiencies are important as contributing factor for exaggerated inflammation (see ref for lipoprotein-endotoxin hypothesis: Rauchhaus et al. Lancet 2000), for lack of anabolic protection (protein in general and essential amino acids are required for muscle growth), as well as factors that contribute to deterioration of co-morbidities (like anemia) and impaired intermediary metabolism and function of skeletal musculature leading to impaired symptoms, exercise intolerance and poor quality of life. Correcting such deficiencies like iron deficiencies can improve all these parameters in patients with heart failure (Anker et al. FAIR-HF trial. NEJM 2009).

Our research suggests that nutritional support alone cannot significantly improve the long-term situation of patients with frank cardiac cachexia, unless anti-catabolic and/or pro-anabolic therapies are actively used.
Also outcomes after exercise training may be improveable with the use of nutritional support.

Of note, some of the results of cardiac cachexia related research may also be very relevant for treatment development in cancer cachexia.