Nutritional markers and prognosis in cardiac cachexia

https://doi.org/10.1016/j.ijcard.2009.07.042Get rights and content

Abstract

Background

Cachexia frequently complicates chronic heart failure (CHF) and predicts an ominous prognosis. Hormonal and inflammatory environment differ between cachectic and non-cachectic patients. Nutritional markers of cardiac cachexia and prognostic predictors in this context are not completely understood.

Objectives

To study biochemical markers of nutritional status in cardiac cachexia and to investigate variables associated with worse prognosis.

Methods

A total of 94 ambulatory patients — 38 cachectics and 56 non-cachectics — were recruited. Cardiac cachexia was defined as a weight loss of ≥ 7.5%. An anthropometric evaluation was performed in all patients and blood was collected for several laboratory determinations: haemoglobin, lymphocytes, albumin, transferrin, pre-albumin, cholesterol and triglycerides. Patients were included in a prospective cohort study.

Results

Cachectics had lower albumin and pre-albumin levels. They also had lower haemoglobin, lymphocytes and triglycerides. Levels of high-sensitivity C-reactive protein, and catabolic hormones were higher in the cachectic group. Low pre-albumin was the only nutritional marker independently associated with cardiac cachexia. (OR = 1.08, CI: 1.01–1.17). During a follow-up of 16.2 ± 5.2 months, 15 (39.4%) cachectic patients and 6 (10.7%) non-cachectics died. In the cachectic group, lower cholesterol was independently associated with worse outcome (HR = 1.32, CI: 1.11–1.57).

Conclusions

Pre-albumin seems to be the best laboratory marker of undernutrition in CHF. Low cholesterol independently associates with worse outcome in cardiac cachexia.

Introduction

Chronic heart failure (CHF) is a major public health problem in western countries [1]. Cardiac cachexia, i.e. body wasting, is a serious complication of CHF, which is associated with poor prognosis, independently of age, New York Heart Association (NYHA) class, peak oxygen consumption and left ventricular ejection fraction (LVEF) [2]. Approximately 15% of CHF patients develop cachexia [3].

The development of cachexia in CHF patients is not well understood. Several mechanisms have been implicated in this pathophysiologic process: pro-inflammatory cytokines [4], imbalance between anabolic and catabolic hormones [5] and changes in the hormonal environment that regulates energy metabolism, lean/fat body composition and appetite — leptin, adiponectin and ghrelin [6], [7], [8]. Decrease in food intake [9] and gut malabsorption resulting from bowel oedema and reduced perfusion [10] may also be important factors contributing for this process of losing weight.

Cardiac cachexia has been recognised for centuries [11], but only recently became a growing field of investigation. Catabolic and anabolic abnormalities characteristic of cachexia have already been described [5], [12], [13] and several studies [4], [14] consistently reported increased levels of inflammatory cytokines. Not yet investigated is the possible association between cardiac cachexia and biochemical markers of undernutrition. Although cachexia is recognised as a condition associated with worse prognosis, little is known about factors predicting worse outcome in cachectic patients.

We compared the biochemical markers of undernutrition in CHF patients with or without cachexia in order to investigate cachexia predictors. We also aimed to assess variables associated with worse outcome in the subgroup of patients with established cardiac cachexia.

Section snippets

Study design

We screened clinical records of patients attending our heart failure clinic (Hospital S. João, Porto, Portugal) and identified all cachectic patients. They were contacted by phone or mail and scheduled to a recruitment visit. The control group consisted of patients without weight loss, attending the clinic during the recruitment time.

Chronic heart failure diagnosis was based on the European Society of Cardiology criteria [15]. Cardiac cachexia was defined as a non-intentional, non-oedematous,

Results

From the 358 records screened we found 38 (11%) cachectic patients. The cachectic group (n = 38) had 11.0 ± 4.4% documented weight loss (minimum 7.6%, maximum 28.2%), during a mean time of 28 months since CHF diagnosis. No significant differences concerning weight loss was documented in the control group (n = 56). Clinical characteristics and laboratory data of both groups are shown and compared in Table 1. No significant differences concerning age, sex, time since CHF diagnosis and severity of left

Discussion

Our results suggest that pre-albumin may be a good biochemical marker of cardiac cachexia and be used as an ancillary tool in this diagnosis. This finding is important, because in chronic heart failure the weight change history is often not available, making cardiac cachexia diagnosis difficult to establish and often delayed.

Pre-albumin and other laboratory nutritional markers were significantly different between groups despite normality and similarity of BMI (cachectic group 23.2 ± 3.0;

Acknowledgements

We thank Gabriela Couto, Bruno Ribeiro and Adélia Mão-de-Ferro for their precious help. We also thank Dra Conceição Gonçalves for the careful handling of laboratory measurements.

The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [25].

This study was supported by a grant from the Portuguese Ministry of Health (Project number 62/2007).

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      In addition to albumin and prealbumin, laboratory abnormalities commonly associated with malnutrition, including low total cholesterol, lymphopenia and anaemia, have been evaluated in patients with CHF and related with unintentional weight loss of ≥7.5% in this population. Low total cholesterol was also associated with worse outcomes [56]. Furthermore, there are other biochemical parameters which have been considered to be possible modern biomarkers of nutritional status, such as ghrelin, leptin, adiponectin, myostatin or growth differentiation factor 8 (GDF-8) and the C-terminal agrin fragment (CAF).

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