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Gastro-intestinal protein loss in elderly patients with cardiac cachexia.

Introduction

Malnutrition due to chronic heart failure has been termed cardiac cachexia. It may be present in up to 50% of patients with heart failure [1] and is associated with increased morbidity and mortality. It is likely to be particularly common in elderly people [2] because of the high incidence of both heart failure and undernutrition from other causes in this age group. The aetiology of cardiac cachexia is probably multifactorial [3]. It has been claimed that a protein-losing enteropathy is an important cause [4, 5]. We have therefore quantified gastro-intestinal protein loss in a group of elderly patients with cardiac cachexia and compared the results with a group of healthy controls.

Methods

Twenty-nine patients (20 women) with cardiac cachexia [mean age = 76.1(4.1) years] and 29 (20 women) healthy controls [mean age = 74.9(4.8) years] were studied. The study was approved by the District Ethics Committee and the Administration of Radioactive Substances Advisory Committee (ARSAC). All subjects gave informed consent.

All patients had clinical evidence of left ventricular failure and a chest radiograph showing pulmonary oedema at the time of initial diagnosis. Congestive heart failure had been present for at least 3 months and patients had been on optimal medical treatment. Patients were selected on the basis of a minimum weight loss of 6kg within the preceding 12 months. Healthy controls were recruited from local GP registers and luncheon clubs. Subjects were excluded if they had other diseases causing undernutrition (diabetes, thyrotoxicosis, cancer, gastro-intestinal disease or previous gastro-intestinal surgery).

All subjects underwent a clinical history, examination, chest radiography and electrocardiography (ECG). Fasting blood samples were drawn for albumin (Alb) and total protein (TP). Samples were analysed in one hospital laboratory (Excel Analyser, Indianapolis, USA). For control subjects the results of a full blood count, liver function tests and electrolytes were within normal reference ranges.

Anthropometric measurements were performed by a single experienced observer (D.K.). Height (m) and weight (kg) were recorded and body mass index (BMI) was calculated as weight/[height.sup.2] (kg/[m.sup.2]). Triceps skin-fold thickness (TS) (mm) was measured using Harpenden calipers. Mid-arm circumference (MAC) (cm) was measured using a plastic tape at the midpoint between the acromion and olecranon process. The mean of three measurements for TS and MAC was recorded. Arm muscle circumference (AMC) (cm) was derived from the formula:

AMC = MAC-(TS x 0.3142)

Two-dimensional echocardiography (Hewlett Packard, Sonos 500 machine) was used to calculate ejection fraction (EF) and pulmonary artery pressure (PAP) was measured by continuous-wave Doppler.

Gastro-intestinal protein loss was measured using the [.sup.51]chromic chloride test ([.sup.51]CrC[l.sub.3]) [6]. [.sup.51]CrC[l.sub.3] labels transferrin in vivo and its recovery in faeces after intravenous administration is a measure of gastro-intestinal protein loss. All subjects received 2MBq [.sup.51]CrC[l.sub.3] intravenously. Stool collection began 12 hours after the injection and continued for 5 days. [.sup.51]CrC[l.sub.3] is excreted by the kidney and therefore detailed instructions were given to avoid contamination by urine. The percentage of administered activity excreted in the stools was measured by standard bulk assay counting. All tests were performed on an outpatient basis. Results are reported as mean (SD), and differences between patients and controls were analysed using Student's t test. All variables followed a normal distribution.

Results

The mean duration of congestive heart failure was 83.4(102.2) months. The mean weight loss of the patients in the preceding 12 months was 8.5(3.2)kg, and there had been no weight loss in the control group. The aetiology of congestive heart failure was rheumatic valvular heart disease (12), idiopathic dilated cardiomyopathy (5), ischaemic heart disease (4), unknown (3), atrial septal defects (2), patent ductus arteriosus (1) and hypertension (2). The severity of heart failure (New York Heart Association classification) was: II(9), III(15). Thirteen patients were taking more than 120 mg of frusemide daily, four were also taking a thiazide diuretic and 18 had been prescribed an angiotensin-converting enzyme inhibitor.

The patients were clinically undernourished compared with the controls (Table). Although patients had a lower serum albumin they could not be considered hypoproteinaemic as the reduction was minimal. The ejection fraction was lower in the patients. The mean pulmonary artery pressure was technically measurable in 26 patients and 23 controls and was higher in the patients. The mean PAP in the patients was higher than the expected normal range (< 18 mmHg).

The 5-day stool collection was completed by all subjects but was contaminated by one control subject and therefore discarded. There was no difference in the percentage of administered activity recovered from the stools of patients and controls [1.00(0.7)% vs. 0.98(0.6)%, p = 0.90] (Figure). These results are within the normal range.
Table. Nutritional and cardiac measurements in patients
and controls

                                  Controls     Patients
                                  (n= 29)      (n = 29)    p

Nutritional measurements
 Weight (kg)                     67.5(14.8)   39.4(19.9)   < 0.001
 Height (m)                       1.63(0.1)    1.62(0.1)   NS
 Body mass index (kg/[m.sup.2])  25.3(3.9)    19.6(2.5)    < 0.001
 Triceps skin-fold (mm)          23.7(9.6)    10.5(3.4)    < 0.001
 Mid-arm circumference (cm)      29.2(3.3)    23.0(2.0)    < 0.001
 Arm muscle circumference (cm)   21.7(3.2)    19.7(2.2)    < 0.01
 Plasma albumin (g/1)            42.9(2.5)    41.0(4.1)    < 0.05
 Plasma total protein (g/l)      71.7(2.6)    72.0(5.5)    NS
 Cardiac measurements
 Ejection fraction (%)           65.5(11.8)   41.5(18.3)   < 0.001
 Pulmonary artery pressure       19.3(8.1)    39.4(19.9)   < 0.001
 (mmHg)




Discussion

Gastro-intestinal protein loss in patients with heart failure has mainly been found in association with constrictive pericarditis [4, 5]. Davidson et al. [4] described three patients with constrictive pericarditis and one with an atrial septal defect who were all hypoproteinaemic and showed evidence of significant gastro-intestinal protein loss. The hypoproteinaemia resolved after correction of the cardiac defects. Other workers have demonstrated protein-losing enteropathy associated with primary myocardial disease [7] and tricuspid regurgitation [8]. Although these cardiac diagnoses are diverse they are all characterized haemodynamically by raised right heart pressures with elevation of right atrial and central venous pressures. The histology of the gut in these patients ranged from`mild hyperaemia and slight dilatation of the capillary and lymphatic vessels' [6] to`dilatation of the lacteals of the villi' [5]. The latter group are similar to patients with intestinal lympangiecatasia, a congenital disease of the lymphatics characterized by a protein-losing enteropathy (`idiopathic hypoproteinaemia').

It has been postulated that the elevated venous pressure results in oedema of the bowel wall and exudation of protein. All the cases previously described were associated with a raised right heart pressure and had evidence of uncontrolled heart failure with marked peripheral oedema. We have shown that patients with controlled heart failure and evidence of undernutrition have no gastro-intestinal protein loss even in the presence of significantly increased right-sided heart pressures.

Gastro-intestinal protein loss is likely to be rare in patients with cardiac cachexia and is therefore not a significant factor in its production. Further research to elucidate the significance of other mechanisms is required.

Acknowledgements

This work was supported by a grant from the British Heart Foundation. We would also like to thank Dr J. H. Silas for his support.

References

[1.] Carr JG, Stevenson LW, Walden JA, Heber D. Prevalence and haemodynamic correlates of malnutrition in severe congestive heart failure secondary to ischaemic and idiopathic dilated cardiomyopathy. Am J Cardiol 1989;63:709-13. [2.] King D. Cardiac cachexia in the elderly. Cardiol Elderly 1994;2:102-6. [3.] Pittman JG, Cohen P. The pathogenesis of cardiac cachexia. N Engl J Med 1964;27:403-9,453-9. [4.] Davidson JD, Waldman TA, Goodman DS, Gordon RS. Protein-losing gastroenteropathy in congestive heart failure. Lancet 1961;i:899-902. [5.] Wilkinson P, Pinto B, Senior JR. Reversible protein-losing enteropathy with intestinal lymphangiectasia secondary to chronic constrictive pericarditis. N Engl J Med 1965;273:1178-81. [6.] Merrick MV. Essentials of nuclear medicine. Edinburgh: Churchill Livingstone, 1984. [7.] Valberg LS, Corbett WEN, McCorriston JR, Parker JO. Excessive loss of plasma protein into the gastrointestinal tract associated with primary myocardial disease. Am J Med 1965;39:668-73. [8.] Stober W, Cohen LS, Waldmann TA, Braunwald E. Triscuspid regurgitation: a newly recognised cause of protein-losing enteropathy, lymphocytopenia and immunologic deficiency. Am J Med 1968;44:842-50.

Authors' addresses

D. King(*) Clatterbridge Hospital, Bebington, Wirral, Merseyside, L63 4JY

M. L. Smith, M. Lye Royal Liverpool University Hospital, PO Box 147, Liverpool, Merseyside, L69 3BX

(*) Address correspondence to Dr D. King, Department of Medicine for the Elderly, Wirral Hospital NHS Trust, Arrowe Park, Arrowe Park Road, Upton, Wirral, Merseyside, L49 5PE

Received in revised form 18 October 1995
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Author:King, D.; Smith, M. L.; Lye, M.
Publication:Age and Ageing
Date:May 1, 1996
Words:1483
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