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European Journal of Heart Failure 2000 2(3):261-263; doi:10.1016/S1388-9842(00)00066-0
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© 2000 European Society of Cardiology

Catecholamine levels in heart failure due to dilated cardiomyopathy and their relationship to the severity of heart failure

Ajit Kumar Agarwala,*, Poothirikovil Venugopalana, Ceryl Woodhouseb and David de Bonoc

a Division of Cardiology, College of Medicine, Sultan Qaboos University Hospital Muscat, Sultanate of Oman
b Department of Biochemistry, Sultan Qaboos University Hospital Muscat, Sultanate of Oman
c Department of Cardiology, Glenfield General Hospital Leicester, UK

Received October 4, 1999; Revised January 10, 2000; Accepted February 16, 2000


   1. Background
Top
 Notes
 1. Background
2. Aims
 3. Methods
 4. Results
 5. Conclusion
 References
 
Persistent sympathetic stimulation, a major factor responsible for continuing myocardial injury and worsening chronic heart failure due to idiopathic dilated cardiomyopathy (IDC), is reflected in raised plasma catecholamine levels. Raised noradrenaline levels quantify the sympathetic response and have been reported to be of prognostic value [1,2]. Therapy with beta-blockade improves outcome [3]. Recently, Richards et al. have demonstrated elevated levels of atrial natriuretic peptide, brain natriuretic peptide (BNP) and/or noradrenaline in heart failure. In nearly a quarter of their study patients having supramedian BNP but inframedian levels of noradrenaline, carvedilol was able to reduce the hospital admission rate for heart failure significantly [4].


   2. Aims
Top
 Notes
 1. Background
 2. Aims
3. Methods
 4. Results
 5. Conclusion
 References
 
The purpose of this study was to investigate the catecholamine levels in an Omani population with stable chronic heart failure due to IDC and to see if these related to the severity of heart failure.


   3. Methods
Top
 Notes
 1. Background
 2. Aims
 3. Methods
4. Results
 5. Conclusion
 References
 
Fifty-five patients with IDC diagnosed as per WHO criteria [5] who were on treatment for chronic heart failure with diuretics, angiotensin-converting enzyme inhibitor (ACEI) and/or digoxin formed the subject of this study. Clinical history was recorded and the severity of heart failure assessed using the New York Heart Association (NYHA) functional classification. Ischaemic heart disease was excluded by coronary arteriography in all patients. Blood samples were drawn after an 8-h period of rest with the patient in a supine position for estimation of noradrenaline, adrenaline and dopamine levels. Ten millilitres of blood was collected in ethylene diamine triacetate (EDTA) tubes and transported to the biochemistry laboratory protected from sunlight. Analysis was performed using high-performance liquid chromatography with electrochemical detection. The catecholamines were separated on reverse phase columns and component retention and peak shape were enhanced by adding ion-pairing reagents to the mobile phase. The reference ranges for normotensive healthy Omani population (data in file) were used as controls (noradrenaline, 164–2360 pmol/l; adrenaline, 152–542 pmol/l; and dopamine, 181–653 pmol/l). Patients were divided based on severity of symptoms into Group A (NYHA class I and II) and Group B (NYHA class III and IV). Levels of catecholamines in the two groups of patients were compared using the Wilcoxon test. The investigation conforms to the principles outlined in the Declaration of Helsinki.


   4. Results
Top
 Notes
 1. Background
 2. Aims
 3. Methods
 4. Results
5. Conclusion
 References
 
Patients were aged 18–70 years (median 50 years) with 34 males and 21 females (M:F=1.6:1). There were 39 patients in Group A and 16 patients in Group B. The treatment profile of patients in the two groups at the time of evaluation is given in Table 1. None of the patients were on beta-blocker therapy. Noradrenaline levels were elevated in 46/55 (83.6%) patients and adrenaline and dopamine in 32/55 (58%). The levels of catecholamines in Group A and Group B were compared (Table 2). The mean levels of noradrenaline were higher in Group A, but the difference was not statistically significant. A similar analysis with adrenaline and dopamine levels in the two groups also failed to show significant difference.


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  		Table 1 Treatment profile of patients in Group A (NYHA class I and II) and Group B (class III and IV)

 


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  		Table 2 Comparison of plasma catecholamine levels in Group A (NYHA class I and II) and Group B (class III and IV)

 

   5. Conclusion
Top
 Notes
 1. Background
 2. Aims
 3. Methods
 4. Results
 5. Conclusion
References
 
Our study reaffirms raised catecholamine levels in heart failure. An interesting observation, however, appeared that comparatively higher levels of noradrenaline were recorded in patients with mild heart failure, but the difference was not statistically significant. Possible explanations for lower levels in severe heart failure include decompensation and/or resetting of adrenergic reflexes, inter-individual differences in sympathetic response, varying degrees of activation of counter-regulatory mechanisms, such as release of atrial natriuretic peptide, and negating effect of ACEI therapy [6]. The difference in the treatment received by the two groups could also be an important contributing factor. Although beta-blockers were not used in any of the patients, a more aggressive use of ACEI in severe heart failure could have lowered the catecholamine levels in Group B.

It is well established that catecholamine levels are elevated in chronic heart failure, their reduction by pharmacological or non-pharmacological means to effect patient survival was disputed until recently, when studies [7–9] demonstrated the significance of plasma noradrenaline levels and survival benefits. However, Anker in his review [10] opined against such benefit and stated that spot catecholamine estimation was of limited value. Reduction of catecholamine levels by beta-adrenergic blockade has been shown to account for the beneficial effects [11,12]. Two recently published studies (CIBIS II and MERIT-HF) have recorded significant survival benefits of beta-blocker therapy [13,14]. However, these did not investigate the effect of therapy on catecholamine levels.

Despite the fact that the neuroendocrine activation is an important component of chronic heart failure, its assessment neither forms part of the routine work up of patients with heart failure, nor is there such a recommendation in the guidelines set by recognised scientific authorities [15–17]. A survey conducted in Italian hospital cardiology units [18] showed that only less than 4% of patients undergo any kind of neuroendocrine assessment. This aspect merits review. Although our observation of comparatively high noradrenaline levels in mild heart failure did not reach statistical significance, the gathering evidence [4,19–21] suggests that monitoring of catecholamine levels and BNP in early stages of IDC be more widely used for its prognostic value. This will also help to use beta-blockade optimally in IDC.


   Notes
Top
 Notes
1. Background
 2. Aims
 3. Methods
 4. Results
 5. Conclusion
 References
 
* College of Medicine, P.O. Box 35, PC 123, Muscat, Sultanate of Oman. Tel.: +968-513355-3404; fax: +968-513419. E-mail address: ajitka{at}hotmail.com (A.K. Agarwal). Back


   References
Top
 Notes
 1. Background
 2. Aims
 3. Methods
 4. Results
 5. Conclusion
 References
 

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