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European Journal of Heart Failure 1999 1(3):293-295; doi:10.1016/S1388-9842(99)00030-6
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© 1999 European Society of Cardiology

Plasma viscosity and fibrinogen in relation to haemodynamic findings in chronic congestive heart failure

Albrecht Hoffmeistera,*, Jürgen Hetzela, Silvia Sanderb, Martina Kronb, Vinzenz Hombacha and Wolfgang Koeniga

a Department of Internal Medicine II-Cardiology, University of Ulm Robert-Koch Str. 8, D-89081 Ulm, Germany
b Department of Biometry and Medical Documentation, University of Ulm Ulm, Germany

* Corresponding author. Tel.: +49-731-5024441; fax: +49-731-5024442


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Conclusion
 References
 
The aim of this study was to investigate an inflammatory response indicated by fibrinogen and plasma viscosity in relation to haemodynamic and clinical findings of patients with stable CHF due to coronary heart disease (CHD).

Key Words: Chronic heart failure • Inflammation • Viscosity • Fibrinogen • Ejection fraction

Accepted June 23, 1999


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Conclusion
 References
 
Elevated levels of proinflammatory cytokines (i.e. TNF{alpha} and IL-6) has been reported in many patients with severe heart failure [1–3]. Therefore, effects mediated by cytokines such as inflammation or increased nitric oxide production are of new interest in understanding the pathophysiology of chronic heart failure (CHF) [4,5]. However, reports on a general inflammatory response in patients with CHF are rare and results are contradictory [6,7].


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Conclusion
 References
 
2.1. Patients
Patients with CHF due to CHD and a history of at least one myocardial infarction older than six months were included. All patients were clinically stable in NYHA functional class II or III, and had a left ventricular ejection fraction (LVEF) <50%. Patients had participated in a randomized controlled trial to study the additional effect of nitrates on exercise tolerance to a baseline treatment with converting enzyme inhibitors and diuretics in CHF. Thus, at time of measurements all patients had received diuretics and converting enzyme inhibitors for at least 12 weeks and nitrates had been withdrawn for 6 weeks.

Beside patients with severe concomitant diseases, we excluded patients with CHF due to (idiopathic) dilated cardiomyopathy or rheumatic heart disease.

2.2. Laboratory methods
Haematocrit and leukocytes (1.5 mg EDTA/ml) were measured on a Coulter-Counter. Fibrinogen (citrate-plasma) was determined by the Clauss method. Plasma viscosity was measured by a rolling-ball viscometer at 37°C (Haake microviscometer, Karlsruhe, Germany).

2.3. Haemodynamic studies
LVEF was quantified in all patients by means of radionuclide ventriculography. Calculation was done by an automated edge detection algorithm. Further haemodynamic variables were determined by right heart catheterization using a Swan Ganz 7F-thermodilution catheter.

2.4. Statistics
Data were evaluated by explorative analysis. For descriptive statistical analysis median, minimum and maximum were calculated. In addition we provided 95% confidence intervals. To describe the correlation between haemodynamic and laboratory findings Spearman’s rank correlation coefficient was calculated.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Conclusion
 References
 
Overall 41 patients (37 men/4 women) aged 42–70 years were included. Twenty-five patients were in NYHA functional class II, and 16 patients were in NYHA functional class III; baseline data and haemodynamic parameters of both groups are shown in Table 1.


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  		Table 1 Baseline characteristics and haemodynamic parameters related to New York Heart Association functional class (n=41)a

 
We found no association between NYHA functional class II or III and plasma viscosity, fibrinogen, leukocytes, or haematocrit in this study population.

A moderate strong negative correlation between plasma viscosity and LVEF (r=–0.51) (Fig. 1) was seen. LVEF and fibrinogen were moderately negatively correlated (r=–0.32). No correlation was found between leukocyte count (r=–0.11) or haematocrit (r=–0.27) and LVEF.


Figure 1
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  		Fig. 1 Correlation between left ventricular ejection fraction and plasma viscosity in 41 patients with chronic heart failure.

 
In contrast to patients with moderately depressed LVEF (31–50%), those with severely depressed LVEF (≤30%) showed increased plasma viscosity values (1.22mPa·s (95%CI 1.21–1.25) vs. 1.26mPa·s (95%CI 1.25–1.34)) and elevated levels of fibrinogen (2.6g/l (95%CI 2.1–2.8) vs. 3.1g/l (95%CI 2.4–3.2)). Haematocrit (43.7% (95%CI 42.3–46.9) vs. 45.9% (95%CI 43.4–48.4)) and leukocyte count (7.2µmol/l (95%CI 5.8–8.4) vs. 7.2µmol/l (95%CI 5.3–9.2)) were not different between both groups.

Patients with a high-normal or increased PCWP (>10mmHg) showed a trend to increased plasma viscosity (1.28mPa·s (95%CI 1.23–1.38) vs. 1.24mPa·s (95%CI 1.22–1.27)) and to elevated levels of fibrinogen (3.0g/l (95% CI 2.3–4.3) vs. 2.5g/l (95%CI 2.1–2.9)) compared to patients with a PCWP ≤10mmHg. Haematocrit (45.7% (95%CI 40.6–50.7) vs. 43.4% (95%CI 41.1–48.4)) and leukocyte count (6.3µmol/l (95%CI 5.3–8.8) vs. 7.5µmol/l (95%CI 5.6–8.6)) again were similar in both groups.

No correlation was found between further haemodynamic parameters (i.e. systemic vascular resistence or right atrial pressure) and inflammatory markers.


   4. Conclusion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Conclusion
References
 
Our study shows that plasma viscosity in patients with CHF is negative correlated to LVEF. Furthermore, patients with a severely impaired haemodynamic situation showed increased plasma viscosity and elevated levels of fibrinogen compared to patients with a moderately impaired haemodynamic situation.

These findings cannot be explained by diuretic therapy, because all patients received constant doses of diuretics, and the haematocrit was not different between haemodynamic subgroups. Thus, moderately increased plasma viscosity or elevated levels of fibrinogen indicate a low grade inflammation in patients with CHF and depressed LVEF. This inflammatory response might be induced by increased cytokine production, and confirms previous reports on elevated cytokine levels (TNF{alpha}, IL-6, IL-2 and IL-1β) in severe heart failure and cardial cachexia [1–3]. Furthermore, an increased erythrocyte sedimentation rate in patients with CHF with, however, inverse prognostic value [6], and elevated CRP-levels in patients with acute heart failure have been reported [7].

The source of increased production of proinflammatory cytokines and low grade inflammatory response in CHF is unclear at present. Damaged cells of peripheral organs in advanced heart failure may provide the stimulus for an increased production of cytokines by activated macrophages and endothelial cells [2,3,8].

A limitation of the present study is the lack of controls; however, an increased plasma viscosity compared to controls has been reported elsewhere [9].

These results confirms an involvement of inflammation in pathogenesis of CHF which might be clinically important, because increased inflammatory activity and haemostatic abnormalities together could contribute to the deterioration of CHF and predispose to thromboembolic events [9].


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Conclusion
 References
 

  1. Levine B, Kalman J, Mayer L, Fillit H.M, Packer M. Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N Engl J Med (1990) 223:236–241.
  2. Testa M, Yeh M, Lee P, et al. Circulating levels of cytokines and their endogenous modulators in patients with mild to severe congestive heart failure due to coronary artery disease or hypertension. J Am Coll Cardiol (1996) 28:961–971.
  3. Tsutamoto T, Hisanaga T, Wada A, et al. Interleukin-6 spillover in the peripheral circulation increases with the severity of heart failure, and the high plasma level of interleukin-6 is an important prognostic predictor in patients with congestive heart failure. J Am Coll Cardiol (1998) 31:391–398.[Abstract/Free Full Text]
  4. Givertz M.M, Colucci W.S. New targets for heart-failure therapy: endothelin, inflammatory cytokines, and oxidative stress. Lancet (1998) 352(Suppl_I):34–38.[CrossRef][Web of Science][Medline]
  5. Finkel M.S, Oddis C.V, Jacob T.D, Watkins S.C, Hattler B.G, Simmons R.L. Negative inotropic effects of cytokines on the heart mediated by nitric oxide. Science (1992) 257:387–389.[Abstract/Free Full Text]
  6. Haber H.L, Leavy J.A, Kessler P.D, Kukin M.L, Gottlieb S.S, Packer M. The erythrocyte sedimentation rate in congestive heart failure. N Engl J Med (1991) 324:353–358.[Abstract]
  7. Pye M, Rae A.P, Cobbe S.M. Study of serum C-reactive protein concentration in cardiac failure. Br Heart J (1990) 63:228–230.[Abstract/Free Full Text]
  8. Lommi J, Pulkki K, Koskinen P, et al. Haemodynamic, neuroendocrine and metabolic correlates of circulating cytokine concentrations in congestive heart failure. Eur Heart J (1997) 18:1620–1625.[Abstract/Free Full Text]
  9. Sbarouni E, Bradshaw A, Andreotti F, Tuddenham E, Oakley C.M, Cleland J.G.F. Relationship between hemostatic abnormalities and neuroendocrine activity in heart failure. Am Heart J (1994) 127:607–612.[CrossRef][Web of Science][Medline]

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This Article
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