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European Journal of Heart Failure 2002 4(3):331-336; doi:10.1016/S1388-9842(02)00021-1
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© 2002 European Society of Cardiology

C-reactive protein as a predictor of improvement and readmission in heart failure

J.L. Alonso-Martíneza,*, B. Llorente-Dieza, M. Echegaray-Agaraa, F. Olaz-Preciadob,*, M. Urbieta-Echezarretaa and C. González-Arencibiaa

a Department of Internal Medicine, Hospital de Navarra Irunlarrea 3, 31008 Pamplona, Spain
b Department of Cardiology, Hospital de Navarra Irunlarrea 3, 31008 Pamplona, Spain

* Corresponding author E-mail address: jalonsom{at}cfnavarra.es


   Abstract
Top
 Abstract
1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Acknowledgments
 References
 
Objectives: Only recently, new risk factors to explain atherosclerotic disease have been identified. One of the most important clinical manifestations of atherosclerosis is heart failure. Our study was aimed at investigating C-reactive protein (CRP), a marker of systemic inflammation, in the context of heart failure, and to determine its usefulness in predicting the need for readmission in patients with heart failure and their degree of improvement.

Design: We studied patients admitted to our hospital due to heart failure, independent of the cause. CRP levels were measured with a sensitive standard assay on a Nephelometer analyser. Patients were classified on admission and discharge following New York Heart Association (NYHA) functional criteria; left ejection fraction was also determined by transthoracic echocardiography. Patients presenting clear sources of infection or inflammatory disease were excluded. Our control group consisted of patients admitted for syncope. Each patient was followed up through a computer system controlling admissions to and discharge from the hospital, for a period of 18 months after initial admission. End points considered were NYHA functional class on discharge, readmission and death.

Results: We studied prospectively 76 patients with a mean age of 73.5±11 [95% confidence interval (CI) 71.2–75.8]; 44 were male (58%) and 32 female (42%). The mean CRP level in patients with heart failure was 3.94±5.87 (95% CI, 1.26–7.60), while in 15 patients with syncope it was 0.84±1.95 (95% CI, 0.96–2.94) (P=0.0007). The principal causes of heart failure included dilated cardiomyopathy due to coronary arterial disease (30%), valvular disease (28%) and heart failure secondary to hypertension (25%). The mean left ejection fraction adequately measured in 72 (95%) patients was 50.41±9.88 (95% CI, 41.20–59.65). We observed a trend of higher CRP levels in relation to ejection fractions below 35%: 7.50±9.88 vs. 3.75±4.57, (P=0.09). Our results showed that on discharge CRP levels increased in relation to NYHA class: I: 0.74±0.69; II: 3.78±3.76; III: 7.4±8.65; IV: 12.2±15.27 (P<0.05). On follow-up of each patient for 18 months, 32 (43%) were readmitted due to deterioration of their heart condition. For patients who were readmitted, those presenting CRP levels >0.9 mg/dl were identified as candidates for earlier hospitalisation than those with levels below 0.9 mg/dl (P=0.02) RR=1.43. In logistic-regression analysis the only group of tested variables predicting readmission were levels of CRP, NYHA class and plasmatic K on discharge and left ventricle ejection fraction. Analysis of covariates yields CRP levels as being an independent predictor of readmission.

Conclusions: An inflammatory response is present in deteriorating heart failure. We observed higher CRP levels in patients with higher NYHA functional class, perhaps signalling a poor therapeutic response. Higher CRP levels were also related to higher rates of readmission and mortality and it could be an independent marker of improvement and readmission in heart failure.

Key Words: C-reactive protein • Heart failure • Chronic inflammatory response

Received May 22, 2001; Revised August 31, 2001; Accepted October 23, 2001


   1. Introduction
Top
 Abstract
 1. Introduction
2. Materials and methods
 3. Results
 4. Discussion
 Acknowledgments
 References
 
C-Reactive protein (CRP) is a pentameric protein (pentraxin) comprised of five identical units [1]. In humans, the gene for CRP subunits is encoded in chromosome 1 [2]. A similar protein has been identified in virtually all mammals and in fish and chickens [3], indicating great evolutionary conservation. Several functions have been attributed to C-reactive protein: CRP is capable of binding various biological substrates [4]; it participates in the activation of the complement system and modulates the function of phagocytic leukocytes. CRP is also located at sites of inflammation [5]; it enhances macrophage action on tumours [6]; it is implicated in the synthesis of interleukine-1 and tumour necrosis factor [7,8] and is capable of binding and blocking platelet activating factor. CRP is mainly produced in the liver in response to interleukine-6.

Recently, evidence suggesting a process of low grade systemic inflammation has been implicated in atherosclerotic disease [9–12]. Heart failure is one of the main consequences of atherosclerosis, and is a frequent cause of hospital admission [13–15] and mortality, despite recent developments in therapy [16–19].

Elevated levels of CRP have been observed in patients with heart failure [20], and activation of the immune response may play a role in heart failure through modifications in the renin–angiotensin–aldosterone and sympathetic systems [22,23]. We studied the role of CRP in patients admitted due to heart failure, with a follow-up of 18 months.


   2. Materials and methods
Top
 Abstract
 1. Introduction
 2. Materials and methods
3. Results
 4. Discussion
 Acknowledgments
 References
 
Our intervention group consisted of patients admitted consecutively to our hospital due to heart failure, independent of the cause. Heart failure was assumed to be present when dyspnea, secondary to pulmonary congestion demonstrated by thoracic X-ray, fatigue or oedema without other obvious cause were present. Each patient was classified according to NYHA functional class and stroke volumes were determined by transthoracic echocardiography. We recorded stroke volumes during echocardiography, along with the type of ventricular failure and the potential origin of heart failure.

Left ventricle failure was considered when symptoms of pulmonary congestion were present (manifested by dyspnea or orthopnea and existence of at least B lines, dilated veins in upper lung fields or pleural effusion). Right ventricle failure was considered when evidence of increased systemic venous pressure was present (manifested as a jugular venous distension in a 45° lying position and oedema). The presence of both was considered as two-sided heart failure. Dilated cardiomyopathy due to coronary artery disease was denominated ischaemic dilated cardiomyopathy. Ischaemic cardiomyopathy was based on localised defects in systolic contraction associated with pathological Q waves in the EKG and or history of angina. Hypertensive cardiomyopathy refers to changes provoked by arterial hypertension, in general secondary to chronic pressure overload (hypertrophy of the left ventricle without other explicit lesions). Diastolic failure was diagnosed following directions of European Study Group in diastolic heart failure [24]. Valvular disease refers mainly to aortic stenosis and mitral valvular disease. Other causes of heart failure are represented in Table 2.

We determined CRP levels in patients with heart failure during hospitalisation and compared them with CRP levels in the control group, consisting of 15 patients consecutively admitted due to syncope. The control group was only used to compare levels of CRP with those of heart failure; they did not participate in any other comparison.

CRP levels were measured in plasma samples on the first day of admission by a sensitive nephelometric method (Image Immunochemistry System, Beckman Coulter INC Fullerton Ca 92834-31100); the lowest levels found were 0.07 mg/dl, and we assigned this value to those patients with undetectable values. Based on the current CRP levels measured, we constructed our hypothesis that those patients with higher CRP levels subsequently presented higher admission and mortality rates.

Patients with a clear cause for elevated CRP levels such as infection or inflammatory disease were excluded from the study, especially patients with endocarditis. Specifically presence of fever, pulmonary infiltrates, productive cough, arthralgia, rash, diarrhoea and urinary symptoms suggesting infection were criteria for exclusion. We also excluded those patients who died during the course of hospitalisation considered as the admission index.

On discharge, patients were classified according to NYHA functional criteria. Each patient was treated with the standard medication for heart failure: diuretics (furosemide), angiotensin-converting enzyme inhibitors depending on renal tolerance, digoxin when patients presented systolic failure or atrial fibrillation; β-blockers in selected cases and anticoagulant or antiplatelet agents when indicated. We did not consider the impact of doses of aspirin or ticlopidine on CRP levels.

We followed up each patient for a period of 18 months, through our computer controlled system, monitoring dates of admission and discharge, departments of admission, diagnosis and vital events. End points considered were degree of improvement following the NYHA functional class, readmission and death.

2.1. Statistical analysis
Results were expressed as mean±standard deviation (S.D.). We employed the t-test for unpaired data and the Mann–Whitney U-test to compare differences between groups. The Kruskal–Wallis test for two-way analysis of variance (ANOVA) was used to evaluate differences between NYHA classes. Length of readmission was defined as the time between initial admission to the intervention group and readmission measured in weeks from the initial discharge. The Log Rank (Mantel–Haenszel) test was used for this purpose. The best cut-off point to predict early readmission was a level of CRP of 0.9 mg/dl.

P values less than 0.05 were considered significant and those less than 0.1 as statistical trend.

To assess the impact of several variables in readmission, logistic-regression analysis was used. We built a stepwise model with all potentially influencing variables on readmission. Afterwards a hierarchical backward elimination process was carried out to determine the best fit for the model, calculating a maximal likelihood equation with a minimal P<0.05. Specifically age, gender, levels of blood pressure and renal function data were eliminated from the model. Besides, to evaluate the independence of variables included in logistic-regression analysis influencing readmission, we used a multivariate covariance analysis, using level of CRP as dependent variable, adjusted for possibly confounding covariates.


   3. Results
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
4. Discussion
 Acknowledgments
 References
 
Our intervention group consisted of 76 patients with a mean age of 73.5±11 (95% CI 71.2–75.8, P<0.05): 44 (58%) were male with a mean age of 77.5±2.3 and 32 (42%) female, with a mean age of 71.8±10.3, (P=0.018). Mean length of stay was 7.7±4.3 days.

The mean value of CRP in patients with heart failure was 3.94±5.87 (CI 1.26–7.60, P<0.05), while mean CRP levels in patients with syncope was 0.84±1.95 (CI 0.96–2.94, P<0.05) (P=0.0007).

Table 1 shows the differences in CRP levels among patients according to type of ventricle failure and NYHA class.


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  		Table 1 Pattern of ventricle failure and CRP levels

 
Table 2 shows the relation between CRP levels and the different causes of heart failure.


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  		Table 2 CRP levels in relation to cause of heart failure

 
The left ventricular ejection fraction was adequately measured in 72 (95%) patients, with a mean value of 50.4±17.7% (CI 41.2–59.6, P<0.05). In the remaining four patients, poor visualisation of heart cameras prevented measurement of left ventricle ejection fraction. We observed a trend for higher CRP levels when the ejection fraction was below 35%: 7.5±9.8 vs. 3.7±4.5 (P=0.09).

The relationship between NYHA functional class on discharge and CRP values are depicted in Table 3.


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  		Table 3 Mean CRP levels found in relation to NYHA functional class on discharge

 
During the 18 month follow up of patients, 32 (43%) required readmission (mean age 74.4±11.2 years) to the hospital due to exacerbation of heart failure, whereas 42 (57%) patients (mean age 74.1±9.4 years) did not present any need for readmission. These patients presented CRP levels of 5.24±5.46 and 4.01±6.70, respectively (P=0.036). Readmission of patients occurred after a mean of 4.01±3.61 months of the first admission and each patient readmitted had a mean of 1.87±1.53 subsequent readmissions (CI 1.34–2.40, P<0.05). Those patients presenting CRP levels of >0.9 mg/dl were readmitted sooner than those with levels below 0.9 mg/dl (Fig. 1). The adjusted relative risk of CRP levels>0.9 mg/dl was 1.43, while for CRP levels ≥3 mg/dl it was 1.96.


Figure 1
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  		Fig. 1 Readmission in patients with levels of CRP higher and lower 0.9 mg/dl (P=0.02).

 
Thirteen patients (17%) died during the follow up period. Mean CRP levels in these patients was 9.35±9.97, while the mean CRP values in those patients who survived was 3.42±4.50 (P=0.002). Mortality occurred after a mean of 5.44±4.77 months (CI 2.85–8.03, P<0.05).

In logistic-regression analysis the best model to explain readmission was fitted by levels of CRP, left ventricle ejection fraction, NYHA class and levels of plasmatic K both on discharge, (P=0.03). In Table 4 standard b coefficients and standard odds ratios (CI 95%) are shown.


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  		Table 4 Logistic-regression model for readmission

 
On analysing influence of covariates we met parallel regression lines among levels of CRP and plasmatic K, NYHA class on discharge and left ventricle ejection fraction, meaning CRP is an independent variable in prediction of readmission (Table 5).


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  		Table 5 Influence of covariates on CRP

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
Acknowledgments
 References
 
Chronic heart failure is a major health problem in developed countries and is responsible for a great number of hospitalisations and rising health costs [13–15]. In most cases heart failure represents the final stage of several diseases that affect different constitutive parts of the human heart. Each of these pathologies may eventually lead to hemodynamic failure and is reflected as heart failure [25].

There is increasing research into new risk factors that may serve as markers of cardiac dysfunction, mainly in ischaemic disease [9–11] where chronic inflammation may play a role in the pathogenesis of atherosclerosis. CRP is a long-term marker of risk of cardiovascular events [10,28]. In addition coronary heart disease has been associated with a variety of infections e.g.: Chlamydia pneumoniae, Helicobacter pylori and herpes virus [11]. These associations are based on epidemiological data and on trials with antibiotics [26,27]. At present, however, it is unknown whether inflammation is an epiphenomenon or, on the contrary an active agent in atherosclerosis.

There is evidence that chronic activation of the immune system exists during heart failure. Some patients present evidence of monocyte-macrophage and lymphocyte activation [20–23]. It appears clear that patients with either ischaemic or non-ischaemic heart failure show activation of proinflammatory cytokines (tumour necrosis factor-{alpha}, IL-1, IL-6). What factor triggers this immune response is unknown, but at present, possible agents include the renin–angiotensin–aldosterone system and the sympathetic nervous system [21–23]. The initial mechanism remains elusive, although bacterial translation from the intestine, particularly in right ventricle failure causing mesenteric venous congestion, or primary lymphocyte dysfunction by down-regulation of lymphocyte β2-receptors (β-blockers preventing these modifications) have been implicated.

In our study, we observed significantly increased levels of CRP in patients hospitalised due to heart failure compared with patients admitted for syncope. We did not find differences in CRP levels between left and two-sided heart failure nor between left and right heart failure. Our results therefore do not support the role of bacterial translation in activation of the immune response. There was no significant variation between NYHA functional class on admission and CRP levels. This finding is difficult to interpret: it could mean activation of the immune system independently of the degree of hemodynamic dysfunction, or it could be related to the effect of some drug (e.g. aspirin, ACE inhibitors) on CRP levels, thus explaining the lack of variation of CRP on admission, since several patients were sub-optimally treated before admission.

We observed different CRP levels on discharge in relation to NYHA class, indicating that there is variation in improvement with standard therapy. The higher the level of CRP, the higher the NYHA functional class. Since in this study, we did not control the effects of drugs on CRP levels, it was not possible to determine the influence of a particular drug on CRP. Although we found differences in CRP levels amongst the several causes of heart failure, the groups were too small and no clear conclusion can be drawn. Levels of CRP were higher, however, in heart failure due to ischaemia, thus supporting the present theory of atherogenesis.

The left ejection fraction values found were not low enough for heart failure. This could be explained by the inclusion of a large number of patients with valvular disease and hypertensive cardiomyopathy. However, we found a trend to decreasing values of left ejection fraction in relation to higher CRP levels.

The natural course of heart failure is a deterioration of cardiac function manifested by worsening symptoms despite therapy, thus leading to the need for subsequent readmission. It may be of interest that CRP was higher in those patients who required readmission due to worsening symptoms of heart failure. Here CRP may serve as a biochemical marker to predict subsequent readmission of patients with heart failure.

As expected, NYHA class on discharge and left ventricle ejection fraction were factors implicated in readmission. Level of plasmatic K was also an influencing factor in readmission; in this sense we could speculate with these patients need higher doses of ACE inhibitors used in therapy for controlling symptoms of heart failure. CRP also participated in prediction of readmission in multivariate analysis, and it presented an independent behaviour when analysed jointly with NYHA class, plasmatic K and left ventricle ejection fraction working as covariates. In addition, CRP may serve as a marker of the length of time leading up to readmission: those patients with CRP levels >0.9 mg/dl presented shorter periods before readmission.

CRP also increased in patients who died during the follow-up period. The relationship between mortality and CRP levels could be an expression of increased cardiovascular deterioration and decline in the gradient of cardiac function up to death.

We conclude that CRP levels measured once during hospitalisation in patients with heart failure may predict, in an independent way, a higher hospitalisation rate and readmission within a shorter period in cases of deteriorating heart failure. Increased CRP levels are also associated with increased mortality and may also be associated with a worse therapeutic response. However, these preliminary data about the value of CRP in heart failure need to be confirmed with larger studies.


   Acknowledgments
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Acknowledgments
References
 
We thank Professor Miguel Anderiz for his invaluable advice and review of statistical methods.


   References
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Acknowledgments
 References
 

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