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C-reactive protein, infarct size, microvascular obstruction, and left-ventricular remodelling following acute myocardial infarction

Stein Ørn, Cord Manhenke, Thor Ueland, Jan K. Damås, Tom Eirik Mollnes, Thor Edvardsen, Pål Aukrust, Kenneth Dickstein
DOI: http://dx.doi.org/10.1093/eurheartj/ehp070 1180-1186 First published online: 19 March 2009


Aims This study assessed the relationship between inflammatory mediators and indices of infarct size and left-ventricular (LV) remodelling following successful primary percutaneous coronary intervention (PCI) in patients with first time ST elevation myocardial infarction (MI).

Methods and results Forty-two patients admitted with an occluded single vessel were recruited consecutively. Cardiac magnetic resonance was used for serial assessment (2 days, 1 week, 2 months) of infarct size, microvascular obstruction (MO), and LV remodelling. Inflammatory mediators were analysed before and after PCI. Our major findings were: (1) Following PCI, there was a marked increase in plasma levels of C-reactive protein, closely correlated with an increase in interleukin-6 and terminal complement complex, reaching maximum 2 days after PCI; (2) C-reactive protein 2 days after PCI was significantly correlated with infarct size and parameters of LV remodelling 2 months after PCI; (3) Patients with persistent MO had significantly higher C-reactive protein levels 2 days following PCI.

Conclusion We suggest that the rapid increase in C-reactive protein levels in this model of successful revascularization of a single, totally occluded vessel reflects the degree of inflammation within the infarcted area. Our findings support a role for C-reactive protein-mediated complement activation as both a marker and mediator of myocardial damage following MI.

Clinical study no.: NCT 00465868.

  • Inflammation
  • C-reactive protein
  • Interleukin-6
  • Terminal complement complex
  • Acute myocardial infarction
  • Remodelling
  • Primary percutaneous intervention
  • Cardiac magnetic resonance


Following acute myocardial infarction (MI), cytokines are released by the myocardium to modulate tissue repair and adaptation after injury.1 The effects of inflammatory cytokines can be favourable, leading to healing and restoration of function, or unfavourable, leading to left-ventricular (LV) remodelling and myocardial failure.2 C-reactive protein, known to activate the classical pathway of complement, is a global marker of inflammation produced by the liver partly as a response to stimulation by interleukin-6 (IL-6), that is released from the ischaemic zone after MI.3 Increased C-reactive protein levels in MI have been associated with adverse clinical outcomes and larger infarctions as assessed by enzymatic assays.4,5 In an animal model, C-reactive protein was deposited together with complement within the infarct, suggesting that it might increase infarct size by activating the complement cascade.6 Interestingly, inhibition of exogenously added human C-reactive protein combined with therapeutic complement depletion during acute MI reduced the scar size in a rat model and C-reactive protein has been recently identified as a potential target for treatment for cardiovascular disease.6 Taken together, these findings suggest that C-reactive protein, at least partly through its interaction with the complement, is not only a marker but also a mediator of the inflammatory reaction following acute MI. However, the relationship between C-reactive protein, complement activation, and the degree of myocardial damage following acute MI has not been elucidated.

The objective of this study was to assess the relationships between myocardial damage and mediators both up-stream (IL-6) and down-stream (terminal complement activation) to C-reactive protein following acute MI. This study was designed to isolate the effects of the acute ischaemic injury from other factors caused by residual ischaemia, activation of proteinases using thrombolytic therapy, and previous MI. Therefore, only patients with first time ST segment elevation MI (STEMI) who were successfully treated with primary percutaneous coronary intervention (PCI) were included. Moreover, in order to allow baseline blood sampling with a minimal influence from the ischaemic zone, only patients with a single, occluded infarct-related artery were included.

Myocardial damage was assessed by cardiac magnetic resonance (CMR), allowing reliable determination of the amount of necrotic tissue, and sequential monitoring during follow-up to assess the healing process.7,8 Cardiac magnetic resonance was also used to assess the relationship between C-reactive protein and microvascular obstruction (MO). Microvascular obstruction represents an impairment of flow in the centre of the infarct region due to plugging and damage of capillaries.9 The presence of MO following acute MI is associated with a poor prognosis and increased LV remodelling,10,11 but its relationship to inflammation has not been addressed.



Consecutive patients admitted with STEMI and selected for primary PCI were enrolled prospectively at a single centre. The diagnosis of STEMI was defined by typical chest pain and ST elevation on electrocardiogram at admission. Patients were included if they had: (i) no previous MI, (ii) demonstrated acute proximal/mid-occluded single-vessel disease, (iii) underwent successful PCI with stent implantation without significant residual stenosis, (iv) had no contraindications to CMR imaging, and (v) could be scanned within 48 h of PCI. Patients were assessed by Troponin T (TnT) every 24 h during the first 4 days and at the time of the second CMR scan at 7 days to ensure a steady wash-out of the infarcted territory. All patients were treated with aspirin, clopidogrel, and a statin. Other medication was prescribed by the treating physician without the knowledge of the CMR results. The study was approved by the regional Ethics Committee at the University of Bergen and all patients provided written informed consent prior to inclusion.

Cardiac magnetic resonance protocol

All patients were scanned at 2 days, 1 week, and 2 months following PCI. Scans were obtained during repeated breathholds with patients in a supine position by a 1.5 T whole body scanner (Intera R 10.3 Philips Medical Systems, Best, The Netherlands) using a dedicated cardiac coil. Resting LV function was determined with cine images using a steady-state free precession technique in short- and long-axis views in the true heart axis. The short-axis covered the whole LV with 10–14 contiguous slices. Left-ventricular mass, ejection fractions and volumes were determined using short-axis volumetry.

Microvascular obstruction was defined as regional hypoperfusion on first-pass perfusion (60 heartbeats), using a turbo field echo sequence with three short-axis slices per heart beat (prospective triggering) and a selective saturation recovery prepulse, using a dosage of 0.075 mmol/kg gadolinium-based contrast agent (Omniscan®, Amersham Health, Little Chalfont, UK).12 Immediately following the completion of the first pass imaging, another 0.175 mmol/kg of contrast agent was infused (total 0.25 mmol/kg), and 10–15 min following the latter infusion, late-enhancement images were acquired, using an inversion recovery prepared T1 weighted gradient-echo sequence. Infarct size was assessed manually with planimetry on each short-axis slice, delineating the hyperenhanced area including areas of hypo-enhancement surrounded by hyperenhanced area, the latter considered a sign of MO. The same density (1.05 g/cm3) was assumed for both hyperenhanced (scarred) and non-hyperenhanced (non-scarred) myocardium.

All post-processing was performed on the View Forum™ Software (Philips Medical Systems). With the exception of LV ejection fraction (LVEF), volumes and mass were indexed to the body surface area: LV end-diastolic volume index (LVEDVI), LV end-systolic volume index (LVESVI), LV stroke volume index (LVSVI), and LV mass index.

Blood sampling protocol

Venous blood samples were collected on admission to the hospital, immediately prior to PCI, and 2 days, 1 week, and 2 months following hospitalization. The pyrogen-free blood collection tubes were immediately immersed in melting ice [ethylenediaminetetraacetic acid (EDTA) containing tubes, plasma] or placed in room temperature (tubes without any additives, serum) and centrifuged within 20 min at 2500 g for 20 min to obtain platelet-poor plasma or centrifuged at 1000 g for 10 min after coagulation (serum). All samples were stored at −80°C and thawed only once.

Biochemical measurements

C-reactive protein concentrations were measured by a particle-enhanced immunoturbidimetric method with the use of Roche ModularP automated clinical chemistry analyser (Roche Diagnostics, Basel, Switzerland) and reagents of Tina-quant C-reactive protein (latex) assay (Roche Diagnostics). Interleukin-6 was measured by a high-sensitivity enzyme immunoassay (EIA) obtained from R&D Systems (Minneapolis, MN). The soluble terminal C5b–9 complement complex (TCC) was measured as described previously using an EIA developed in our laboratory.13 The results are given in arbitrary units (AU)/mL, related to a standard of zymosan activated serum, defined to contain 1000 AU/mL. Troponin T concentrations were measured on Roche Elecsys 2010 (Roche Diagnostics), with the immunoassay Troponin T (Roche Diagnostics), using biotinylated monoclonal troponin T-specific antibody and a monoclonal troponin T-specific antibody labelled with ruthenium forming a sandwich complex. N-terminal pro B-type natriuretic peptide (NT-proBNP) was measured with a Roche Diagnostics NT-proBNP assay on an Elecsys 2010 analyser.


Using commercially available power calculation software (Biostat Inc., Englewood, New Jersey, USA), we calculated the minimum sample-size of the study: based upon data from a previous CMR study,17 with a power of 80%, a two-sided significance of 5%, a R2 = 0.25 for infarct size (the increment) and a two-sided significance of 0.05, we needed 27 patients. However, to decide the final sample size, we also consulted the literature. The three most relevant publications available at the time of design of this study all used a sample size of 40–45 patients.1416 Based upon these publications and the power calculation we decided to include between 40 and 45 patients. Biochemical parameters were assessed for characteristics of distribution by use of the Kolmogorov–Smirnov test. Levels of inflammatory markers were identified as not normally distributed. Therefore, those variables were expressed as medians and interquartile range (IQR) and non-parametric test were used. Kruskal–Wallis ANOVA was used to test for differences among more than two groups at each time point, followed by Mann–Whitney U-tests where appropriate to examine for differences between groups. Friedman test was used to test-time related changes within each group of patients, and if significant changes were found Wilcoxon signed-rank test was used to test for particular comparison. Correlations were assessed by Spearman correlations. A two-tailed P-value of <0.05 was considered significant. However, since a number of statistical calculations were made, and to adjust for multiple testing, particular attention should be given to P-values <0.01.


Baseline characteristics

Patients were included from September 2004 until May 2006. A total of 271 patients with first time STEMI treated by primary PCI were screened during the inclusion period. Reasons for non-inclusion (some patients had more than one reason) were multivessel disease 136 (60%) patients, non-occluded infarct related artery at coronary angiography 73 (33%) patients, thrombolytic therapy 5 (2%) patients, active inflammatory or autoimmune disease treated with anti-inflammatory medication 8 (4%) patients, prior infarction 5 (2%) patients, death before inclusion 8 (4%) patients, and contraindications to CMR [significant claustrophobia/unwilling to undergo CMR 8 (4%) patients, inability to cooperate during CMR examination 5 (2%) patients, and haemodynamic instability 6 (3%) patients]. Of the 46 patients that were included in the study, two patients were excluded due to re-infarction during the first week, and two patients refused to undergo more than one CMR examination. No patient died during follow-up. Patient characteristics of the remaining 42 patients are presented in Table 1. The first CMR imaging (‘2 days’) was performed at a mean of 2.2 ± 0.4 days following PCI, the second (‘1 week’) at 7.3 ± 0.8 days, and the third (‘2 months’) at 61 ± 3.7 days following PCI. In 11 (26%) patients there was no evidence of MO at any time point, 16 (38%) patients showed MO at 2 days but not at 1 week, and 15 (34%) patients showed MO both at 2 days and 1 week. As assessed by CMR, there was a significant reduction in infarct size (P < 0.001) and LVESVI (P < 0.001), and a significant increase in LVEF (P < 0.002) from 2 days until 2 months of follow-up, whereas LVEDVI did not change (Figure 1).

Figure 1

Changes in left-ventricular volumes, ejection fraction, and infarct size in 42 patients with ST segment elevation myocardial infarction 2 days, 1 week, and 2 months following primary percutaneous coronary intervention. Data are given as median and ranges. P-values vs. pre-percutaneous coronary intervention values.

View this table:
Table 1

Baseline characteristics of the study group

Variablesn = 42
Age (years)58 ± 12
Male gender (%)34 (81)
Body surface area (m2)2.0 ± 0.2
Systolic blood pressure (mmHg)140 ± 27
Diastolic blood pressure (mmHg)84 ± 20
Heart rate (b.p.m.)74 ± 17
Current smoker (%)20 (48)
Diabetes mellitus (%)3 (7)
Hypertension (%)10 (24)
Time from symptoms to reperfusion (min)261 ± 202
ECG changes
 Q-waves prior to PCI (%)14 (33)
 Q-waves at discharge (%)24 (57)
Culprit vessel
 Left anterior descending artery (%)21 (50%)
 Right coronary artery (%)17 (40)
 Circumflex artery (%)4 (10)
Lesion location (proximal/mid/distal)18/22/2
Patients with more than one stent (%)10 (24)
Drug eluting stents (%)4 (10)
Thrombus aspiration (%)24 (57)
TIMI flow Post-PCI (3/2)35/7
 Gp IIb/IIIa antagonists (%)31 (74)
 Heparin (%)42 (100)
 Clopidogrel (%)42 (100)
 Aspirin (%)42 (100)
 Statin (%)42 (100)
 ACE-I/ARB (%)38 (91)
 Beta-blocker (%)23 (55)
 Aldosterone antagonist (%)8 (19)
  • ACE-I, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; PCI, percutaneous coronary intervention.

  • Where indicated, data are given as mean±SD.

Plasma levels of C-reactive protein, interleukin-6, and terminal complement complex following percutaneous coronary intervention

There was a marked increase in C-reactive protein levels in all patients following PCI, reaching maximum after 2 days (∼20-fold increase) (Figure 2). Moreover, this increase in C-reactive protein was accompanied by a significant rise in plasma levels of IL-6 (∼10-fold increase) and TCC (∼5-fold increase) (Figure 2). Interleukin-6 was significantly correlated with C-reactive protein at all time points (r = 0.44, P = 0.009; r = 0.64, P < 0.001; r = 0.69, P < 0.001; r = 0.48, P < 0.002; prior to PCI and 2 days, 1 week, and 2 months after PCI, respectively). In contrast, the correlation between TCC and C-reactive protein reached statistical significance only at 2 days (r = 0.51, P < 0.001) and 1 week (r = 0.37, P < 0.02) after PCI. There was no difference in C-reactive protein levels at 2 days between the 32 patients treated with 1 vs. the 10 patients treated with more than one stent (median and IQR): one stent 30[14–75] mg/L vs. more than one stent 32[10–57] mg/L; P = 0.76). Significant correlations between total ischaemic time and biomarkers were only found for TnT (r = 0.51, P = 0.004) and NT-BNP (r = 0.40, P = 0.02) prior to PCI. No correlations were found between total ischaemic time and any of the biomarkers following PCI.

Figure 2

Time profiles of interleukin (IL)-6, C-reactive protein (CRP), and terminal complement complex (TCC) in 42 patients with ST segment elevation myocardial infarction before and 2 days, 1 week, and 2 months following primary percutaneous coronary intervention. Data are given as median and ranges. P-values vs. pre-percutaneous coronary intervention values.

The relationship between inflammatory mediators, infarct size, and left-ventricular function at corresponding time points

Two days following PCI, C-reactive protein levels were strongly correlated to NT-proBNP, LVEF, and in particular to infarct size as assessed by both CMR and enzymatic methods (Table 2). C-reactive protein was not correlated to LV volumes, but was inversely correlated to non-infarcted mass (Table 2). A similar pattern of correlations was seen at 1 week, but not after 2 months (Table 2). In contrast to C-reactive protein, IL-6 was correlated with infarct size only at 2 days as assessed by CMR (0.38, P = 0.01), but not by enzymatic methods. However, IL-6 was strongly correlated with NT-proBNP levels at 2 days (0.49, P = 0.001), 1 week (0.40, P = 0.009), and 2 months (0.45, P = 0.003) following PCI. Terminal complement complex was not correlated to NT-proBNP, TnT, or any of the CMR parameters at any time-point.

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Table 2

The relationship between C-reactive protein and corresponding cardiac magnetic resonance measurements, Troponin T, and N-terminal pro B-type natriuretic peptide in 42 patients with STEMI at 2 days, 1 week, and 2 months following primary percutaneous coronary intervention

C-reactive protein
2 days1 week2 months
 Infarct size (g/m2)0.500.0010.58<0.00010.230.14
 LVEF (%)−0.390.01−0.410.007−0.090.58
 LVESVI (mL/m2)
 LVEDVI (mL/m2)0.020.910.140.370.080.62
 Non-infarct size (g/m2)−0.340.03−0.160.300.030.85
  • LVEF, left-ventricular ejection fraction; LVESVI, left-ventricular end-systolic volume index; LVEDVI, left-ventricular end-diastolic volume index; NA, not applicable; CMR, cardiac magnetic resonance; STEMI, ST segment elevation myocardial infarction.

The relationship between inflammatory mediators and cardiac magnetic resonance parameters 2 months after percutaneous coronary intervention

Infarct size and parameters of LV function 2 months after primary PCI reflect the final myocardial damage following MI. Notably, early measurement of C-reactive protein (i.e. 2 days and 1 week) significantly predicted LVEF, LVESVI, and in particular infarct size after 2 months (Table 3). Interleukin-6 levels after 2 days, but not TCC levels, were also related to these parameters of myocardial function after 2 months (Table 3).

View this table:
Table 3

Correlation between inflammatory parameters (C-reactive protein and interleukin-6), infarct size, left-ventricular ejection fraction, and left-ventricular volumes as assessed by cardiac magnetic resonance 2 months following primary percutaneous coronary intervention in 42 patients with STEMI treated with primary percutaneous coronary intervention

CMR at 2 monthsC-reactive protein 2 daysC-reactive protein 1 weekIL-6 2 days
Infarct size (g/m2)0.560.00010.430.0040.370.02
LVEF (%)−0.420.006−0.380.01−0.320.04
LVESVI (mL/m2)0.400.0090.370.020.300.05
LVEDVI (mL/m2)
Non-infarcted myocardial mass (g/m2)−0.170.29−0.020.92−0.070.67
  • LVEF, left-ventricular ejection fraction; LVESVI, left-ventricular end-systolic volume index; LVEDVI, left-ventricular end-diastolic volume index; CMR, cardiac magnetic resonance; IL-6, interleukin-6; STEMI, ST segment elevation myocardial infarction.

The relationship between inflammatory mediators and microvascular obstruction

When the patients were divided into three groups according to the degree of MO [no MO, (n = 11), MO at 2 days, but not at 1 week (subacute MO, n = 16), and MO both at 2 days and 1 week (persistent MO, n = 15)], we found that the latter group had increased C-reactive protein levels at 2 days compared with the other two groups (Figure 3). A similar pattern was seen for IL-6, although the differences between the groups reached statistical significance only after 2 months (Figure 3). No differences were seen between the different MO groups for TCC (Figure 3).

Figure 3

Time profiles of interleukin (IL)-6, C-reactive protein (CRP), and terminal complement complex (TCC) in 42 patients with ST segment elevation myocardial infarction before and 2 days, 1 week, and 2 months following primary percutaneous coronary intervention. The patients were divided into three groups according to degree of microvascular obstruction (MO): no microvascular obstruction (n = 11), microvascular obstruction at 2 days, but not at 1 week (subacute microvascular obstruction, n = 16) and microvascular obstruction both at 2 days and 1 week (persistent microvascular obstruction, n = 15). Data are given as median and ranges. P-values vs. the other two microvascular obstruction groups.


In the present study, we found a marked rise in C-reactive protein levels 2 days following successful primary PCI. Notably, C-reactive protein and IL-6, a potent inducer of C-reactive protein, were correlated to sub-acute and chronic infarct size measured by contrast-enhanced CMR. These findings are in accordance with studies that demonstrate a relationship between biochemical markers of infarct size and C-reactive protein,5 but in apparent contrast to the study by Haase et al.16 that did not find a correlation between C-reactive protein and infarct size measured by CMR. There may be several reasons for this discrepancy. The study by Haase et al. included patients admitted for rescue PCI, 30% of whom had previous MI that may preclude accurate assessment of new myocardial damage. Furthermore, 60% of patients had multivessel disease and there was no information on the patency of the infarct-related artery at the time of PCI. In contrast, our study was designed to isolate the effect of acute reperfusion from potential confounders such as previous MI, residual ischaemia following restoration of blood flow, varying patencies of the infarct-related artery prior to revascularization and any co-morbidity likely to interfere with the inflammatory response following acute MI. Only patients with first time MI, occluded single-vessel disease of a large coronary artery, successfully revascularized by primary PCI were included in the current study.

There is still controversy regarding the stimuli of C-reactive protein release following revascularized MI. Gottsauner-Wolf et al.14 found a significant increase in circulating C-reactive protein levels following elective PCI, and suggested that this reflected the inflammatory response to vascular damage. In contrast, our findings suggest that the majority of the increase in the C-reactive protein levels following revascularized MI reflects the systemic inflammatory response to myocardial damage rather than to vascular damage following PCI. First, there was a strong correlation between C-reactive protein levels and infarct size and biochemical markers of myocardial necrosis. Second, the magnitude of C-reactive protein increase in our study was far greater compared with the study by Gottsauner-Wolf et al., i.e. ∼20 vs. ∼2-fold increase. Third, although the use of more than one stent indicates larger and more complex vascular damage, we found no difference in C-reactive protein response between patients treated with one or more than one stent in our study. Fourth, we have previously shown that the inflammatory response to PCI is attenuated in patients with acute coronary syndromes when compared with those with stable disease.18

Studies in animal models have demonstrated that the binding of C-reactive protein to ligands exposed in damaged tissue within the infarcted area promote complement activation with secondary increase in MI size.6 Moreover, in vivo depletion of complement has been shown to substantially attenuate the C-reactive protein-mediated effects on myocardial tissue damage after coronary ligation in rats.6 In an autopsy study by Nijmeijer et al.19 it was found that both reinfarction and reperfusion therapy significantly increased the extent of C-reactive protein and complement depositions in human myocardial infarcts. An interaction between C-reactive protein and TCC has also been suggested in plaque destabilization in patients with coronary artery disease.20 We extend these findings by demonstrating a marked systemic increase in TCC 2 days after successful revascularization in STEMI patients potentially reflecting a high degree of complement activation within the infarcted area. Moreover, we found a significant correlation between C-reactive protein and TCC levels only during the subacute phase following successful PCI, further supporting a role for C-reactive protein-mediated complement activation during MI.

Increased C-reactive protein level in the acute phase of MI has been identified as an independent predictor of development of heart failure.4 The size of the healed infarction is a major determinant of long-term remodelling,20 and has been demonstrated to be a stronger predictor of outcome than LVEF.21 Our study provides a potential pathophysiological explanation for the association between C-reactive protein levels and LV remodelling by linking peak C-reactive protein levels with infarct size after 2 months. Furthermore, our findings suggest an association between persistent MO and enhanced C-reactive protein levels. In the present study, we show that the peak level of C-reactive protein, 2 days after successful PCI, was increased in those with persistent MO 1 week following PCI, when compared with other patients. Interestingly, compared with patients with persistent MO at 1 week, C-reactive protein levels were significantly lower in patients that only had evidence of MO at 2 days. This finding may suggest a different inflammatory response in patients with persistent MO, possibly related to a more extensive structural damage in the core of the infarction in these patients. Although MO impairs microcirculation in the infarct zone, there is slow diffusion from the necrotic myocardium in these patients.22 Necrotic debris and inflammatory mediators from the infarct zone will therefore be released to systemic circulation, with a subsequent increase in the hepatic release of acute phase reactant such as C-reactive protein.


The small sample size in this study makes the results susceptible to the impact of biological heterogeneity. However, the trial was designed with rigorous selection criteria in order to reduce the number of confounders such as prior MI, multi-vessel disease, differences in revascularization techniques (only primary PCI, not thrombolysis), and varying patency in the infarct related artery prior to and after PCI. The cohort therefore represents a unique and homogenous patient sample that facilitates interpretation of the prospectively selected parameters. However, to ensure that the findings are applicable in non-selected STEMI populations, larger-scale studies in these populations are required. Moreover, correlations do not necessarily mean causal relationship and further mechanistic studies are needed to elucidate the role of inflammatory mediators in MI and post-MI myocardial remodelling.

Although our findings may suggest a direct pathogenic role of C-reactive protein during MI and myocardial remodelling, it is important to underscore that the leading role of C-reactive protein as a stable and reliable inflammatory biomarker in cardiovascular disease is based on its long circulating half-life and its ability to reflect upstream inflammatory activity including IL-6 activation. Thus, the strong correlation between C-reactive protein and indices of infarct size and remodelling when compared with a weaker correlation between these indices and IL-6 and TCC, does not necessarily suggest a more important pathogenic role of C-reactive protein in the development of MI and post-MI remodelling, but rather the strong ability of C-reactive protein to mirror the inflammatory responses that are involved in these processes.


In patients following successful revascularization of a total occluded single vessel in STEMI, we suggest that the rapid systemic increase in C-reactive protein levels 2 days after PCI reflects the degree of inflammatory response within the infarcted area including enhanced IL-6 activation. C-reactive protein levels in these patients were strongly related to the size of myocardial damage and to the severity of MO as well as to the degree of complement activation, potentially reflecting C-reactive protein-mediated complement activation during these processes. Although further studies are needed, these findings suggest a role for C-reactive protein not only as a marker but potentially also as a mediator of myocardial damage following MI.


The study was financed by Helse Vest grant no. 911017, The Norwegian Association of Heart and Lung Patients, Helse og Rehabilitering grant no. 2003/2/0211, The Norwegian Council on Cardiovascular Disease, and The Family Blix Foundation.

Conflict of interest: none declared.


The authors wish to thank Torbjørn Aarsland, Jorunn Nielsen, Fredrikke Wick, Bent Erdal, and Øyvind Skadberg for their important contributions during the study.


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