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European Heart Journal Advance Access originally published online on January 13, 2006
European Heart Journal 2006 27(5):547-552; doi:10.1093/eurheartj/ehi709
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oupjournals.org

Effects of metoprolol therapy on cardiac troponin-I levels after elective percutaneous coronary interventions

Ilyas Atar1,*, Mehmet Emin Korkmaz1, Inci Asli Atar1, Oyku Gulmez1, Bulent Ozin1, Huseyin Bozbas1, Tansel Erol1, Alp Aydinalp1, Aylin Yildirir1, Muammer Yucel2 and Haldun Muderrisoglu1

1Department of Cardiology
2Department of Biochemistry, Faculty of Medicine, University of Baskent, Maresal Fevzi Çakmak cad. 10. sok. Bahçelievler 06490, Ankara, Turkey

Received 27 March 2005; revised 6 December 2005; accepted 8 December 2005; online publish-ahead-of-print 13 January 2006.

* Corresponding author. Tel: +90 312 2126868/1404; fax: +90 312 2237333. E-mail address: iatar{at}tkd.org.tr


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Acknowledgement
 References
 
Aims Beta-blockers (BBs) have been shown to improve survival and reduce the risk of re-infarction in patients following myocardial infarction. There are conflicting data about the effects of BB therapy on cardiac biomarkers after percutaneous coronary interventions (PCIs). The aim of the study was to investigate the effects of BB use on cardiac troponin-I (cTnI) levels in patients who had undergone elective PCI.

Methods and results In this prospective study, 287 patients with coronary artery disease were included. Patients were randomized either to BB or control groups prior to the intervention. Blood samples for cTnI were obtained before and at 6, 24, and 36 h after the procedure. Of the 287 patients included, 143 received metoprolol succinate 100 mg/day, and 144 received no BB and served as the control group. Baseline clinical characteristics of both groups, except for history of coronary artery bypass graft surgery, were similar. We observed no significant difference in the elevation of cTnI levels between the two groups after PCI (BB group, 17 patients, 11.9%; control group, 10 patients, 6.9%; P=0.2).

Conclusion Metoprolol succinate therapy seems to have no cardioprotective effect in limiting troponin-I rise after PCI.

Key Words: Beta-blocker • Cardiac troponin-I • Percutaneous coronary interventions


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Acknowledgement
 References
 
Cardiac troponins are sensitive markers of myocyte necrosis, with demonstrated diagnostic and prognostic value in the setting of acute coronary syndromes. Elevated cardiac troponin-I (cTnI) levels have been reported in 13.6–48% of patients after percutaneous coronary interventions (PCIs).1–11 Some studies have shown that elevations in cTnI levels after PCI are associated with increased major adverse clinical events during follow-up.1,4,9,11

Numerous secondary prevention trials have shown that beta-blockers (BBs) prevent death and reduce the risk of re-infarction after acute myocardial infarction (AMI).12–16 There are conflicting data about the effects of BB therapy on cardiac biomarkers after successful PCI.17–19 An observational study suggests that oral BB use before PCI reduces creatine kinase-MB (CK-MB) elevation and improves long-term survival.17 However, a second large observational study failed to confirm this finding.18 A randomized study showed that intracoronary administration of propranolol protects the myocardium during PCI and significantly reduces the incidence of cTnI and CK-MB elevations.19 To our knowledge, there are no randomized studies in the literature that evaluate the effects of oral BBs on cTnI levels after PCI.

The aim of this study was to investigate the effect of oral metoprolol succinate use on cTnI in patients undergoing elective PCI.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Acknowledgement
 References
 
Patients population and study protocol
This study was a prospective, randomized, open-controlled trial. Patients with coronary artery disease who were undergoing elective PCI were considered for inclusion. Random-generated numbers table were used for randomization. Exclusion criteria were Q-wave MI during the previous 7 days; patients with elevated pre-procedural cTnI and CK-MB levels; use of BBs prior month; those in whom use of a special device (laser, rotational atherectomy, brachy-therapy, etc.) was planned; those in whom BBs were contraindicated. The research protocol was approved by the local Ethics Committee of Baskent University. Informed consent was obtained from all patients.

Between 1 November 2000 and 1 December 2002, a total of 512 patients underwent elective PCI; 160 patients were excluded because of prior month treatment with BBs, 48 because of elevated pre-procedural cTnI and CK-MB levels or Q-wave MI during the previous month, 10 because of contraindications to BB treatment, and seven because of the use special device. Thus, a total of 287 patients [mean age, 59±10 (60) years; 210 men, 77 women] fulfilling the inclusion criteria were scheduled for elective PCI and were included in the study; 144 patients were randomized to control group and 143 to BB group.

Metoprolol succinate slow releasing form (Beloc ZOC, AstraZeneca®, Sweden) 100 mg/day po was given to the patients (n=143) in the BB group and no BBs were given to the patients (n=144) in the control group. The first doses of metoprolol succinate were given to patients the morning of the procedure. According to our standard protocol, all patients without contraindications were pre-treated with ticlopidine 250 mg bid at least 3 days before the procedure or with clopidogrel 300 mg at least 6 h before the procedure. All patients continued ticlopidine 250 mg bid or clopidogrel 75 mg/day for 3 months. We did not use intracoronary BBs, intravenous nitrate infusion, glycoprotein IIb/IIIa inhibitors, adenosine, and drug eluting stents. Other medical therapies were planned according to clinical necessity. In the BB group, the effectiveness of BB therapy evaluated using the effects of metoprolol succinate therapy on heart rate, systolic blood pressure, diastolic blood pressure, and rate pressure product (Heart ratexsystolic blood pressure).

The type of PCI (angioplasty only, angioplasty and stent, or primary stenting) was determined by the physician according to the lesion characteristics. Total balloon inflation times and inflation pressures were determined according to the technical properties of the balloon and the stent. The interventional procedures were all performed through femoral artery sheaths, with weight-adjusted heparin administered at the outset. PCI was considered successful if the final percentage diameter of stenosis was <50% with TIMI III flow in the absence of death, recurrent ischaemia, AMI, or urgent coronary bypass graft surgery during hospitalization.

Laboratory analyses
In all patients, blood samples were obtained before PCI and at 6, 24, and 36 h after the PCI for analysis of cTnI. cTnI samples were analysed by a Microparticle Enzyme Immunoassay (Axsys System Abbott, Abbott Park, IL, USA) with a normal range of cTnI value from 0.02 to 2.3 ng/mL. The measuring range was 0.02–50 ng/mL. cTnI was considered elevated if the measurement was above the normal limit in any of the follow-up measurements.

Statistical analyses
The statistical package SPSS (Statistical Package for the Social Sciences, version 9.0, SSPS Inc., Chicago, IL, USA) was used for statistical analyses. Continuous variables are expressed as means±standard deviation (median). All continuous variables were checked with Kolmogorov–Smirnov normality test to show their distributions. Continuous variables with normal distributions, such as age, levels of total cholesterol, haemoglobin were compared using the unpaired Student's t-test. Continuous variables with abnormal distributions, such as body mass index, mean LVEF, levels of fasting blood glucose, blood urea nitrogen, creatinine, triglyceride, C-reactive protein, basal CK-MB, and cTnI levels at basal, 6th, 24th, and 36th h were compared using the Mann–Whitney U test. For categorical variables, the {chi}2 test was used. P-values <0.05 were considered statistically significant.

A multivariable logistic regression model was used to assess the independent predictors of elevated cTnI levels. The alternative test hypothesis was built as two-sided for each statistical analysis. The tests were independent and so the experiment-wise Type I error did not exceed 0.05 alpha levels. In univariate analysis, age, sex, body mass index, incidence of hypertension, diabetes mellitus, smoking, stable angina and unstable angina, history of PCI, coronary artery bypass graft surgery and AMI within 1 month, usage of BBs, calcium channel-blockers, angiotensin-converting enzyme inhibitors and statins, dilated coronary artery, incidence of multivessels PCI, stent usage, incidence of spasm, dissection, blood transfusion, and subacute occlusion were assessed. Significant univariate variables with P<0.05 and BB use were included in the multiple logistic regression analysis for odds ratios and 95% confidence intervals.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Acknowledgement
 References
 
Baseline clinical and laboratory characteristics of both groups, except for history of a coronary artery bypass graft surgery, were similar (Table 1). History of coronary artery bypass graft surgery was significantly more prevalent in patients in the control group than in patients in the BB group (P=0.02). PCI procedure properties, except left anterior descending artery intervention, were similar in the two groups (Table 2). The number of left anterior descending artery interventions was higher in patients in the control group than in patients in the BB group (P=0.02).


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  		Table 1 Baseline clinical and laboratory features of patients in the BB and control groups
 

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  		Table 2 Details of PCI procedures for patients in the BB and control groups
 
In the BB group, heart rate [78±9 (78) vs. 62±8 (63) b.p.m.; P<0.001], systolic blood pressure [141±19 (140) vs. 117±14 (117) mmHg; P<0.001], diastolic blood pressure [85±11 (82) vs. 71±9 (70) mmHg; P<0.001], and rate pressure product [11 077±2116 (10 913) vs. 7298±1331 (7197); P<0.001] decreased significantly after the metoprolol succinate therapy when compared with the baseline values.

Baseline CK-MB and cTnI levels were similar in patients in the BB and control groups (Tables 1 and 3). During follow-up, cTnI levels increased above normal values in 17 patients (11.9%) in the BB group and in 10 patients (6.9%) in the control group (P=0.2). Mean cTnI levels at 24 and 36 h after PCI were higher in patients in the BB group than in patients in the control group; however, this difference was not statistically significant (Table 3).


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  		Table 3 Mean cTnI levels of the groups during follow-up
 
In the univariate analysis, baseline cTnI levels, baseline CK-MB levels, blood urea nitrogen levels, subacute coronary occlusion, and calcium channel-blocker use were significantly correlated with elevated cTnI levels (Table 4). In the multivariable analysis, baseline cTnI levels, blood urea nitrogen levels, subacute occlusion, and calcium channel-blocker use appeared as independent factors predictive of cTnI elevation (Table 5).


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  		Table 4 Factors statistically significantly associated with elevated cTnI levels: univariate analysis
 

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  		Table 5 Factors statistically significantly associated with elevated cTnI levels: multivariable analysis
 
No patients died during the study period. Major adverse effects which included coronary artery spasm or dissection, the need for blood transfusion, and subacute occlusion were not different between the groups (Table 2).


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Acknowledgement
 References
 
BB therapy is associated with a marked short- and long-term survival benefit among patients undergoing successful elective PCI.17,20,21 Previous studies have shown contradictory data about the effects of BB therapy on cardiac biomarkers after successful PCI.17–19 In the present study, no effects of oral metoprolol succinate therapy on cTnI levels after elective PCI were observed.

Sharma et al.17 demonstrated that BB use prior to PCI reduced CK-MB elevation and improved long-term survival in 1675 patients. In that study, only 643 (38.4%) patients were on BB drug therapy before the PCI. In that observational study, BB therapy was the single independent factor for lower CK-MB release after PCI. In another large observational study, Ellis et al.18 did not support these findings in 6200 patients undergoing PCI. Of these patients, 47.2% had been on BB therapy before the procedure. In another study, Wang et al.19 showed that intracoronary administration of propranolol decreased the incidence of MI after coronary intervention when compared with placebo.

Our study is a prospective, randomized study that investigated the effect of oral metoprolol succinate use on cTnI in patients who underwent PCI. All of the other trials published so far, evaluating the effects of BBs on cardiac biomarkers release after coronary interventions, have been retrospective observations and have included patients taking a wide variety of BBs at different dosages.17,18 In our study, the BB group was a homogenous group with all the patients receiving metoprolol succinate 100 mg/day. Two of the three BB studies mentioned earlier analysed only CK-MB levels,17,18 but Wang et al.19 analysed CK-MB and cTnI levels after PCI. It has been shown that troponins are more sensitive markers of myocardial necrosis than CK-MB after PCI;22 therefore, we tested only cTnI levels to evaluate myocardial damage in this study. Methodological issues such as the design of the study, the dose, and the administration route of the drug might be important in the discrepancy of the results obtained in different trials evaluating the effects of BBs on cardiac biomarker release after PCI.

The mechanisms underlying the beneficial and harmful effects of BBs after PCIs are not completely clear. The heightened sympathetic activity associated with PCI, which is caused by ischaemia or pain, may increase oxygen demand by increasing heart rate, blood pressure, and contractility. Sharma et al.17 have suggested that BBs decrease oxygen demand by preventing increases in heart rate and blood pressure. This may be the mechanism responsible for preventing periprocedural cardiac biomarkers release in patients who have been on prior BB therapy. Wang et al.19 have proposed that the effects of micro-embolization during PCI are often transient, and that reperfusion of small myocardial areas occurs after dissolution of these microemboli. Intracoronary administration of BBs before PCI results in a high local concentration of the drug and minimal, if any, systemic effects of the drug, such as changes in heart rate or myocardial depression in the non-PCI territory. Coronary collateral flow plays an important role in the prevention of myocardial ischaemia and limits the infarct size in patients with coronary artery disease. Recently, Billinger et al.23 demonstrated that intravenous metoprolol therapy reduced coronary collateral flow after angioplasty, probably due to an increase in coronary collateral resistance or a reduction in oxygen demand.

The pathophysiological mechanism for elevated cTnI and CK-MB after PCI is unclear. Factors related to the procedure, such as complications (e.g. side-branch occlusion, intimal dissection, coronary spasm, and distal embolization); number, duration, and pressure of balloon inflations; and stent implantation have been suggested as possible causes of increased cTnI and CK-MB after PCI.2,5–10 Ricciardi et al.,24 using contrast-enhanced magnetic resonance imaging, found an association between elevations of CK-MB and either side-branch occlusion or embolization to the vascular bed, leading to myocardial necrosis. In our study, we demonstrated that baseline cTnI and blood urea nitrogen levels, subacute occlusion, and usage of calcium channel-blocker use appeared as independent factors predictive of cTnI elevation after PCI. We found no relation between BB use and cTnI levels after elective PCI in univariate and multivariable analyses. In previous studies, treatments proposed to prevent myocardial injury during PCI that include nitrate infusion,25 statins,26,27 oral BBs,17 intracoronary BBs,19 glycoprotein IIb/IIIa inhibitors,28 and adenosine29 have been used. In the current study, we did not use intracoronary BBs, intravenous nitrate infusion, glycoprotein IIb/IIIa inhibitors, or adenosine.

In univariate and multivariable analysis, we demonstrated that calcium channel-blocker usage decreases cTnI levels after elective PCI. Previous studies demonstrated that calcium channel-blockers may improve anterograde flow, may be effective for resolving coronary spasm, and decrease micro vascular spasm after reperfusion.30,31 These mechanisms might explain the myocardial protective role of these agents. Our data also showed that increased levels of blood urea nitrogen were associated with elevated cTnI levels. This is in accordance with the previous studies showing a positive correlation between serum creatinine and blood urea nitrogen levels.32

Study limitations
The sample size in the present study is relatively small, and the study is open labelled. There were not enough data in the literature on the effects of the BBs on cTnI levels after PCIs and this prevented us to do power calculations at the beginning of the study. This study did not evaluate the effects of different types of BBs. The only BB used was metoprolol succinate. We did not include patients who were treated with atherectomy, laser, or brachy-therapy. History of coronary artery bypass graft surgery and the number of saphenous vein graft interventions were significantly more prevalent in patients in the control group than in patients in the BB group and the number of left anterior descending artery interventions was higher in patients in the control group than in patients in the BB group. The present results were collected at a single centre, which raises the issue of whether the results are generalizable and reproducible.

In conclusion, this prospective, randomized, open study suggests that metoprolol succinate therapy seems to have no effect on cTnI levels after elective PCI.


   Acknowledgement
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgement
References
 
The authors are greatly indebted to Dr Ayse Canan Yazici for statistical analysis. No financial support from any organization was used.

Conflict of interest: none of the authors has associations that might pose a conflict of interest.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgement
 References
 

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