Methods

The present single-center, retrospective cohort study included patients with STEMI who were treated with primary percutaneous coronary intervention from March 2010 to March 2011 from an ongoing clinical registry. The patients were treated according to the institutional protocol (MISSION!), based on the most recent international guidelines. Our protocol includes a prehospital, in-hospital, and outpatient framework for clinical decision making and treatment of patients with acute myocardial infarction ≤1 year after discharge. Since the implementation of the protocol in 2004, the data from consecutive patients with STEMI were prospectively collected in the departmental electronic patient information system (EPD-Vision). The MISSION! care program is the standard of acute myocardial infarction care in the district of Hollands-Midden, The Netherlands.

Consecutive patients with STEMI were eligible for inclusion when presenting with symptoms of acute myocardial infarction, with an electrocardiogram demonstrating STEMI (ST-segment elevation of ≥0.2 mV in ≥2 contiguous leads in V ₁ through V ₃ or ≥0.1 mV in other leads) and a typical rise and/or fall course of cardiac biomarker levels. At least 1 value of hs-cTnT had to exceed the diagnostic decision limit (0.05 μg/L) in the present study based on clinical experience. Furthermore, treatment according to the protocol, including primary percutaneous coronary intervention and monitoring at the MISSION! outpatient clinic, was required. The exclusion criteria were a history of acute myocardial infarction and severe renal failure (serum creatinine >2.5 mg/dl). All patients received pharmacotherapy according to the MISSION! care program, including upfront abciximab, periprocedural heparin, in-hospital enoxaparin, and loading and maintenance doses of aspirin and clopidogrel. After discharge, the patients were treated with dual antiplatelet therapy, β blockers, angiotensin-converting enzyme inhibitors, and statins. The patients were examined at the outpatient clinic at 30 days and 3, 6, and 12 months. At 3 months, echocardiography and radionuclide ventriculography were performed to assess LV function.

For the measurements of the cardiac biomarkers, serum samples were obtained at presentation and subsequently at 6-hour intervals for 48 hours after the primary percutaneous coronary intervention. The samples were centrifuged immediately after collection, followed directly by measurements of cTnT in serum. The cTnT concentration was assayed using the fifth-generation cTnT reagent (Roche Diagnostics, Indianapolis, Indiana) using Modular E analyzers, with a 99th percentile upper reference limit of 0.014 μg/L. The hs-cTnT values at 6, 12, 18, and 24 hours after the onset of symptoms were retrospectively calculated by interpolation of the serial 6-hour samples collected during the hospitalization.

CK activity was measured at 37°C with an International Federation of Clinical Chemistry and Laboratory Medicine-traceable method (Roche Diagnostics) using Modular P analyzers. The upper reference limit was 200 U/L. As a measure of infarct size, the quantity of CK cumulatively released in the first 48 hours after the onset of symptoms was calculated using the 2-compartment model, which has been previously described in detail. In a few patients, the 48-hour cumulative CK release could not be calculated owing to a lack of samples during the first 48 hours. In those patients, the 48-hour cumulative CK release was estimated by multiplying the quantity of cumulatively released CK after 24 hours (if available) with the average ratio between 24- and 48-hour cumulative CK release (1:1.50) of patients with both quantities available. The laboratory staff and investigators responsible for the measurements and calculation of the biomarker parameters were unaware of the patient data.

All patients underwent 2-dimensional echocardiography 3 months after discharge in the left lateral decubitus position (Vivid 7 and e9, GE-Vingmed Ultrasound AS, Horten, Norway). Images were acquired during breath hold using a 3.5-MHz transducer in the parasternal and apical views with simultaneous electrocardiographic signal and saved in cine-loop format. The analyses were performed offline (EchoPac, version 110.01, GE-Vingmed). The left ventricle was divided into 16 segments. The segments were analyzed individually and scored according to the degree of motion and systolic thickening (1, normokinetic; 2, hypokinetic; 3, akinetic; and 4, dyskinetic). The wall motion score index was calculated by dividing the sum of all segment scores by the number of segments and considered to be a measure of LV function.

Single photon emission computed tomography was routinely performed 3 months after discharge. Since January 2011, routine stress echocardiography was implemented in the MISSION! protocol as a replacement. Therefore, single-photon emission computed tomography was performed in a subgroup of the present study population. The patients underwent myocardial perfusion imaging using technetium-99m tetrofosmin (500 MBq; Myoview, GE-Healthcare, Little Chalfont, Buckinghamshire, United Kingdom) including radionuclide ventriculography. Electrocardiographic gating was applied at 16 frames/cardiac cycle with a tolerance window of 50%. The images were acquired 45 minutes after tracer administration and processed after the procedure using the Corridor4DM, version 6.1, software (INVIA Solutions, Ann Arbor, Michigan). The automatically calculated LV ejection fraction at rest was considered to reflect LV function.

The patients were monitored at the MISSION! outpatient clinic for 1 year after discharge. Major adverse cardiac events were recorded and prospectively collected by attending cardiologists not involved in the present study. The vital status of the entire cohort was retrieved from the municipality records. Patients for whom ≥2.5 months of clinical follow-up data (other than vital status) were lacking were considered lost to clinical follow-up. Data were included until the last follow-up date. The clinical end point was defined as the composite of all-cause death, implantable cardioverter-defibrillator implantation, or any hospitalization for heart failure within 1 year.

The categorical variables are presented as numbers and proportions and continuous variables as mean ± SD or median and interquartile range. The correlations were evaluated using Spearman’s correlation. Linear regression analysis was performed to examine the association between the cTnT values and infarct size and LV function. First, clinical variables with p <0.10 on univariate analysis were included in the multivariate linear regression models. To prevent multicollinearity, a cTnT parameter was added one at a time to the multivariate model, keeping the combination of the other clinical variables in the model constant. The independent additional contribution of a cTnT parameter was determined by calculating the increase in the variation in outcome explained by the variables in the model (R ² ). To examine the predictive value of the cTnT values for the composite clinical outcome, Cox proportional hazards regression analysis was performed. Owing to the limited number of events, a stepwise forward selection procedure was performed, using clinical variables with p <0.05 on univariate analysis. Just as with the other outcomes, the predictive value of a cTnT parameter for this outcome was determined by adding 1 cTnT parameter at a time to the multivariate model, keeping all other variables constant. The magnitude of the effect on the adverse outcomes of the individual cTnT parameters was reflected by the hazard ratio. All p values were 2-sided, and p <0.05 was considered to be statistically significant. Analyses were conducted using SPSS, version 17.0.1, statistical analysis software (SPSS, Chicago, Illinois).

Results

The study population included 188 patients treated with primary percutaneous coronary intervention for a first STEMI. The baseline characteristics are summarized in Table 1 . The 12, 18, 24, and peak hs-cTnT values were missing in 5, 6, 7, and 11 patients, respectively, because of transfer or death within the first few hours after intervention. The median peak hs-cTnT value was 3.15 μg/L (interquartile range 1.21 to 7.22), median peak CK was 1,205 U/L (interquartile range 622 to 2,703). In the present population, discordant release patterns of cTnT and CK were occasionally observed. Plotting these release patterns revealed a prolonged plateau phase for cTnT, and the CK quantities quickly diminished to the normal steady state level ( Figure 1 ).

Discordant release patterns of CK and troponin T.

The 48-hour cumulative CK release was available for 177 patients. Of the 177 patients, it was calculated for 123 patients and was estimated using the aforementioned method for 54 patients. The peak and all fixed-time hs-cTnT values correlated significantly with the 48-hour cumulative CK release. The value at 24 hours after the onset of symptoms demonstrated the greatest correlation coefficient (r = 0.86; Figure 2 ) compared to the other hs-cTnT values (6-hour hs-cTnT, r = 0.53; 12-hour hs-cTnT, r = 0.70; 18-hour hs-cTnT, r = 0.85; and peak hs-cTnT, r = 0.83). Linear regression analysis (adjusted for gender, ischemic time, out-of-hospital cardiac arrest, number of diseased—major epicardial coronary—vessels, proximal lesion, preprocedural Thrombolysis In Myocardial Infarction flow, stent implantation, and multiple stents implanted) revealed that the peak and all fixed-time hs-cTnT values were independently associated with the 48-hour cumulative CK release ( Table 2 ). The 24-hour hs-cTnT value was demonstrated to have the greatest effect on 48-hour cumulative CK release, ensuring a substantial increase in the variation in outcome explained by the model (R ² ).

Spearman’s correlation between (A) 24-hour hs-cTnT value (hs-cTnT ₂₄ ) and 48-hour cumulative CK release (Q ₄₈ CK), (B) 24-hour hs-cTnT value and wall motion score index (WMSI) at 3 months, and (C) 24-hour hs-cTnT value and LV ejection fraction (LVEF) at 3 months.

Table 2

Multivariate linear regression analysis for 48-hour cumulative creatine kinase (CK) release, wall motion score index, and left ventricular (LV) ejection fraction

	β	Increase R 2	Total R 2	p Value
48-Hour cumulative creatine kinase release
High-sensitive cardiac troponin T
At 6 h	0.528	0.200	0.469	<0.001
At 12 h	0.648	0.313	0.582	<0.001
At 18 h	0.809	0.489	0.757	<0.001
At 24 h	0.835	0.513	0.782	<0.001
Peak	0.765	0.476	0.748	<0.001
Wall motion score index
High-sensitive cardiac troponin T
At 6 h	0.136	0.015	0.239	0.076
At 12 h	0.208	0.033	0.259	0.009
At 18 h	0.343	0.085	0.312	<0.001
At 24 h	0.357	0.093	0.318	<0.001
Peak	0.312	0.074	0.310	<0.001
LV ejection fraction (%)
High-sensitive cardiac troponin T
At 6 h	−0.271	0.064	0.253	0.005
At 12 h	−0.366	0.114	0.312	<0.001
At 18 h	−0.453	0.168	0.366	<0.001
At 24 h	−0.470	0.176	0.374	<0.001
Peak	−0.421	0.155	0.358	<0.001

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