Methods

The present study is a subanalysis of the prospective, randomized, multicenter abciximab intravenous versus intracoronary in ST-Elevation Myocardial Infarction (AIDA STEMI) trial. The study randomized 2,065 patients with STEMI reperfused by primary PCI <12 hours after symptom onset to either intracoronary or intravenous abciximab bolus. The trial showed no differences between the treatment groups with respect to the occurrence of major adverse cardiac events (MACE) after 90 days and 12 months. CMR was performed in 795 patients in the predefined AIDA CMR substudy. The design, rationale, and final results including the CMR substudy of AIDA STEMI have previously been published. The study was approved by national regulatory authorities and ethics committees of the participating centers. All patients provided written informed consent. Coronary angiography of the target vessel was performed before and after PCI with the same projections. Visual assessments were performed offline in the angiographic core laboratory by 2 blinded observers. Impaired coronary flow was defined by an initial TIMI flow ≤1 and preserved coronary flow was defined by an initial TIMI flow ≥2. CMR was performed between days 1 and 10 after infarction on a 1.5 or a 3.0 T scanner ( Figure 1 ). A standardized protocol was used to assess IS, MSI, MVO, and left ventricular (LV) ejection fraction and volumes as described before. In brief, cardiac edema imaging was conducted using T2-weighted imaging and cine sequences were used for analysis of function and volume and contrast-enhanced T1-weighted imaging for visualization of myocardial necrosis (15 minutes after contrast injection). Image analysis was performed by blinded observers in a CMR core laboratory. Certified CMR evaluation software (Circle CVI42; Calgary, Alberta, Canada) was used for the quantitative analyses. Semi-automated computer-aided threshold detection was used to identify regions of edema, hypointense core, infarcted myocardium, and MVO, as previously described. MSI was calculated as the area of myocardial edema minus IS divided by the area of myocardial edema multiplied by 100. The primary clinical end point of the study was the time to MACE defined as death, reinfarction, or new onset of congestive heart failure within 12 months after infarction, as previously described.

Contrast-enhanced image (late gadolinium enhancement) depicting a patient with STEMI with TIMI 0 flow of the right artery pre-PCI. (A) Short-axis and (B) 2-chamber view showing high signal intensity of the inferior and lateral wall indicating transmural necrosis.

Continuous data are presented in medians with interquartile range and were compared using the nonparametric Mann-Whitney U test. Categorical and ordinal variables are presented as counts and percentages. Differences between groups with categorical or ordinal variables were evaluated using Pearson’s chi-square test. Univariable and stepwise multivariable linear regression analyses were performed to identify predictors of IS, MVO, and MSI. Multivariable regression was performed using only variables with a p value <0.05 in univariate regression analyses. For univariate analyses, all variables listed in Table 1 were tested. The Kaplan-Meier estimator was used for survival and MACE calculation, and differences between groups were compared using the log-rank test. Univariable and stepwise multivariable Cox regression analyses were performed to identify predictors of MACE. Multivariate regression was again performed using only variables with a p value <0.05 in univariable regression analyses. A 2-tailed p value <0.05 was defined as statistically significant. IBM SPSS, version 23, was used for all statistical analyses.

Results

From July 2008 to April 2011, 795 patients were enrolled in the AIDA STEMI CMR substudy. Patients with previous infarction and incomplete or insufficient CMR data were excluded. The final study group comprised 738 patients ( Figure 2 ). The baseline characteristics are listed in Table 1 according to impaired or preserved TIMI flow before PCI. Most cardiovascular risk factors (smoking, hypertension, and diabetes mellitus) and reperfusion times did not differ significantly between the groups. In the impaired TIMI flow group, less patients had hypercholesterolemia and a higher peak CK value within 48 hours was observed ( Table 1 ). No significant differences could be found between groups regarding the number of diseased vessels and/or the infarct-related artery. Thrombectomy devices and intra-aortic balloon pumps were used more frequently in patients with impaired TIMI flow pre-PCI ( Table 1 ). The median time between the index event and CMR was 3 days (interquartile range 2 to 4 days) for both groups (p = 0.70). Most patients underwent CMR on a 1.5-T scanner (97%). The main findings from CMR analyses are presented in Table 2 . Almost all CMR parameters of myocardial injury showed significant differences between both groups. Patients with impaired TIMI flow had significantly larger IS, a higher extent of MVO, and less MSI. Impaired TIMI flow before PCI was an independent predictor of IS, MVO, and myocardial salvage ( Tables 3 to 5 ). Furthermore, there was a clear evidence for a graded inverse relation between TIMI flow pre-PCI and IS ( Figure 3 ) or MVO ( Figure 4 ) and a graded relation between TIMI flow pre-PCI and MSI ( Figure 5 ). The follow-up after 12 months was completed in all patients. The combined primary clinical end point and the individual clinical end points did not differ between both groups ( Table 6 ). Kaplan-Meier curves demonstrated also no significant differences according to the initial TIMI-flow pre-PCI ( Figure 6 ). Using Cox regression analysis, impaired TIMI-flow before PCI was not an independent predictor for MACE (data not shown).

Study flowchart.

Table 2

Cardiovascular magnetic resonance results

Variable	Total Study (n=738)	TIMI-flow grade		p-value
		0-1 (n=507)	2-3 (n=231)
Left ventricular ejection fraction (%)	51 (44-58)	49 (42-56)	55 (47-61)	<0.001
End-diastolic volume (ml)	146 (121-172)	149 (124-176)	138 (113-162)	<0.001
End-systolic volume (ml)	72 (54-91)	76 (58-96)	62 (48-82)	<0.001
Infarct size (%LV)	17 (8-25)	19 (12-27)	9 (3-18)	<0.001
Microvascular obstruction (%LV)	0.0 (0.0-1.7)	0.6 (0.0-2.7)	0.0 (0.0-0.2)	<0.001
Myocardial salvage (%)	17 (9-27)	17 (9-25)	18 (10-30)	0.01
Myocardial salvage index	51 (33-69)	46 (29-62)	65 (46-89)	<0.001
Hypointense core of infarcted myocardium	224/654 (34%)	189/447 (42%)	35/207 (17%)	<0.001
Hypointense core (%LV)	0.0 (0.0-1.6)	0.0 (0.0-2.7)	0.0 (0.0-0.0)	<0.001
Edema (%LV)	35 (25-48)	35 (25-47)	38 (27-49)	0.08

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