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Microvascular obstruction is a major determinant of infarct healing and subsequent left ventricular remodelling following primary percutaneous coronary intervention

Stein Ørn, Cord Manhenke, Ole Jacob Greve, Alf Inge Larsen, Vernon Vijay Singh Bonarjee, Thor Edvardsen, Kenneth Dickstein
DOI: http://dx.doi.org/10.1093/eurheartj/ehp219 1978-1985 First published online: 6 June 2009


Aims We studied the time-dependent relationships between microvascular obstruction (MO), infarct size, and left ventricular (LV) remodelling after acute myocardial infarction (MI).

Methods and results Forty-two consecutive patients with first-time ST-elevation MI, single-vessel disease, successfully treated with primary percutaneous coronary intervention (PCI) were included. Microvascular obstruction, infarct size, and LV remodelling were assessed by cardiac magnetic resonance. Cardiac magnetic resonance was performed at: 2 days, 1 week, 2 months, and 1 year following PCI. Microvascular obstruction was assessed by first-pass perfusion. Patients were divided into three groups according to the presence or absence of MO at 2 days and 1 week: no detectable MO at any time point (11 patients), MO detectable only at 2 days (16 patients), and MO detectable both at 2 days and 1 week (15 patients). In multivariable analysis adjusting for infarct size at 2 days, detectable MO at 1 week was an independent predictor (P = 0.003) of infarct size at 1 year follow-up, associated with adverse infarct healing, adverse LV remodelling, increased LV volumes, and lower ejection fractions when compared with the rest of the cohort.

Conclusion Microvascular obstruction is an important determinant of infarct healing. The effect of MO on infarct size translated into distinct patterns of LV remodelling during long-term follow-up.

Clinical study no.: NCT 00465868

  • ST elevation myocardial infarction
  • Primary percutaneous coronary intervention
  • Microvascular obstruction
  • Infarct size infarct healing
  • Left ventricular remodelling
  • Cardiac magnetic resonance
  • Temporal relationships


Infarct size is a major determinant of left ventricular (LV) remodelling following myocardial infarction (MI).1 Recent studies suggest that infarct size may be a more important predictor of outcome than LV ejection fraction (LVEF)2,3 following MI. The presence of microvascular obstruction (MO) has been related both to LV remodelling and adverse outcome.4,5 There are limited data on the complex interrelationship between MO, infarct healing, and LV remodelling; no study has addressed the time-dependent changes in these relationships. Comprehension of the temporal associations between infarct size, MO, and LV remodelling is important for our understanding of the pathophysiology following acute MI. Appreciation of these relationships is also important for treatment strategies in this patient population. We therefore studied the time-dependent relationships between MO, infarct size, and LV remodelling. Cardiac magnetic resonance (CMR) was used as a reference method for serial assessment of infarct size, MO, and LV remodelling during 1 year of follow-up in patients with ST-elevation MI (STEMI), occluded single-vessel disease, successfully revascularized by primary percutaneous coronary intervention (PCI). Patients were examined by CMR four times during the first year following primary PCI: 2 days, 1 week, 2 months, and 1 year. Microvascular obstruction was assessed by first-pass perfusion (FPP). In order to study the effects of the duration of MO, patients were divided into three groups according to the presence or absence of detectable MO at 2 days and 1 week: no detectable MO at any time point (‘no MO’), detectable MO only at 2 days (‘MO 2 days’), detectable MO both at 2 days and 1 week (‘MO 1 week’).



Forty-six consecutive patients admitted to our hospital treated with primary PCI were prospectively enrolled. The diagnosis of STEMI was defined by typical chest pain and ST-elevation on ECG at admission.6 Patients were included if they had no previous MI, demonstrated acute proximal/mid-occluded single-vessel disease, and underwent successful PCI with stent implantation without significant residual stenosis. Patients were excluded if they had evidence of previous MI based on any source, such as history, ECG findings, or evidence of MI from angiography, or in more than one vascular territory on CMR examination. Patients were required to have no contraindications to CMR imaging. Patients with evidence of re-infarction during the first week were excluded from the study. All patients were treated with aspirin, heparin, clopidogrel, and statins in relation with the PCI procedure. Other medication was prescribed by the treating physician without the knowledge of the CMR results. Blood samples were taken from all patients, during hospitalization and at each CMR assessment. The blood-sampling protocol and the assessment of Troponin T (TnT) and N-terminal pro B-type natriuretic peptide (NT-proBNP) have been described previously.7 All patients were followed up with an exercise ECG within 6 months following PCI, and patients with signs or symptoms of restenosis underwent repeat angiography. 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 four times: 2 days, 1 week, 2 months, and 1 year following PCI (Figure 1). The CMR images were ECG gated and obtained during breath hold. Patients were scanned in a supine position by a 1.5T whole body scanner (Intera R10.3 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. In-plane resolution was 1.3 × 1.3 mm2 with a slice thickness of 8 mm and inter slice gap of 2 mm. The whole LV was covered with 10–14 contiguous slices. Left ventricular mass, LVEF, and volumes were determined using short-axis volumetry.

Figure 1

Typical pattern of microvascular obstruction (MO) in a patient with ST-elevation myocardial infarction due to an occluded left anterior descending artery, treated with primary percutanous coronary intervention (PCI). Images are short-axis views, right ventricle (RV), left ventricle (LV). (A) Microvascular obstruction is visualized on first-pass perfusion with a gadolinium-based contrast agent as areas of reduced signal intensity (black areas) within the myocardium. Microvascular obstruction areas are smaller in size at 1 week and are absent 2 months following myocardial infarction. (B) With the use of a gadolinium-based contrast agent, the late enhancement technique visualize infarcted myocardium as white areas. Non-infarcted myocardium is black. Areas of MO are seen as black regions within the white areas at 2 days and 1 week, but not at 2 months.

For FPP, a turbo field echo sequence with three short-axis slices per heart beat (prospective triggering) and a selective saturation recovery prepulse were used. In plane resolution typically 1.4 × 1.4 mm2, slice thickness was 10 mm. A dosage of 0.075 mmol/kg gadolinium-based contrast agent (Omniscan®, Amersham Health) was infused via an antecubital vein at a rate of 6 mL/s, and images were acquired for 60 heartbeats immediately following contrast infusion. Immediately following the completion of the first-pass imaging, another 0.175 mmol/kg of contrast agent was infused, and 10–15 min following the latter infusion delayed hyper enhancement (DHE) images were acquired, using an inversion recovery prepared T1 weighted gradient-echo sequence,8 with a pixel size of 0.82 × 0.82 mm2, covering the whole ventricle with short-axis slices of 10 mm thickness, without inter-slice gap. Inversion time was individually adapted aiming to null normal myocardium (typically 200–300 ms). To aid the assessment of apical portions of the ventricle, six images were recorded with 30° separation through the long axis of the LV.

All post-processing was performed using the View Forum™ Software (Philips Medical Systems, Best, The Netherlands). Assessments of LV volumes, mass, as well as myocardial infarct size were performed in a random, blinded fashion, and indexed for body surface area.9 Infarct size was assessed manually with planimetry on each short-axis slice, delineating the hyperenhanced area including areas of hypoenhancement surrounded by the hyperenhanced area, the latter considered a sign of MO. The same density (1.05 g/cm3) was assumed for both hyperenhanced (infarcted) and non-hyperenhanced (non-infarcted) myocardium. Transmurality was calculated as the average transmurality of all segments with evidence of infarction in a 17-segment model. Non-scarred LV mass index was calculated by subtracting scarred myocardial mass index from LV mass index. Microvascular obstruction was identified on FPP images as an area of persistent subendocardial hypoenhancement.10 The presence of MO was assessed by two experienced observers (S.Ø., O.J.G.) in a random fashion unaware of the other assessments. The size of FPP MO was assessed as a percentage of LV mass.


Continuous variables are expressed as mean ± standard error of mean (SEM). Non-parametric tests (Kruskal–Wallis ANOVA) were used to test for differences among the three groups at each time point, followed by Mann–Whitney U-tests where appropriate to examine for differences between groups. Friedman's 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. General linear models were used for the multivariable analyses that included infarct size, transmurality, infarct-related artery, and MO group as independent variables. In order to assess the temporal effects of MO in the early phase following MI, patients were categorized according to the presence or absence of detectable MO at 2 days and 1 week following MI. A mixed effects model was used to assess the time-dependent changes in the relationship between infarct size and remodelling. A two-tailed P-value of less than 0.05 was considered significant. For all statistical analyses, a commercially available statistical package (SPSS system 14.0) was used.


Baseline characteristics

A total of 46 patients were included in the study. Two patients withdrew from the study following the first CMR examination and two patients had re-infarctions between the first and second CMR assessments. With the exception of one patient who was unable to attend the final CMR examination at 1 year, all 42 patients underwent all CMR examinations. The first CMR examination was performed at a mean of 2.2 ± 0.1 days following PCI, the second at 7.3 ± 0.1 days, the third at 61 ± 0.6 days, and the fourth 364 ± 1.2 days following PCI. In 11 (26%) patients, there was no evidence of FPP MO at any time point (‘no MO’), 16 (38%) patients showed MO at 2 days but not at 1 week (‘MO 2 days’) and 15 (34%) patients demonstrated MO both at 2 days and 1 week (‘MO 1 week’).

At 2 days, there was a highly significant (P<0.0001) difference in MO size between patients with ‘MO 2 days’ (5.4 ± 0.8%) compared with ‘MO 1 week’ patients (16.1 ± 2.7%). Of note, there was no difference (P = 0.25) between the three groups in average transmurality of the infarctions at 2 days: 63 ± 4% in patients with ‘no MO’, 61 ± 2% in patients with ‘MO 2 days’, and 70 ± 4% in patients with ‘MO 1 week’. Patient characteristics are presented in Table 1. Seven patients were re-assessed with coronary angiography due to suspected recurrent ischaemia (‘no MO’: n = 3, ‘MO 2 days’: n = 1,‘MO 1 week’: n = 2). All events occurred between 2 months and 1 year. Restenosis was discovered in two of these patients (‘no MO’: n = 1,’MO 1 week’: n = 1) and both were successfully treated with PCI.

View this table:
Table 1

Baseline characteristics

Variables‘No MO’ (n = 11)‘MO 2 days’ (n = 16)‘MO 1 week’ (n = 15)P-value
Age (years)60 ± 356 ± 359 ± 40.70
Male sex9 (82%)13 (81%)12 (80%)0.99
Body surface area (m2)1.9 ± 0.12.0 ± 0.052.0 ± 0.040.44
Systolic blood pressure (mmHg)131 ± 7140 ± 4146 ± 90.27
Diastolic blood pressure (mmHg)77 ± 782 ± 492 ± 60.17
Heart rate (min−1)75 ± 571 ± 376 ± 60.75
 Pre-infarction angina4 (36%)9 (56%)3 (20%)0.22
 Current smoker2 (18%)11 (69%)7 (47%)0.04
 Diabetes mellitus1 (9%)0 (0%)2 (13%)0.35
 Hypertension3 (27%)2 (13%)5 (33%)0.39
Cholesterol (mmol/L)5.9 (1.2)5.8 (1.1)5.3 (0.8)0.23
TnT prior to PCI (µg/L)0.16 ± 0.10.15 ± 0.070.15 ± 0.040.39
Time from symptoms to reperfusion (min)234 ± 53241 ± 42288 ± 550.81
ECG changes
 Q-waves prior to PCI3 (27%)5 (33%)6 (43%)0.79
 Culprit vessel
  Left anterior descending artery6 (54%)5 (31%)10 (67%)0.14
  Right coronary artery5 (46%)8 (50%)4 (27%)0.40
  Circumflex artery0 (0%)3 (19%)1 (7%)0.25
Lesion location (proximal/mid/distal)3/8/08/7/17/7/10.74
Patients with more than one stent2 (18%)4 (27%)4 (26%)0.81
Drug eluting stents2 (18%)1 (6%)1 (7%)0.53
Thrombus aspiration5 (46%)11 (69%)8 (53%)0.46
TIMI flow Post-PCI (3/2)9/215/111/40.32
 GpIIb/IIIa antagonists8 (73%)11 (69%)12 (80%)0.78
 Heparin11 (100%)16 (100%)15 (100%)1.0
 Clopidogrel11 (100%)16 (100%)15 (100%)1.0
 ASA11 (100%)16 (100%)15 (100%)1.0
 Statin11 (100%)16 (100%)15 (100%)1.0
 ACEI/ARB11 (100%)14 (88%)13 (87%)0.41
 Beta-blocker4 (36%)9 (56%)10 (67%)0.31
 Aldosterone antagonist0 (%)3 (19%)5 (33%)0.11

Microvascular obstruction assessed by first-pass perfusion (FPP) vs. delayed hyper enhancement (DHE)

Microvascular obstruction was detectable on DHE images in 14 patients at 2 days and in 9 patients at 1 week following primary PCI. Delayed hyper enhancement MO was only found in patients with detectable MO by FPP: at 2 days MO was detectable on DHE images in 11 of 15 (73%) patients with ‘MO 1 week’ and in 3 of 16 (19%) patients with ‘MO 2 days’. At 1 week, 9 of 15 (60%) patients with ‘MO 1 week’ had evidence of MO by DHE. Multivariable models were constructed comparing the relationship between infarct size at 1 year and MO assessed by DHE vs. FPP. All models included infarct-related artery, transmurality, and infarct size at 2 days as independent variables. At 2 days, both MO assessed by DHE (P = 0.02, R2 = 0.68) and FPP (P = 0.04, R2 = 0.67) were related to infarct size at 1 year. In contrast, at 1 week only FPP MO (P = 0.004, R2 = 0.70) was significantly related to infarct size at 1 year. Therefore, only the results of FPP MO will be reported.

Microvascular obstruction, infarct size, and left ventricular volumes

There were significant differences in LV end-diastolic volume index (LVEDVI) and end-systolic volume index (LVESVI) and infarct size between the three MO groups at all time points (Figure 2AD); the largest difference was found at 1 year (Table 2). Importantly and in contrast to the other groups, LVEF did not improve in ‘MO 1 week’ during 1 year follow-up. The presence of MO influenced transmurality (Figure 3) and reduction in infarct size (Figure 2A). In contrast to the significant reduction in infarct size in ‘no MO’ patients (P = 0.01) and in ‘MO 2 days’ patients (P = 0.001), there was no reduction in infarct size during the first week in ‘MO 1 week’ patients (P = 0.11). Similarly, there was no significant reduction (P = 0.46) in infarct size between 2 months and 1 year in patients with ‘MO 1 week’ when compared with a small but significant reduction in the other patients (P < 0.0001). Initial infarct size and MO group were the only independent predictors for infarct size at 1 year follow-up (P < 0.0001 and P = 0.008, respectively) correcting for transmurality at 2 days and infarct-related artery (Table 3). In contrast to MO duration, MO size at 2 days was not an independent variable of infarct size at 1 year. There was no change in non-infarcted myocardial mass between 2 days and 1 year for any group.

Figure 2

The relationship between the presence of MO and: (A) infarct size, (B) left ventricular ejection fraction (LVEF), (C) left ventricular end-systolic volume index (LVESVI), (D) left ventricular end-diastolic volume index (LVEDVI) at: 2 days, 1 week, 2 months, and 1 year following successful primary PCI. Dots and vertical bars represent mean and standard error of mean, respectively.

Figure 3

The figure displays the change in transmurality between 2 days (x-axis) and 1 year (y-axis) in relation to the presence and duration of MO. All myocardial segments are conventionally classified according to the transmural extent of infarction at 2 days: 0: no infarction, 1: 1–25%, 2: 26–50%, 3: 51–75%, 4: 76–100% transmurality. The y-axis displays the mean transmurality at 1 year.

View this table:
Table 2

Differences in cardiac magnetic resonance recordings between 2 days and 1 year

‘No MO’ (mean ± SEM)‘MO 2 days’ (mean ± SEM)‘MO 1 week’ (mean ± SEM)P-value
End-diastolic volume index (mL/m2)
 2 days79.5 ± 5.091.8 ± 3.195.2 ± 2.90.03
 1 year74.7 ± 5.091.1 ± 4.3100.7 ± 6.80.007
 Per cent change−5.5 ± 3.4−0.5 ± 4.04.9 ± 4.60.47
End-systolic volume index (mL/m2)
 2 days40.0 ± 3.647.1 ± 3.155.2 ± 3.20.03
 1 year29.4 ± 3.941.8 ± 2.755.9 ± 6.50.001
 Per cent change−28.1 ± 3.8−9.2 ± 4.91.7 ± 5.80.003
Left ventricular ejection fraction (%)
 2 days50.5 ± 2.849.3 ± 2.442.9 ± 2.00.09
 1 year61.8 ± 3.054.7 ± 1.345.4 ± 2.6<0.001
 Per cent change23.7 ± 5.213.9 ± 4.45.9 ± 3.70.05
Infarct size (g/m2)
 2 days10.8 ± 1.816.2 ± 1.620.0 ± 2.00.01
 1 year3.7 ± 0.98.5 ± 0.814.2 ± 2.0<0.001
 Per cent change−66.1 ± 6.7−43.7 ± 5.1−29.9 ± 3.9<0.001
Non-infarcted myocardial mass (g/m2)
 2 days51.4 ± 2.748.8 ± 1.749.8 ± 2.70.69
 1 year47.4 ± 2.848.2 ± 1.850.1 ± 2.90.77
 Per cent change−7.0 ± 4.7−0.4 ± 3.32.2 ± 5.60.43
  • P-value denotes significant differences between the three MO groups (Kruskal–Wallis).

View this table:
Table 3

Multivariable model (general linear model) including MO categories, infarct size at 2 days, transmurality of the infarction, and infarct-related artery

Dependent variable: infarct size (g/m2) 1 year following MI
Infarct size 2 days0.600.12<0.0001
‘MO 1 week’5.731.800.003
‘MO 2 days’2.061.670.23
‘no MO’0a
Transmurality 2 days−1.441.700.40
  • The table demonstrates that the presence of MO at 1 week is an independent predictor of infarct size at 1 year, after correction for infarct size, transmurality, and infarct-related artery. This model explained 72% of the variance (R2 = 0.72) of infarct size at 1 year.

  • aThese parameters are set to zero as they serve as references.

Microvascular obstruction, N-terminal pro B-type natriuretic peptide, and Troponin T

The profiles of TnT are illustrated in Figure 4. In multivariable analysis, including infarct size at 2 days, there was no independent effect of MO on NT-proBNP levels. In contrast, at 2 days, both infarct size (P < 0.0001) and ‘MO 1 week’ (P < 0.0001) were independent predictors of max TnT levels at a median of 11 h following PCI (R2 = 0.78). Only persistent MO (P = 0.003) was an independent predictor of TnT levels at 1 week (R2 = 0.38).

Figure 4

The figure displays the time profiles of Troponin T (TnT) during the first week following primary PCI, categorized according to MO group. Blood samples were acquired prior to PCI, and at each CMR examination. An extra blood sample (max TnT) was acquired according to hospital routines mean 11 h following PCI. Bars and vertical lines represent mean and ± SEM.

Infarct size and left ventricular remodelling

There were strong correlations between infarct size and LVEDVI, LVESVI, and LVEF at corresponding time points during 1 year follow-up (Figure 5). These correlations were augmented over time, as demonstrated by the statistically significant (P < 0.001) increase in the slope of the relationship between infarct size and both LV volumes and LVEF during the observation period (Figure 5). At corresponding time points, infarct size was the only independent predictor (P < 0.0001) of LVEDVI, LVESVI, and LVEF in a multivariable model which included infarct-related artery and transmurality.

Figure 5

Time-dependent relationship between infarct size and indices of left ventricular (LV) remodelling and function [LV end-diastolic volume index (LVEDVI), LV end-systolic volume index (LVESVI), LV ejection fraction (LVEF)] 2 days, 1 week, 2 months, and 1 year following ST-elevation myocardial infarction treated with primary PCI.


This study is the first human study to use multiple contrast enhanced CMR assessments to explore temporal changes in the relationship between MO, infarct size, and LV remodelling following primary PCI in STEMI. This study demonstrates that the duration of MO is a major independent determinant of the size of the healed MI and subsequent remodelling of the LV. Moreover, distinct time-dependent patterns of infarct healing and LV remodelling were found implying that the timing of CMR examination is important for the assessment of infarct size and prediction of LV remodelling in patients following acute MI.

Microvascular obstruction, infarct size, and the healing process of myocardial infarction

The time course of resorption of hyperenhanced volume on CMR is directly related to the removal of necrotic tissue and inversely related to the deposition of connective tissue within the infarction.11 We found a time-dependent reduction in hyperenhanced volume (infarct size) that was strongly related to the presence and duration of MO (Figures 2A and 3). In multivariable models adjusting for infarct size at 2 days, ‘MO 1 week’ was an independent determinant of infarct size at 1 year (Table 3). In these patients, a significant reduction in infarct size was only observed between 1 week and 2 months. This finding was in contrast to the two other groups that demonstrated a significant shrinkage in infarct size between all time points. The presence and duration of MO also appeared to influence TnT levels: in patients with ‘MO 1 week’, there was an increased maximal TnT release independent of infarct size, suggesting a more severe myocardial damage within the infarcted territory. Moreover, persistent MO was associated with prolonged elevation of TnT levels independent of initial infarct size. Interestingly, in the same population, we recently demonstrated that there is an increased acute inflammatory response in patients with persistent MO.7 However, in accordance with a previous study that did not demonstrate an independent relationship between infarct size and NT-proBNP, there was no independent relationship between MO and NT-proBNP.12 Taken together, these data support that persistent MO at 1 week is a different entity than MO resolving during the first week, possibly reflecting more severe damage to myocardial architecture. Future studies should address the pathophysiology of MO. Assessment of haemorrhage is particularly encouraged since myocardial haemorrhage may affect infarct healing and LV remodelling.13,14

Infarct size and left ventricular remodelling

At all time points, infarct size was the major determinant for LV volumes and LVEF (Figure 5). This finding is in accordance with prior observations in long-term survivors of MI.1 The major changes in LV volumes occurred within the first 2 months. These changes in LV volumes coincide with infarct healing and the reduction in infarct size observed during this time frame. However, the relationship between infarct size and LV volumes became increasingly strong over time, and there is a statistically highly significant increase (P < 0.0001) in the beta value of the regression line for the relationship between LV volumes and infarct with time (Figure 5). Our data indicate that, while most LV remodelling occurs by 2 months after STEMI, this process continues at least to 1 year, particularly for patients in whom MO is prolonged after the acute event. The effect of MO on infarct size translated into three distinct patterns of LV remodelling during follow-up (Figure 2BD): patients with normal wound healing (‘no MO’), patients that dilate but manage to adapt functionally (‘MO 2 days’), and patients that dilate without the ability to functionally adapt (‘MO 1 week’). These findings underscore the impact of the temporal effects of MO on scar size and subsequent LV remodelling.

Assessment of microvascular obstruction

This study used FPP as the primary assessment of MO, as FPP compared with the other techniques has a higher sensitivity for the detection of MO.10,15 In accordance with these publications, we found that MO was more frequently detected by FPP compared with DHE. However, MO detected by DHE was more frequently observed in patients with the most severe MO. At 2 days, both MO detected by DHE and FPP predicted infarct size at 1 year. In contrast, at 1 week, only FPP MO was a predictor of infarct size at 1 year. Taken together, these findings support previous observations that FPP and DHE may reflect different aspects of myocardial damage following MI.10 Moreover, our results suggest that the timing of assessment may be important for the diagnostic accuracy of these techniques.

Clinical implications

Several important clinical implications are suggested by these findings. First, the results underscore the impact of the temporal effects of MO on scar size and subsequent LV remodelling, and emphasize the need to take these important effects into consideration when designing management strategies. Second, MO-related effects on LV remodelling occur early, and significant changes can be observed within the first week following MI. Third, these early changes appear to have long-term detrimental effects on LV remodelling and may identify high risk patients who should be targeted for comprehensive anti-remodelling therapy. Fourth, MO remains an important determinant for LV remodelling in spite of adequate treatment with inhibitors of neurohormonal activation. It is therefore reasonable to assume that early treatment strategies that reduce MO are likely to attenuate LV remodelling. Fifth, the present study provides data facilitating calculation of sample size for larger studies by describing the relationship between infarct size and LV remodelling at different time points (Figure 5).


The following limitations should be noted: first, the relatively 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. The cohort therefore represents a unique and homogenous patient sample that facilitates interpretation of the prospectively selected parameters. Second, treatment of the present cohort was according to conventional guidelines. As expected, there was a non-significant trend towards an increased use of comprehensive neurohormonal inhibition in patients with decreased LV function. The use of neurohormonal inhibition has been shown to attenuate LV remodelling following MI.16 If less comprehensive neurohormonal inhibition had been administered, a larger difference in LV remodelling might have been anticipated. Therefore, the observed incremental use of comprehensive neurohormonal inhibition in the patients with the most severe MO should not compromise our results. Moreover, our results on LV remodelling only applies to patients treated with neurohormonal inhibition. Third, the use of CMR in the assessment of these patients represents a selection bias. Patients who are to be assessed by CMR need to cooperate and remain in a supine position for the entire duration of the examination, which require breath holds. As demonstrated by Figure 4, there is one extremely large value for one patient at 1 year and partly also at 2 months. Such an extreme value will influence the slope and the correlation. However, since the value of this extreme case is plausible, it will in this case not greatly alter the fit, but it will slightly inflate the correlation at these time points.


Infarct size is the major determinant of LV remodelling at all time points following successful restoration of epicardial blood flow in patients with STEMI. There are large dynamic changes in infarct size reflecting the different phases of infarct healing and scar formation. The presence and duration of MO are important determinants of infarct healing. The presence of MO 1 week after primary PCI was associated with attenuated infarct healing, increased volumes, and subsequent reduction in LV function at long-term follow-up. Detection of MO 1 week following MI may identify patients of high risk for adverse LV remodelling likely to benefit from aggressive pharmacological therapy.


The study was financed by Helse Vest grant no. 911017, and The Norwegian Association of Heart and Lung Patients, Helse og Rehabilitering grant no. 2003/2/0211 and SR-Bank Fund for Public Welfare Purposes.

Conflict of interest: none declared.


The authors wish to thank Torbjørn Aarsland, Jorunn Nielsen, Fredrikke Wick, Bent Erdal, Tore Wentzel-Larsen and Christian Lycke Ellingsen for their important contributions during the study.


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